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10 Best CBD Oil for Arthritis & Joint Pain – 2021 Product …

Friday, May 14th, 2021

Many arthritis sufferers use CBD as an alternative remedy for easing joint pain. Weve put together a list of the best CBD oil for arthritis and a guide to help you get the most out of CBD.

Arthritis is a common condition characterized by joint pain and inflammation. The United States witnessed a significant increase in the prevalence of arthritis in recent years. Standard treatments typically focus on pain relief but arent always effective and can cause notable side effects.

As a result, more and more people are opting for safe, natural options such as CBD oil. Still, with so many products available and a lack of regulation, finding a high-quality CBD product can be difficult.

Thats why we researched and compared numerous leading brands to find the best CBD oil for arthritis as well as the best CBD cream.

Heres our list of the top 10 CBD oils and creams for this debilitating condition, based on the formula, potency, hemp source, third-party testing, pricing, and other factors.

CBD oil and topical CBD products are an increasingly popular option for arthritis sufferers. Although more research is needed, early studies[1] indicate that CBD and other cannabinoids may relieve the pain and inflammation involved in arthritis. Some of the suitable CBD oil for pain can be found here.

This means CBD can help with symptom relief in common types of arthritis, including osteoarthritis and rheumatoid arthritis.

Better yet, theres some evidence that CBD may have a positive effect on the inflammation that causes some types of arthritis, which means it may help the condition directly.

CBD can also offer indirect benefits for arthritis sufferers, such as improving sleep and mood-related issues.

In comparison, prescription drugs typically only focus on pain relief instead of improving the root cause of certain types of arthritis. They can also cause significant side effects and other issues such as withdrawal in the case of opioids..

Editors Choice

Spruce CBD

Why is it better?

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The Lineup At A Glance

Best Formula

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Most Natural

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For those who dont mind paying a little more for high-quality CBD from a family-run company with hundreds of satisfied customers, Spruce CBD is a solid pick.

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Spruce CBD was founded in North Carolina in 2018. The company stands out for being a relatively small, family-run business and having hundreds of satisfied customer reviews.

Spruce sources its CBD products from a 200-year-old strain of hemp grown organically in Kentucky and North Carolina. It uses a time-tested alcohol extraction process to create full-spectrum products rich in all of hemps beneficial components.

The company also posts detailed third-party test reports for everyone to see. Besides working well on adults, Spruce CBD is also safe for kids, which makes it one of the most popular choice on the market.

Spruces CBD oil comes in two strengths: regular, with 25 mg CBD per ml and 750 mg total, and high-strength, with 80 mg/ml and 2400 mg CBD in total. Both tinctures are formulated with hemp seed oil and the regular version is also flavored with peppermint.

The 2400 mg tincture may be particularly suited for arthritis thanks to its high potency.

If youre looking for a CBD oil designed for arthritis, CBDfxs wellness tincture is a great choice because it contains multiple anti-inflammatory ingredients backed by evidence-based research.

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CBDfx is an established CBD brand out of California. It offers many different kinds of CBD products with unique formulas, flavors, and other features that make it stand out from the competition.

CBDfx sources its hemp from organic farms in Kentucky. All of its products go through extensive third-party testing to verify their potency and safety.

CBDfxs unique take on CBD products can be seen with their wellness tincture. It contains not only CBD but also a large amount of CBG, another beneficial cannabinoid,

More importantly, this CBD oil carries two natural anti-inflammatory compounds that have been demonstrated to help with arthritis symptoms in research studies: coenzymeQ10[2] (CoQ10)- a rat-based study and curcumin[3] study in humans.

Thats why this CBD oil is especially suitable for dealing with arthritis. Its available in four strengths:

High-quality and all-natural ingredients are what makes Royal CBD a great option. Its all back by lab tests and a 30-day guarantee.

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CBD oils effectiveness in relieving pain is one reason people consider it as an option. Its also attractive because its a natural remedy, working with your bodys natural healing abilities. If its natural healing youre looking for, the Royal CBDs oil may be a good option for you.

Its derived from hemp that is organically grown, as well as grown in a sustainable way to ensure there will be more in the future. Once grown, the hemp is extracted using the CO2 process, which is the safest and cleanest option. You also wont find any added flavors in Royal CBD oil either, just the natural flavoring of the oil.

Some people prefer CBD oils that are as close to natural as possible. In that case, CBDPure is a decent option.

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Washingtons CBDPure has been around since 2016. The company offers a simple yet effective lineup of full-spectrum CBD oil, capsules, and cream sourced from organic hemp grown in Colorado and Washington.

As demonstrated by the companys third-party lab reports, the full-spectrum extract used in its products contains significant amounts of minor cannabinoids like CBC, CBDV, and CBG.

Thats a sign of a high-quality full-spectrum product since these compounds add to the beneficial effects of CBD.

CBDPure offers a 60 ml CBD oil containing full-spectrum CBD extract blended with hemp seed oil and no other extra ingredients. It comes in three strengths:

This isnt the most potent CBD oil on the market. However, if youre looking for a quality low-medium potency tincture made with pure ingredients, CBDPure fits the bill. We also have details of CBDPure brand you can read here.

Medterra is a top-tier CBD brand with competitive prices and is a particularly great option when you need pure CBD oil without any other active ingredients.

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Founded in 2017, Medterra is a leading CBD company known for offering quality products at affordable prices. All of its offerings are completely free of THC and sourced from organic hemp cultivated in Kentucky.

Medterra publishes detailed third-party lab test reports of its products. The company is also certified by the U.S. Hemp Authority, which means it passed a strict independent audit confirming that it follows strict hemp manufacturing standards.

Some people prefer to use CBD oil containing pure CBD (also called isolate) for arthritis and other conditions. In that case, Medterra is a great choice. Its CBD oil comes in three strengths:

It has a straightforward formula combining CBD isolate with coconut MCT oil.

Joy Organics is a good choice when you need CBD oil that doesnt contain any THC but still provides all of the cannabinoids, terpenes, and other beneficial hemp compounds alongside CBD.

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Joy Organics is a family-run CBD company out of Fort Collins, Colorado. It differentiates itself by offering only broad-spectrum CBD products.

Broad-spectrum CBD is a type of whole-plant hemp extract that contains all of the plants beneficial cannabinoids, terpenes, flavonoids, and other ingredients, but with zero THC.

In that sense, its ideal for those who want to get the most out of hemp while completely avoiding THC.

Joy Organics products are derived from organic Colorado-grown hemp. Theyre comprehensively tested by a third-party lab to make it easy to verify their potency and safety. It is also found to be the best CBD for high blood pressure patients

Joy Organics offers broad-spectrum CBD oil in four strengths:

It uses virgin olive oil as the carrier oil and has four flavor options natural, tranquil mint, summer lemon, and orange bliss.

NuLeaf Naturals is one of the most respected names in the U.S. CBD industry, known particularly for its high-quality full-spectrum CBD oil tinctures.

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Founded in 2014 in Colorado, NuLeaf Naturals is one of the leading CBD brands in the country. Until recently, NuLeaf sold only one type of CBD product full-spectrum CBD oil which highlights the companys unrivaled expertise and a strong reputation.

NuLeaf uses organic Colorado-grown hemp-extracted with CO2 to make its products, which undergo comprehensive third-party testing for cannabinoid levels and contaminants.

The test results confirm that NuLeafs full-spectrum CBD extracts contain the full range of beneficial cannabinoids.

The best CBD oil for arthritis should use a potent, full-spectrum formula, and NuLeaf Naturals certainly meets that requirement.

Its CBD oil has a high potency of 60 mg per ml and comes in five bottle volumes ranging from 5 ml to 100 ml, with 300-6000 mg of CBD. Its formulated with hemp seed oil without any added flavoring.

Many people with arthritis prefer a high-potency CBD oil for significant relief. In that case, CBDistillery is an excellent pick because it offers tinctures containing as much as 167 mg of CBD per ml.

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One of the biggest names in the CBD industry, CBDistillery was founded in Colorado in 2016. The company offers a full range of affordable, high-quality CBD products with multiple strength options.

Theyre derived from organic hemp grown in Colorado and tested by a third-party lab to confirm their potency, safety, and consistency.

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10 Best CBD Oil for Arthritis & Joint Pain - 2021 Product ...



Friday, May 14th, 2021

Practicing these habits can slow down OA, keep you healthy and put off surgery as long as possible.

Maintain a Healthy Weight

Excess weight worsens OA. Combine healthy eating with regular exercise to maintain a healthy weight.

Control Blood Sugar

Many people have diabetes and OA. Having high glucose levels can make cartilage stiffer and more likely to break down. Having diabetes causes inflammation, which also weakens cartilage.

Maintain Range of Motion

Movement is medicine for joints. Make a habit of putting your joints through their full range of motion, but only up to the point where it doesnt cause more pain. Gentle stretching, raising and lowering legs from a standing or seated position, daily walks and hobbies such as gardening can help. But listen to your body and never push too hard.

Protect Joints

Make sure to warm up and cool down when doing exercise. If you play sports, protects joints with the right gear. Use your largest, strongest joints for lifting, pushing, pulling and carrying. Watch your step to prevent falls. Balance rest and activity throughout the day.


Find ways to reduce or avoid stress through meditation, listening to music, connecting with friends and family, doing fun activities, and finding ways to relax and recharge.

Choose a Healthy Lifestyle

Eating healthy food, not smoking, drinking in moderation and getting good sleep will help you to feel your best.



Is there a link between mouth bacteria and rheumatoid arthritis? – Medical News Today

Friday, May 14th, 2021

An estimated 1.5 million people living in the United States alone have RA, an autoimmune disease that causes joint pain, swelling, and eventually damage.

Researchers continue to look for new ways to diagnose RA, especially in its early stages. That is because the earlier a person receives a proper diagnosis of and treatment for RA, the better their chances of good outcomes, such as limiting joint damage and functional loss.

Researchers also remain uncertain as to what exactly causes RA to develop, although it seems to depend on a mix of genetic and environmental factors.

In more recent years, RA researchers have been exploring the link between ERA, people at risk of RA, and the changes in their oral and intestinal microbiota, or community of microbes.

It seems people with ERA and at risk of RA have abnormal levels of certain bacteria in the mucus that lines the mouth and intestines. They also seem to be more likely than other people to have periodontal disease, or gum disease.

What is more, some research indicates RA may begin in the oral cavity.

That is why a team of researchers from the Academic Centre for Dentistry of Amsterdam (ACTA) set out to analyze the microbial populations and periodontal condition of people with ERA, those at risk of RA, and a control group of people without these conditions for comparison.

Their study appears in the journal Arthritis & Rheumatology.

Researchers have long speculated that autoimmune diseases, such as RA, are triggered or caused by microorganisms.

For quite some time, researchers have been aware there are links between periodontal disease, changes in the oral and intestinal microbiome, and RA.

Several studies seem to show that oral microbes in particular anaerobic bacteria, which do not require oxygen may play a role in the development of RA.

A 2009 study highlights three types of anaerobic bacteria occurring in the oral cavity that have been identified in joint fluid from people with RA. Several studies show that antibodies for certain types of anaerobic bacteria associated with periodontal disease may play a role in the development of RA.

Some researchers think these bacteria may cause an RA-associated immune response by producing proteins that trigger the formation of anti-citrullinated protein antibodies (ACPAs).

These compounds appear to promote inflammatory responses in different types of cells, including bone cells. Some studies have shown that this response ACPAs promote may be involved in the mediation of bone damage in the joints of people with RA.

For these and other reasons, the detection of ACPAs is now considered the most specific biomarker for RA in serum, which is the fluid component of blood.

The detection of ACPAs in serum also seems to help predict RA development several years before a person has clinical RA or experiences symptoms and receives an RA diagnosis.

That is why several research teams, including the team involved in the current study, have been exploring how changes in the composition and other components of the oral microbiome may relate to the onset of RA.

In the new study, researchers analyzed the oral microbiome and periodontal status of three groups of 50 people.

People in the first group had ERA, and the second group included people at risk of RA (people with serum ACPAs or arthralgia). People in the third group did not have RA and were not at risk, did not have autoimmune conditions, and were generally healthy.

Each participant was examined by a dentist to assess their periodontal condition. Dentists checked whether their gums bled with probing, the inflamed gum surface area, and how deep into the gum line dental tools could probe.

They also examined how many teeth each participant had, how many of their teeth were missing, decayed, or filled, and whether a person wore a removable denture. They also asked each participant about the last time they brushed their teeth and what their regular oral hygiene measures were.

In addition, the scientists collected from each participant samples of the tongue coating or film, saliva, and subgingival dental plaque, which is found below the gum.

After using devices to amplify the DNA present in the samples, they collected, analyzed, and quantified the microbial populations within the samples. They then compared microbial differences between the three groups.

The team identified no difference in periodontal conditions between the groups. There was also no difference in dental plaque samples.

Yet differences did exist between the oral saliva and tongue coating of people with ERA and at risk of RA compared with the control group.

Levels of bacteria belonging to the genera Prevotella and Veillonella were higher in saliva samples from people with ERA and at risk of RA compared with the control group. Veillonella bacterial levels were also higher in the tongue coatings of the RA groups than in those of people in the control group.

According to the authors, these findings suggest that a possible link between the oral microbe and RA may truly exist.

This also suggests that bacteria from these two genera, as well as some others already reported to be involved in RA onset, could help trigger immune responses that influence the development of RA.

The authors explain that these findings correspond to those of previous studies showing that people with new-onset RA and established RA had increased levels of oral Prevotella bacteria. The results also support research that found increased levels of Prevotella bacteria in the gut microbiome of people at risk of RA or with ERA.

The authors write that some strains of Prevotella can cause chronic inflammation, which can trigger immune cells to be released throughout the body. They add that in some cases, microbial dysbiosis, or microbial imbalances, partially resolves with RA treatment.

Medical News Today spoke with Dr. Vanessa L. Kronzer, who cowrote a recent review on the etiology of RA. She said:

This is an interesting study that, in my mind, achieves two goals. First, it provides further support for the mucosal origin hypothesis for RA. And second, it suggests that dysbiosis occurs even before disease onset and thus may play a role in RA disease pathogenesis.

Dr. Kronzer believes this research is an important step in a long path to understanding the etiology of this important disease.

MNT also contacted Johanna Kroese from ACTA, the corresponding author of the study. She explained:

Our results indicate a possible role for oral bacteria in triggering the onset of RA. Targeting these bacteria might lower the risk of developing RA. Future research can focus on strategies to target these bacteria and improving oral health, and might eventually lead to the development of measures for RA disease prevention.

While the study had many strengths, it also had some notable flaws.

People within the ERA group were receiving treatment for RA, while people at risk of RA and those in the control group were not. The researchers also did not collect information on some factors that may influence dental plaque, such as diet.

To confirm their findings, the authors say future studies must collect multiple datasets over longer periods of time, ideally using large groups of people and consistent collection methods.

Nevertheless, these findings may have uncovered yet another stepping stone in the complex, elusive development process of RA. This could be good news for the millions of people living with RA, and the healthcare professionals trying to diagnose and treat them.

As Johanna Kroese explained to MNT, although further research is needed, improving oral health is relevant for the entire population, and it wouldnt hurt to already pay attention to oral health in persons at risk of developing RA.

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Is there a link between mouth bacteria and rheumatoid arthritis? - Medical News Today


Overcoming Health Disparities by Reaching Patients With Arthritis in Their Preferred Language – Rheumatology Advisor

Friday, May 14th, 2021

The COVID-19 pandemic has highlighted significant health disparities in the Hispanic community. Although these disparities are more apparent now, inequalities, including adequate access to health care and information, among Spanish-speaking communities pre-date the current pandemic. Hispanic individuals are also underrepresented in medical research.1

During the COVID-19 pandemic, Richardae Araojo, the US Food and Drug Administration (FDA) associate commissioner for Minority Health and the director of the Office of Minority Health & Health Equity, agreed with the premise described in a recent CenterWatch article that, Clinical trial researchers should include input from patients before the trial design and consent process even begins to ensure that minority participants feel included and that all study participants stay engaged until the study is complete. He went on to flag the need for more diverse clinical trials, asking that industry and other stakeholders make trial design, logistics, recruitment, and retention practices more patient-centric.2

Latest data made available by the Centers for Disease Control and Prevention (CDC) indicate that 4.4 million individuals who are Hispanic Americans live with some form of doctor-diagnosed arthritis.3 The prevalence of arthritis among Hispanic patients is less than among non-Hispanic White patients4; however, Hispanic patients are nearly twice as likely to become disabled from arthritis and experience joint damage.5

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As part of its ongoing commitment to lead efforts to effectively educate patients who prefer Spanish as their preferred language, CreakyJoints Espaol, the multicultural digital arthritis community for patients and caregivers worldwide and part of the Global Healthy Living Foundation (GHLF), recently launched new digital communication platforms to reach Spanish-speaking families via popular Latino social media platforms.

However, despite the heavy usage of social media, general health information available online for the Hispanic community heavily leans toward misinformation, which has led to low levels of diagnosis and a growing knowledge gap.

With this in mind, CreakyJoints Espaol launched additional communication channels to provide evidence-based health information and support on social media, including WhatsApp. CreakyJoints is the first patient organization to communicate with their members using WhatsApp, which was a priority given its popularity in the Hispanic community. Resources originally developed in English are now available in Spanish (translated with cultural sensitivity) to ensure equitable access to tools needed by patients with arthritis. For example,, a platform that helps patients get the most from their telehealth appointments, is available in both Spanish and English.

CreakyJoints member Yaideliz Acevedo (age 23 years), whose first language is Spanish, is also fluent in English and frequently switches between both languages. However, her mother is more comfortable using Spanish. Yaideliz said to us, When I was first diagnosed with rheumatoid arthritis when I was 21 years and 1 month after having my son, it was overwhelming. There was a lot to learn about managing my disease and my mom was frustrated that she couldnt find on her own enough Spanish-language health information to understand my disease or its expected progression. At first, she didnt even know that people so young could be diagnosed with arthritis. Resources provided by CreakyJoints Espaol help me understand my disease and share information with my family and friends.

CreakyJoints recently launched ArthritisPower Espaol, intended for Spanish speakers, many of whom self-identify as Hispanic, to proactively participate in their disease management and contribute to better understanding of patients living with arthritis and other inflammatory diseases.

Available as a free mobile and desktop application, the ArthritisPower Research Registry first launched in 2015. It includes more than 30,000 people who use the same patient-reported outcome (PRO) measures used in their health care providers office to track their experience of rheumatic, musculoskeletal, and other inflammatory diseases. Patients can select from a large range of PROs to track and email those data to their rheumatologist before their next appointment, which may facilitate shared-decision making based on objective measures of disease activity. Patients can also participate in voluntary research studies, many of which result in presentations at US and international medical meetings or publication in peer-reviewed journals.

Eligible ArthritisPower Espaol participants will be invited to join the existing ArthritisPower Patient Governor Group, which is responsible for co-evaluating research study requests in collaboration with clinicians, researchers, and CreakyJoints. The group also provides feedback on what research questions should be next advanced in ArthritisPower.

Our goal is to increase the Hispanic communitys participation in clinical and observational research. To ensure that Hispanic individuals are part of the conversation about what patients living with rheumatic conditions need to better manage their health, they need to be at the table and part of the conversation from the beginning.

Note: To learn more about CreakyJoints Espaol, visit To learn more and register with ArthritisPower Espaol, visit

Overcoming Health Disparities by Reaching Patients With Arthritis in Their Preferred Language - Rheumatology Advisor


BMI Associated With Higher Disease Activity in Women, But Not Men, With Psoriatic Arthritis – Rheumatology Advisor

Friday, May 14th, 2021

Women vs men with psoriatic arthritis (PsA) were found to have higher disease activity and were less likely to reach their treatment target, particularly if they had a higher body mass index (BMI), according to study results published in Rheumatology.

In PsA, the prevalence of the disease is similar between the sexes; however, the symptoms can vary.

This study was conducted to evaluate the sex differences in the severity of PsA and the factors related to not reaching the treatment target.

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Patients from an outpatient rheumatology clinic in The Netherlands were included in the current cross-sectional study. Clinical and demographic data were used to assess the following differences between women and men: Psoriatic Arthritis Disease Activity Score (PASDAS; individual components included swollen and tender joints [SJC/TJC], enthesitis, C-reactive protein [CRP], dactylitis, physical component summary score of the short form-12 [SF12-PCS], and physician and patient global disease activity visual analog score [VAS]); skin/nail disease; mental component summary score of the short form-12 (SF12-MCS); health assessment questionnaire (HAQ); and inflammatory back pain (IBP).

A total of 855 patients with PsA were included in the study. Results indicated that mean PASDAS was significantly higher in women than men (3.5 vs 2.7, P <.001). Women vs men also had significantly worse scores for SJC, TJC, enthesitis, physician and patient global disease activity VAS, CRP, SF12-PCS, SF12-MCA, and HAQ (all P <.001). PASDAS treatment targets were more frequently not met in women vs men (odds ratio [OR], 2.03; P <.001). Factors significantly associated with not reaching the treatment target for the overall cohort included BMI, nail disease, IBP, and the number of disease-modifying antirheumatic drugs (DMARDs) used in the past or currently. Stratified for sex, BMI was associated with not reaching the treatment target in women, but not men (OR for BMI 25-30, 3.43; P <.001; OR for BMI 30-35, 2.59; P =.019; OR for BMI >35, 2.41; P =.002).

Study limitations included the cross-sectional design, lack of patients with recently diagnosed disease in the cohort, and the inability to determine the causal relationship between BMI and increased disease activity.

Researchers noted, For [rheumatoid arthritis], there is evidence that being overweight is associated with higher disease activity in women, but not in men. To our knowledge, we are the first to show that the same holds true for PsA. Further, A higher BMI in women, but not men, was associated with not reaching the treatment target. This suggests that rheumatologists should pay extra attention to weight loss in the disease management of women with PsA.

Mulder MLM, Wenink MH, Vriezekolk JE. Being overweight is associated with not reaching low disease activity in women but not men with psoriatic arthritis. Rheumatology (Oxford). Published online April 8, 2021. doi:10.1093/rheumatology/keab338

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BMI Associated With Higher Disease Activity in Women, But Not Men, With Psoriatic Arthritis - Rheumatology Advisor


Psoriatic arthritis and the eyes: Dry eye, glaucoma, and more – Medical News Today

Friday, May 14th, 2021

Psoriatic arthritis, or PsA, is a form of arthritis associated with psoriasis. PsA affects the joints and the areas of the body where tendons and ligaments connect to bones.

The National Psoriasis Foundation states that about 30% of individuals with psoriasis will develop psoriatic arthritis during their lifetime.

Sometimes, people living with PsA may develop eye conditions, which can range from irritation to vision loss.

This article explains how PsA affects the eyes and how to treat and prevent these complications.

One eye condition that people living with PsA may experience is chronic dry eye, or keratoconjunctivitis sicca. Experts believe that about 2.7% of people with PsA have this condition. However, some studies suggest that the number may be as high as 18.75%.

In a person with this condition, the tear ducts lose their ability to produce tears, which are vital for proper lubrication of the eyes. A lack of adequate lubrication increases the risk of eye infections and can damage the cornea.

In cases where over-the-counter artificial tears prove ineffective, prescription eye drops may help increase tear production and lower inflammation. For some people, steroid eye drops may offer short-term relief to control inflammation.

Uveitis is a type of eye inflammation that affects the middle layer of tissue within the eyeball, called the uvea. The symptoms of uveitis include redness in the white parts of the eyes, blurred vision, sensitivity to light, pain, and floaters.

There are four types of uveitis:

The treatment for uveitis usually starts with corticosteroid eye drops to reduce inflammation. If these do not work, an eye doctor may recommend injecting the eye with a corticosteroid. In cases of infection, an eye specialist may recommend antibiotics.

Cataracts are the result of cloudy films developing over the eye lens, leading to impaired vision. The Arthritis Foundation notes that inflammatory conditions such as PsA may advance the formation of cataracts.

Symptoms include:

People with cataracts require surgery to remove the cloudy lens and replace it with an artificial one.

Glaucoma is the term for a group of eye disorders that damage the optic nerve. It can lead to vision loss.

Chronic inflammation from arthritic conditions, including PsA, can contribute to glaucoma by increasing the pressure in the eyes.

This eye condition has no symptoms in the early stages when it is the most treatable. However, an ophthalmologist may detect it when they are carrying out a regular eye examination.

Symptoms that a person may experience include pain, blurred vision, and seeing blank spots or halos around lights. A doctor may prescribe eye drops to reduce the pressure in the eyes. Some people may require surgery.

Peripheral ulcerative keratitis causes the cornea, which is the transparent outer layer at the front of the eye, to become inflamed, which makes it prone to thinning.

The symptoms of peripheral ulcerative keratitis include:

Artificial tears and antibiotic drops can promote healing and prevent infection.

A person can mitigate the risk of developing PsA-related eye problems by reducing inflammation in the body.

As PsA is an inflammatory condition, a doctor may prescribe medication to control inflammation within the body, improving eye conditions related to PsA.

Anyone with PsA should consider undergoing annual eye examinations and regular doctor visits to discuss any new or existing eye-related symptoms.

Some eye conditions do not have any signs in the beginning stages. Due to this, it is vital to get regular eye checkups to detect any problems as soon as possible.

Living with PsA can be challenging. In addition to the joint pain that PsA can cause, many people may develop related eye problems.

The good news is that many PsA-related eye conditions are highly treatable.

As some conditions do not have early warning signs, an eye examination is the best way to detect any abnormalities. A doctor can help a person manage any symptoms related to PsA and eye health.

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Psoriatic arthritis and the eyes: Dry eye, glaucoma, and more - Medical News Today


Alvotech Seeks to End AbbVie’s Wrongful Monopoly on Humira and Bring Affordable Arthritis Treatment to U.S. – Business Wire

Friday, May 14th, 2021

VIRGINIA--(BUSINESS WIRE)--Alvotech today filed a federal lawsuit (Case 1:21-cv-00589) seeking to end the monopoly that pharmaceutical giant AbbVie has long-maintained on the adalimumab market, sold as Humira. Humira is the highest grossing prescription drug in the United States with over $16 billion in sales in 2020 (nearly $20Bn globally).

Alvotech has developed a biosimilar (analogous to a generic) of Humira called AVT02, the first-filed biosimilar drug equal in strength to Humiras latest formulation, which AbbVie markets as a high-concentration, pain-free drug. The company is also developing AVT02 as an interchangeable product and it expects results from its ongoing interchangeability study in Q2 of this year. AVT02 could save U.S. taxpayers and the overall healthcare system $8-10 billion annually.

Our new product will be a gamechanger that will provide consumers who are suffering from chronic pain with significant savings, and we look forward to bringing this drug onto the market as soon as possible, said Alvotech Founder and Chairman Robert Wessman.

As alleged in court today, AbbVie seeks to overwhelm Alvotech with 60+ patent claims of questionable validity in order to keep its closest competitor off the market, a tactic it has long used against other competitors. At stake are billions of dollars of cost to the U.S. healthcare system, which is largely driven by AbbVies significant price increases that its Humira monopoly makes possible. Later this month, AbbVie will face questions from Congress about whether the company improperly suppresses competition in order to maintain their monopoly.

As alleged in the filing, AbbVie has taken several improper steps to inflate its patent portfolio, specifically:

Today, affordable biosimilars to Humira are available across Europe and in Japan, Canada and Australia. The settlement agreements that allowed launches in 2018 of biosimilars in Europe were done to delay launches of similar products in the U.S., thus allowing AbbVie the ability to maintain and even increase prices on the U.S. consumer and taxpayer.

As pointed out in Alvotechs lawsuit, AbbVie did not invent adalimumab or the subject matter of the original patents surrounding adalimumab and its use, instead acquiring them from German BASF AG. Nevertheless, despite those original patents expiring in 2016, AbbVie has been able to extend its monopoly to 2023 and beyond by deliberately seeking to block legitimate competition.

In 2010, AbbVie developed and tested a less-painful and higher-concentration version of Humira that was as a 100 mg/ml formulation, which the FDA approved in 2015. Yet the company waited nearly three years before bringing this new formulation to the public, a strategic move meant to entrench their control over the market and hobble the competition. Alvotech has developed and is seeking interchangeability for the less-painful, high-concentration version of Humira, which will offer patients the treatment at a more affordable price point.

Furthermore, AbbVie successfully sought and obtained over 100 additional patents of dubious validity that extended its Humira monopoly beyond 2016. Through settlements reached with their competitors, other biosimilars will not enter the market until 2023.

In just the last four years, since its monopoly should have run its course, AbbVie has reported selling over $75 billion worth of Humira and is forecasted to make an additional nearly $40 billion through 2022.

As alleged in todays filing, this strategy has been called a minefield of IP by those in AbbVies leadership, meaning the company will engage in endless litigation not to protect innovation but to make challenges to its patent claims cost- and resource-prohibitive for competitors.

About Alvotech

Alvotech is a multinational biopharmaceutical company focused on the development and manufacture of high quality biosimilars for global markets. We are specialists in biotechnology, seeking to be a global leader in the biosimilar space by delivering high quality, cost-competitive products and services to our partners and to patients worldwide. Our fully integrated approach, with high-quality in-house competencies throughout the value chain, enables the accelerated development of biosimilar products. Alvotechs shareholder base includes, among others, Aztiq Pharma, led by founder and Chairman Mr. Robert Wessman, Fuji Pharma from Japan, Shinhan from Korea, Baxter Healthcare SA, YAS Holdings, ATHOS (Strngmann Family Office), CVC Capital Partners and Temasek from Singapore.

Alvotechs initial pipeline contains several monoclonal-antibody and fusion-protein biosimilar candidates aimed at treating autoimmunity, oncology and inflammatory conditions to improve quality of life for patients around the world. For more information, please visit our website, or follow us on LinkedIn, Twitter and Facebook.

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Alvotech Seeks to End AbbVie's Wrongful Monopoly on Humira and Bring Affordable Arthritis Treatment to U.S. - Business Wire


Rheumatoid arthritis: Non-joint symptoms that may precede joint symptoms by five years – Express

Friday, May 14th, 2021

Rheumatoid arthritis is an autoimmune condition, which means it's caused by the immune system attacking healthy body tissue. The NHS explains: "If you have rheumatoid arthritis, your immune system mistakenly sends antibodies to the lining of your joints, where they attack the tissue surrounding the joint." Research has also uncovered a host of symptoms that are not related to joint pain.

CreakyJoints, a support, education, advocacy, and research organisation for people living with arthritis, reports on the findings of a study published in the journal RMD Open: Rheumatic and Musculoskeletal Diseases.

The study found that many rheumatoid arthritis patients had visited their doctor with musculoskeletal complaints about their hand/finger, shoulder, or knees within four to six years (and especially the 18 months) prior to their diagnosis.

"But many also presented with issues that might not seem clearly related to rheumatoid arthritis," CreakyJoints reports.

The study found that carpal tunnel syndrome was more common among those who later developed rheumatoid arthritis.

READ MORE:Rheumatoid arthritis: How to spot arthritis bumps - location and size

Carpal tunnel syndrome is a common condition that causes pain, numbness, and tingling in the hand and arm.

The study also found infections of the urinary tract and genitals were common among those who went on to receive a rheumatoid arthritis diagnosis.

Inflammation of the mucous membranes in the gums, lung, or gut also occurred more often in people who were later diagnosed with rheumatoid arthritis.

What's more, some were diagnosed with psoriasis, inflammatory bowel disease (Crohns disease or ulcerative colitis), or gout in the period leading up to their rheumatoid arthritis diagnosis.

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Although more research is needed, the authors of the study suggested that being aware of these findings might help doctors to detect rheumatoid arthritis earlier on.

The authors noted that, in particular, people who see their doctor with new musculoskeletal symptoms such as shoulder pain, chronic knee pain, or carpal tunnel syndrome seem to be more likely to develop inflammatory arthritis within the following 1.5 years.

Consequently, they can consider referring these patients [to a rheumatologist], which may facilitate early diagnosis and treatment, they wrote.

The symptoms of rheumatoid arthritis can be life-limiting but there are proven ways to alleviate them.

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Similarly, improving your diet can provide some relief for rheumatoid arthritis.

"For starters, a diet rich in fruits, vegetables, fish, nuts and beans but low processed foods and saturated fat, is not only great for overall health, but can also help manage disease activity," explains the Arthritis Foundation (AF).

In fact, many of these components are found in a Mediterranean-style diet, "which is frequently touted for its anti-aging and disease-fighting powers", notes the AF.

Among other things, the diet can help arthritis by curbing inflammation and aiding weight loss, the health body adds.

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Rheumatoid arthritis: Non-joint symptoms that may precede joint symptoms by five years - Express


Ten years in the making: Arthritis drug repurposed to fight pancreatic cancer cells – The New Daily

Friday, May 14th, 2021

Are we on the brink of a genuine breakthrough in treating pancreatic cancer, the disease that almost always kills its victims within months of diagnosis?

Associate Professor Phoebe Phillips from the University of NSWs adult cancer program told The New Daily that she has never before been so optimistic and hopeful in her career researching the disease.

Well know soon enough whether that optimism pays off.

Within weeks, Dr Phillips and her team will start recruiting pancreatic cancer patients for a Phase II clinical trial.

The volunteers will receive a repurposed arthritis drug that appears to defeat pancreatic cancers formidable defences against treatment.

Because the drug, Sulfasalazine, has already proven itself to be safe, an expensive Phase I trial isnt necessary, saving valuable time.

Going straight into a Phase II trial is a huge deal, Dr Phillips said.

And because the drug is off patent and listed on the PBS Dr Phillips said patients would be paying about $50 for treatment, instead of many thousands that a new drug ordinarily costs.

Twenty years ago, Phoebe Phillips, then a PhD student, discovered helper cells that build up scar tissue that feed pancreatic tumours but also protect the cancer from being treated with drugs.

These helper cells also called cancer-associated fibroblasts are recruited by cancer cells to support their growth and spread, essentially scouting out and preparing sites for metastasis.

Dr Phillips said helper cells have been ignored in treatment strategies.

This week, Dr Phillips and her team published a paper detailing an intervention that attacks both the cancer cells and the helper cells, thereby thwarting the aggressiveness and drug resistance of the disease.

Its been 10 years in the making, she said.

The potential new treatment targets a protein called SLC7A11, which has been found in high levels in more than half of all pancreatic patients. The arthritis drug Sulfasalazine potently inhibits SLC7A11.

We found that switching off SLC7A11 in mice with pancreatic tumours directly killed pancreatic cancer cells, reduced the spread of tumour cells throughout their body and decreased the scar tissue fortress, said Dr George Sharbeen, a postdoc researcher in Dr Phillips lab who led the experimental work.

In other words, we have identified a novel dual cell therapeutic target tackling both the tumour cells and their helpers which overcomes the current limitations of standard chemotherapy.

The potential is to improve treatment response and ultimately survival of these patients.

In future trials Sulfasalazine will be used in tandem with existing cancer drugs with a view to finding a treatment sweet spot.

As Dr Phillips noted in a prepared statement: Pancreatic cancer has seen minimal improvement in survival for the last four decades and without immediate action, it is predicted to be the worlds second biggest cancer killer by 2025.

The researchers hope to analyse and publish the first set of results of the trial within three years.

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Ten years in the making: Arthritis drug repurposed to fight pancreatic cancer cells - The New Daily


Rheumatoid Arthritis Linked to Adverse COVID-19 Outcomes – MD Magazine

Friday, May 14th, 2021

The COVID-19 pandemic has resulted in adverse effects among vulnerable populations, particularly those with chronic diseases such as cardiovascular (CV) disease and diabetes.

Infections in patients with rheumatoid arthritis often complicate the natural course of RA, while treatment with disease-modifying anti-rheumatic drugs (DMARDs) are associated with an increased risk of infection.

Previous data found immunosuppressants did not lead to increased rates of COVID-19 in patients with immune-mediated inflammatory disease.

However, in a new study, investigators, led by Bryant R. England, MD, PhD of the Nebraska Medical Center, found that patients with RA have an increased risk for COVID-19 and hospitalization or death from COVID-19, compared to patients with non-RA.

The study compared the risk of SARS-CoV-2 infection and the development of severe COVID-19 between patients with RA and a comparator patient group in an at-risk population.

The team hypothesized that patients with RA would have a higher risk of acquiring an infection and were more likely to require hospitalization or die from COVID-19.

To test this hypothesis, investigators conducted a retrospective, matched-cohort study using data from the National Veterans Health Administration (VHA).

Patients active in the VHA system were identified as of January 2020, using algorithms for multiple RA diagnostic codes, a rheumatologist diagnosis of RA, and a DMARD or positive RA autoantibody test.

The team matched RA patients to non-RA patients (1:1) on age, sex, and Department of Veterans Affairs (VA) site. Patients were followed up with from January 2020 to the first COVID-19 diagnosis, death, or end of the study period in December 2020.

Data on COVID-19 outcomes was collected through the VA COVID-19 surveillance database, including positive tests and hospitalization or death within 30 days of infection.

Investigators used multivariable regressions models to assess the COVID-19 risk in both RA patients versus non-RA patients, including adjustment for demographics, comorbidities, health behaviors, and county-level COVID-19 rates as of November 2020.

The team identified 33,866 patients with RA and 33,866 patients without RA, including 84.5% male and a mean age of 67.8 years.

Patients with RA were more likely to be smokers, have a higher BMI, with a greater comorbidity burden, and more hospitalizations within the past year.

Investigators found in over 62,894 patient-years of follow-up, there were 1503 diagnoses of COVID-19.

In a subset of 338 severe COVID-19 cases, 345 resulted in hospitalization and 84 resulted in death. Within the same observation period, there were 288 non-COVID-19 related deaths.

The data show RA was associated with a significantly higher risk of COVID-19, with a 25% higher risk of COVID-19 with a hazard ratio (HR) of 1.25 (95% CI, 1.13, 1.39) and a 35% higher risk of COVID-19 hospitalization or death with an HR of 1.35 (95% CI, 1.10, 1.66).

Other factors in addition to RA status associated with the higher risk included patients treated with DMARDs and prednisone, as well as demographic including Black race and Hispanic ethnicity.

Patients with treated with DMARDs and prednisone were at the highest risk of COVID -19 with a hazard ratio of 1.66 (95% CI, 1.36,2.03), as well as hospitalization or death with a HR of 2.12 (95% CI, 1.48, 3.03), compared to non-RA patients.

Investigators concluded that patients with RA have a significantly increased COVID-19 risk, with immunosuppressive therapy treatment associated with a more severe risk of COVID-19.

Consideration should be given to establishing RA, and potentially other conditions that require treatment with similar immunosuppressive medications, as a chronic condition that receives prioritization for COVID-19 prevention and management strategies, investigators wrote.

The study, Risk of COVID-19 in Rheumatoid Arthritis: A National Veterans Affairs Matched Cohort Study in At-Risk Individuals, was published online in Arthritis & Rheumatology.

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Rheumatoid Arthritis Linked to Adverse COVID-19 Outcomes - MD Magazine


A changing landscape in the treatment of Rheumatoid Arthritis – Irish Medical Times

Friday, May 14th, 2021

The treatment of Rheumatoid Arthritis has been transformed in the last two decades by the introduction of biologic agents. Dr Sharon Cowley looks at how management and treatment of RA has changed

Rheumatoid Arthritis (RA) is a common condition, estimated to affect 1% of the caucasian population and over 45,000 people in Ireland.1 It results from a complex interaction between genes and environment, leading to a breakdown of immune tolerance and synovial inflammation in a characteristic symmetric pattern.

Each year in Ireland 2,000 new cases are diagnosed, and 3 out of 4 are in patients of working age. There have been many recent advances in the treatment of RA and new treatment strategies have substantially changed the course of RA. Many patients can achieve remission if the disease is recognised early, and it is treated promptly and continuously.

In 2019 the European Alliance of Associations for Rheumatology (EULAR) updated its treatment guidelines and the American College of Rheumatology (ACR) is preparing to release updated 2021 guidelines later this year. These guidelines aim to reflect newly licenced drugs, data on long-term efficacy and safety of previously approved drugs, comparative effectiveness studies, and considerations of the cost involved.

Conventional Synthetic Disease Modifying Anti-Rheumatic Agent (csDMARD)Methotrexate (MTX) is the anchor drug in RA and is the preferred first-line treatment agent.2,3

Not only is it efficacious by itself, but it is also the basis for combination therapies, either with glucocorticoids or with other csDMARDs, biological DMARDs (bDMARDs) or targeted synthetic DMARDs (tsDMARDs).3

The efficacy of biological and other targeted therapies are enhanced when administered in combination with MTX.4 Safety screening for MTX includes full blood count, liver and renal function tests, hepatitis B and C serology, assessment of underlying lung and liver disease, determination of alcohol use and potential future pregnancy, although the risks are low.

MTX is commenced at a dose of 10-15mg weekly with folic acid and can be up-titrated to 25mg weekly. It is important to note that its onset of effect can take up to 12 weeks so patients may require additional cover with non-steroidal anti-inflammatories or corticosteroids during this period. Response is monitored in a treat to target fashion with up-titration of MTX dose to achieve clinical response. If a patient has a contraindication to methotrexate, other first line csDMARDs include salazopyrin, hydroxychloroquine can be added.

BiologicsBiologicals are large molecules (80,000-150,000 dalton molecular weight) and produced in living cells using recombinant DNA technology. The biologic era started in the late nineties, with the tumour necrosis factor inhibitors (TNFi) infliximab and etanercept. In the succeeding years, other TNFi and several other biologic molecules with varying targeted mechanisms of action have emerged. Rheumatology was one of the earliest specialties to commence biologic therapy following their availability in the late 1990s.

Pre-biologic screening to ensure safe administration includes full blood count, liver and renal function tests, hepatitis B and C serology, TB screening and an accurate history concerning congestive heart failure, nervous system disorders, malignancies, allergies, vaccination status and plans for future pregnancy.

Despite initial concerns about biologic-associated potential side effects in major areas such as malignancy, pregnancy and in the risk of infection, a growing body of real world data is now available and confirms their agents to high very good benefits/side-effects ratios.

At present bDMARDs are second line treatments in both the EULAR and ACR guidelines. They are typically commenced if a patient has less than optimal response to csDMARDs. Recent head-to-head data comparing various biological medications including the RED SEA trial comparing adalimumab and etanercept,5 the AMPLE study6 comparing abatacept and adalimumab and the ADACTA study comparing tocilizumab and adalimumab,7 have shown comparable outcomes between the treatment arms in all of these studies.

Generally the choice of first biologic is physician-dependant. If one TNFi has failed, patients generally receive an agent with a different mode of action rather than a second TNFi.

BiosimilarsThe end of patents of the original biological agents (originators) has resulted in the availability of cheaper biosimilar agents. These must have identical amino acid sequence with the originator biological agent, and have very similar affinity for the target protein (e.g. TNF or IL-6). Potential differences in glycosylation between originator and biosimilar agents could affect pharmacokinetics, pharmacodynamics or immunogenicity of these agents.

To date however there have been no clinically significant issues found in rheumatic patients treated with biosimilars. Common examples are Inflectra, a biosimilar of Infliximab; Benepali, an Etanercept biosimilar; and Amgevita, a biosimilar of Adalimumab. Data from several studies switching patients with RA from an original biologic to a biosimilar drug showed no changes in efficacy, safety, trough serum drug concentration, or immunogenicity between the biosimilars and their reference product.8

Despite the European Medicines Agency granting market authorisation for 28 biosimilars, introduction was initially slow in Ireland; however the list of biosimilars reimbursable by the State is gradually increasing. Once a biosimilar medicine is available, the price of the originator product must be reduced by 30 per cent, following an agreement reached between the Irish Pharmaceutical Healthcare Association and the State. As a result of lower unit prices of the drug, both biosimilar and reference medicine, the drug can be provided to patients for a substantially lower cost.

Janus Kinase InhibitorsJanus Kinase Inhibitors (JAKi) are the newest players in the treatment of rheumatoid arthritis. They are small molecules, rather than biologicals, and target a key pro-inflammatory intracellular signalling pathway. They compare favourably to existing bDMARDs and have been shown to slow radiographic progression in RA.

The EULAR 2019 guidelines have revised the preference of bDMARDs over targeted synthetic DMARDs because of new evidence regarding the successful long-term efficacy and safety of JAK inhibitors and now both JAK inhibitors and bDMARDs are equally recommended as a second line option.2

Tofacitinib, baricitinib and upadacitinib are the first three JAK inhibitors to become commercially available in Ireland. Similar to bDMARDS the most frequently reported side-effects of JAK inhibitors are increased rate of infection. In contrast to the bDMARDS there are signals for slightly increased incidence of thrombosis, shingles and gastrointestinal perforations, so careful history-taking is important before initiation, and some patients may benefit from shingles vaccination before administration.

Future treatmentsThere are a number of potential future treatments for RA to add to the ever expanding armamentarium.

Sariluzumab is an interleukin 6 inhibitor (IL-6i) approved by the European Medicines Agency but not yet used in Ireland. Olokizumab is another IL-6i in phase III trials and has shown benefit versus placebo in clinical response however concerns are present over the high incidence of treatment-related adverse events.9

Extended studies will be needed to prove safety. Otilimab is another new agent that works by inhibiting granulocyte-macrophage colony-stimulating factor (GM-CSF). Current phase III trials are evaluating both long-term safety and efficacy in patients with active RA who have an inadequate response to DMARDs or JAK inhibitors.10

Targeting of non-immune cells such as RA synovial fibroblasts is an emerging area11 this cell type drives both inflammation and tissue destruction in joints.12

Non pharmacological treatmentIn conjunction with drug-based treatment, non-pharmacological interventions such as dynamic exercises and occupational therapy should be considered as adjuncts to drug treatment. Smoking cessation, dental care, weight control, assessment of vaccination status, and management of comorbidities, especially cardiovascular risk, should be included in overall patient care.

The treatment of rheumatoid arthritis has undoubtedly been transformed in the past two decades with the introduction of targeted biologic agents. Although biologic agents are more costly in the short term than synthetic DMARDs, drug-specific costs may be offset by significant improvements symptoms, slowed disease progression, and improved quality of life for patients.


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A changing landscape in the treatment of Rheumatoid Arthritis - Irish Medical Times


Yale Rheumatology State of the Art Symposium: Pre-autoimmunity and the Prevention of Rheumatic Diseases, on May 19 – Yale School of Medicine

Friday, May 14th, 2021

Yale Rheumatology State of the Art Symposium: Pre-autoimmunity and the Prevention of Rheumatic Diseases

Recent progress in our understanding of the development of autoimmunity suggests the opportunity of intervening in the prodromal phase of rheumatic diseases to prevent the future onset of clinically-apparent disease, such as arthritis or other disease manifestations.

This one-day international symposium will bring thought leaders together to review the conceptual basis and available clinical data for implementing preventive strategies in rheumatoid arthritis, systemic lupus erythematosus, and other autoimmune and rheumatic conditions. Topics will include the definition of at-risk individuals, interventions under study, and prospects for new approaches in basic scientific and clinical investigation, and for the design of therapeutic clinical trials.

Date: Wednesday, May 19, 2021

Time: 8 a.m - 4 p.m.

Live Zoom webinar

Accreditation Statement

The Yale School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Designation Statement

The Yale School of Medicine designates this live activity for a maximum of 7.25 AMA PRA Category 1 Credits. Physicians should claim only the credit commensurate with the extent of their participation in the activity.


Richard Bucala, MD, PhD, Waldemar Von Zedtwitz Professor of Medicine (Rheumatology) and Professor of Pathology and of Epidemiology (Microbial Diseases); Chief, Rheumatology, Allergy, & Immunology; Rheumatologist in Chief, Rheumatology

Ned Calonge, MD, President and CEO, the Colorado Trust

Ben Chong, MD, Assistant Instructor, University of Texas Southwestern Medical Center

Andrew Cope, MD, PhD, Professor of Rheumatology, King's College London

Philip De Jager, MD, PhD, Professor of Neurology, CUMC/Neurological Institute of New York

Kevin Deane, MD, PhD, Associate Professor of Medicine, Division of Rheumatology, University of Colorado Hospital, Veterans Affairs Medical Center

Hani El-Gabalawy, MD, FRCPC, Professor of Medicine and Immunology, University of Manitoba Arthritis Center

Peter C. Grayson, MD, MSc, Tenure Track Investigator, NIAMS Vasculitis Translational Research Program, National Institutes of Health

Mark Harrison, PhD, Associate Professor, Faculty of Pharmaceutical Sciences, University of British Columbia

Andrew Heinrich, JD, MPhil, Lecturer, Yale School of Public Health

Kevan Herold, MD, C.N.H. Long Professor of Immunobiology and of Medicine (Endocrinology)

Judith James, MD, PhD, Vice President of Clinical Affairs, Oklahoma Medical Research Foundation

David Karp, MD, PhD, Professor and Chief, Rheumatic Disease Division, University of Texas Southwestern Medical Center

Nancy Olsen, MD, Department of Rheumatology, Penn State M.S. Hershey Medical Center

Christopher T. Ritchlin, MD, MPH, Professor of Medicine and Chief - Department of Medicine, Allergy/Immunology and Rheumatology (SMD), University of Rochester Medical Center

Event RSVP: Allison Rentfro, PhD

REGISTRATION FEES: Physicians - $50 Nurses/PAs/Allied Health Professionals - $25 Residents/Fellows/Students - Complimentary Exhibits - $1500

Host Organization: Rheumatology, Allergy, & Immunology

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Yale Rheumatology State of the Art Symposium: Pre-autoimmunity and the Prevention of Rheumatic Diseases, on May 19 - Yale School of Medicine


Allogeneic Mesenchymal Stem Cell Segment Is Expected To Lead In the Global Rheumatoid Arthritis Stem Cell Therapy Market over the Forecast Period,…

Friday, May 14th, 2021

The report on the Rheumatoid Arthritis Stem Cell Therapy market provides a birds eye view of the current proceedings and the impact on the COVID-19 pandemic. Further, the report ponders over the various factors that are likely to impact the overall dynamics of the market once the COVID-19 pandemic subsides. The current trends, growth opportunities, restraining factors, and drivers are discussed in the report in detail.

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The growing prevalence and recurrence of rheumatoid arthritis is expected to be the major factor driving the growth of the rheumatoid arthritis stem cell therapy market over the forecast period. Although doctors do not know the exact cause of rheumatoid arthritis, but certain risk factors are observed to be associated with it.

These risk factors include age (most common between the age of 40 and 60), family history, gender, environment (a toxic chemical in the environment can up the odds), obesity and smoking. Changes in lifestyle and eating habits are contributing to the growing prevalence of rheumatoid arthritis.

Rheumatoid Arthritis Stem Cell Therapy Market: Segmentation

Tentatively, the global rheumatoid arthritis stem cell therapy market can be segmented on the basis of treatment type, application, end user and geography.

Based on treatment type, the global rheumatoid arthritis stem cell therapy market can be segmented into:

Based on application, the global rheumatoid arthritis stem cell therapy market can be segmented into:

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Based on distribution channel, the global rheumatoid arthritis stem cell therapy market can be segmented into:

Based on geography, the global rheumatoid arthritis stem cell therapy market can be segmented into:

Rheumatoid Arthritis Stem Cell Therapy Market: Regional Outlook

Geographically, the global rheumatoid arthritis stem cell therapy market can be segmented into viz. North America, Latin America, Europe, Asia-Pacific excluding Japan (APEJ), Japan and the Middle East and Africa (MEA). North America is expected to be the dominant region in the global rheumatoid arthritis stem cell therapy market, owing to the presence of various key players.

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The rheumatoid arthritis stem cell therapy market in Asia Pacific excluding Japan is expected to grow at a significant CAGR due to the expansion of product offerings by key players. Europe is expected to have the second large share in the global rheumatoid arthritis stem cell therapy market throughout the forecast period.

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Allogeneic Mesenchymal Stem Cell Segment Is Expected To Lead In the Global Rheumatoid Arthritis Stem Cell Therapy Market over the Forecast Period,...


State pension: You could get up to 358 a month for arthritis and other health conditions – Express

Friday, May 14th, 2021

TheState Pensionis overseen by the Department for Work and Pensions (DWP), responsible for ensuring everyone gets the amount to which they are entitled. State pension payments revolve around the National Insurance contributions a person has made throughout their lifetime. Some 10 years are needed to get anything at all, while 35 years and above usually ensure a person receives the full state pension sum.

It is worth noting, though, the Government states some individuals will get less than the full sum if they were contracted out before April 6, 2016.

Regardless of what a person receives via the state pension, if they are living with a health condition in old age, this may create additional costs.

With a limited income in retirement, some may struggle with any additional financial burdens.

Bearing this in mind, then, the DWP is making older Britons aware of a payment they could receive to help.

READ MORE:Yorkshire Building Society offers leading 3.5 percent interest rate

Attendance Allowance is issued by the DWP on a weekly basis, but paid at two different rates.

The amount individuals can expect to receive will be based on the level of help and support they need.

Firstly, the lower rate of Attendance Allowance has been laid out in this tax year as 60.00.

This is intended for those who need frequent help or constant supervision during the day, or supervision at night.

There is not a prescriptive list of health conditions or disabilities a person must have in order to claim Attendance Allowance, but it could be especially helpful for those living with arthritis.

The organisation Versus Arthritis has explained the matter further, stating: What matters is how much your arthritis - and any other condition you may have - affects you.

It is based on the help you need - not the help you actually get. It does not matter if you receive a lot of help or support, or very little.

People can use their own discretion to decide how they will use their Attendance Allowance payment if they find they are eligible.

Britons will be able to claim using the dedicated form and sending it by post - and this can be accessed via the Governments official website.

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State pension: You could get up to 358 a month for arthritis and other health conditions - Express


Effect of biologics on cardiovascular inflammation | JIR – Dove Medical Press

Friday, May 14th, 2021


There is now sufficient experimental and clinical evidence to support that atherosclerosis represents a chronic inflammatory process evolving within the wall of large and medium-sized arteries rather than just the result of passive lipid accumulation in the arterial wall.1 In fact, inflammation dominates all steps of the atherogenic process, starting with the recruitment of leukocytes and the expression of pro-inflammatory cytokines at sites of endothelial dysfunction that ultimately result in the formation of and progression to a vulnerable atherosclerotic plaque.2

A complex interplay between the high-grade inflammatory process and classic cardiovascular risk factors has been recognized as the pathogenetic substrate for excessive cardiovascular morbidity and mortality characterizing the whole spectrum of autoimmune rheumatic disorders (ARD), mainly rheumatoid arthritis (RA),3 systemic lupus erythematosus (SLE) and the spondyloarthropathies (SpA).4,5 In particular, the overexpression of several proinflammatory cytokines with an established role in atherogenesis, such as tumor necrosis factor alpha (TNF-) and interleukin 6 (IL-6), leads to endothelial dysfunction and contributes to the development of premature atherosclerosis.6 Given the shared pathogenic features between the inflammatory response and atherosclerosis, sufficient control of disease activity is one of the two main targets of cardiovascular disease (CVD) management in ARDs (the other one being adequate control of classical CVD risk factors).7 Indeed, a remarkable improvement in surrogate markers of atherosclerosis, such as arterial stiffness and carotid intima-media thickness (cIMT) after sufficient control of the disease in patients with RA has been documented.8,9 Beyond subclinical atherosclerosis, cardiovascular inflammation encompasses ischemic cardiovascular events, such as myocardial infarction and strokes, myocardial inflammation, pericardial inflammation and heart failure, all of which are present in patients with ARD as a consequence of chronic high-grade inflammatory state. To that end, interest is now diverting towards novel therapeutic approaches that expand beyond the management of traditional cardiovascular risk factors, targeting specific agents in the inflammatory cascade with promising results.10

Over the last 3 decades, biologic disease modifying drugs (bDMARDs) have proved to be very effective at controlling the inflammatory burden and altering to the better the natural history of ARDs. Designed to block key mediators of the immune response, namely TNF-, IL-1 and IL-6, bDMARDs have radically improved the prognosis and quality of life of patients with ARDs. Beyond their striking efficacy in achieving stable and low disease activity, bDMARDs also appear to associate with overall improved cardiovascular outcomes in these populations.11 Based on the inflammatory hypothesis of atherosclerosis, the addition of biologics as a complementary therapeutic option for CVD beyond the context of systemic inflammatory diseases is steadily gaining attention, although large-scale clinical trials with hard cardiovascular endpoints are still scarce.12,13

The aim of this review is to provide an insight into the inflammatory aspects of atherosclerosis and subsequently critically summarize and discuss current data about the effects of biologic treatments on cardiovascular inflammation, focusing on studies assessing their impact on surrogate markers of CVD and cardiovascular outcomes.

A review of the English literature published in the online databases Medline, Cochrane and Embase was performed to December 2020, searching for randomized controlled trials, observational studies and review articles concerning the association between biologic agents and the risk of cardiovascular events.

The search consisted of three components, each of them represented by specific Medical Subject Headings (MeSH) terms: (a) the autoimmune rheumatic disorder utilizing the terms rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis and spondyloarthropathies; (b) the biologic agent, utilizing the terms biologics, biologic DMARDs, TNF- antagonists, TNF inhibitors, anti-TNFs, anti-IL6, anti-IL1, canakinumab, tocilizumab, rituximab, abatacept, anakinra, etanercept, infliximab, adalimumab, golimumab; certolizumab pegol (c) the cardiovascular outcome, identified by the terms atherosclerosis, arteriosclerosis, cardiovascular disease, cardiovascular risk and myocardial infarction, cardiovascular death, sudden cardiac death, heart failure, stroke, lipids, lipid profile, cholesterol, hypertension, arterial stiffness, augmentation index, endothelial function, flow mediated dilatation, carotid, intima media thickness. Our search strategy was initially developed for PubMed and modified accordingly for other research engines. In order to look for publications referring to the use of biologics in non-rheumatic conditions, an additional search combining the MeSH terms used for the biologic agent and the cardiovascular outcome in the initial search was also conducted.

The identification of eligible articles was initially carried out by screening titles and abstracts, and finally by reading the full text of the publication. The references of the eligible articles were screened to ensure that no important research data relevant to the subject were missed. Full journal articles, reviews and published abstracts in English from international rheumatology and cardiovascular congresses were included in the search. Not accessible abstracts, data from ongoing pharmaceutical research or reports not translated in English were excluded.14

The concept that high-grade inflammation has a central position in the etiopathogenesis of atherosclerosis in ARDs has been primarily based on the observation that various chronic, systemic inflammatory disorders are associated with an excessive risk for cardiovascular events, which cannot be solely explained by the prevalence of traditional cardiovascular risk factors.15,16 For instance, individuals with RA have a 2-fold higher risk for developing CVD than the general population.17 On the other hand, it has been demonstrated that conventional and bDMARDs not only improve markers of systemic inflammation and disease activity parameters,18 but also convey beneficial impact on vascular injury associated with these conditions.18 Figure 1 provides a schematic overview of the complex interrelation between vascular injury and systemic inflammation in ARDs.

Figure 1 Pathogenetic links between systemic and cardiovascular inflammation. Proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-) and interleukin-1 (IL-1), upregulated in the setting of systemic inflammation, trigger endothelial activation. The ensuing overexpression of endothelial leukocyte adhesion molecules leads to increased recruitment and activation of inflammatory cells within the arterial wall, resulting in destabilization of endothelial hemostasis, endothelial dysfunction and vascular inflammation. The heightened synthesis of potent procoagulant molecule tissue factors by activated endothelial cells induces platelet adhesion and aggregation, creating a prothrombotic state. Moreover, systemic inflammation associates with an increase in oxidized low-density lipoprotein (LDL-ox) particles along with a reduction in high-density lipoprotein (HDL). These inflammation-driven mechanisms are responsible for the derangement of vascular architecture which represents the earliest step of atherosclerosis, ultimately resulting in vulnerable plaque formation and rupture.

Endothelial dysfunction is well recognized as one of the earliest steps and major contributors in the development of atherosclerosis.19 It is characterized by the dysregulation of the balance between endothelial-dependent vasoconstriction and vasodilatation, mainly attributed to diminished nitric oxide bioavailability, and the enhanced expression of proinflammatory adhesion molecules, cytokines, chemotactic and prothrombotic factors, all of which participate in the development of atherosclerosis.20 A number of factors may impair endothelial function and act as triggers of endothelial activation. For example, TNF-, stimulates the expression of endothelial leukocyte adhesion molecules and promotes endothelial cell-leukocyte interaction resulting in increased recruitment and activation of inflammatory cells, within the arterial wall21,22 The ensuing disorganization of the vascular architecture and dysregulation of vascular tone lead to reduced endothelial nitric oxide synthase expression and further derangement of nitric oxide metabolism through various inflammation-driven mechanisms.23,24

The interaction between cytokines and endothelial cells activates the coagulation cascade and promotes intravascular fibrin deposition.25 Systemic inflammation induces the expression of the potent procoagulant molecule, tissue factor, by endothelial cells and platelet adhesion and aggregation,26,27 whereas endogenous fibrinolytic mechanisms are downregulated.28 This thrombotic propensity deteriorates the pro-atherogenic state and accelerates plaque formation. The intrinsic coagulation pathway, which also participates in hemostasis, is mainly mediated by the kallikrein-kinin system, a group of plasma proteins with an integral role in many biological processes, including coagulation and inflammation. Activation of the kallikrein-kinin system has been implicated in cardiovascular disease as a result of bradykinin release, an established proinflammatory mediator as well as the induced changes in the hemostatic system, leading to a hypercoagulable state. Moreover, recent data demonstrate that blockade of the kallikrein-kinin system can reduce complement activation and thereby the inflammatory response on the endothelium, providing additional mechanistic links between inflammation and atherosclerosis.29

Beyond their direct impact on endothelial function, systemic inflammation promotes an atherogenic lipoprotein profile. This is mostly characterized by increased levels of both small, highly atherogenic very low-density lipoprotein (VLDL) and oxidized low-density lipoprotein (LDL) particles, in combination with alterations in high-density lipoprotein (HDL) composition and function.30 A paradoxical suppression of total cholesterol, LDL and HDL levels is observed during the active phases of some chronic inflammatory disorders, such as RA and SLE, presenting an inverse association with the subsequent cardiovascular risk.31,32 This is explained by the disproportionate reduction in levels of HDL compared to LDL cholesterol, giving a more atherogenic total-cholesterol:HDL index.33 On top of lipid abnormalities, systemic inflammation exerts adverse effects on other metabolic pathways such as insulin resistance and body composition and is now considered one of the main pathogenetic mechanisms of the metabolic syndrome.34,35 Thus, it is not surprising that the magnitude of atherosclerosis in RA is comparable to that of diabetes mellitus.36

The understanding of the inflammatory background of atherosclerosis has reasonably given rise to the hypothesis that targeting mediators of the inflammatory process may attenuate the progression of the atherosclerotic plaque and, hence, lead to the reduction of cardiovascular events. he Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) trial was a randomized, double-blind, placebo-controlled trial designed to test the hypothesis that interleukin-1 inhibition with the administration of the human monoclonal antibody canakinumab could prevent recurrent cardiovascular events in patients with a history of myocardial infarction and a persistent pro-inflammatory response, as defined by elevated high-sensitivity C-reactive protein (hsCRP) levels (2 mg/L). The trial enrolled over 10,000 patients who were randomly assigned to receive placebo or canakinumab at doses of 50 mg, 150 mg and 300 mg. After a median follow-up period of 3.7 years, it was shown that canakinumab doses of 150 mg and 300 mg significantly reduced the risk for nonfatal myocardial infarction, nonfatal stroke or cardiovascular death by 15% (p = 0.021) and 14% (p = 0.031), respectively, compared to placebo, without any effect on cholesterol levels.37 This favorable effect on cardiovascular events was accompanied by a reduction of about 3540% in interleukin-6 and hsCRP levels as a consequence of direct interleukin-1 inhibition.

On the other hand, the Cardiovascular Inflammation Reduction Trial (CIRT) found that low-dose methotrexate treatment had no effect on major cardiovascular endpoints in patients with stable coronary artery disease and either type 2 diabetes or metabolic syndrome. The study enrolled 4786 patients who were randomized to receive low-dose methotrexate or placebo, followed for a median period of 2.3 years. The concept was to assess the benefits of a broader spectrum anti-inflammatory approach on cardiovascular outcomes, utilizing the ability of methotrexate to reduce the production of several inflammatory biomarkers, including CRP, interleukin-1, interleukin-6 and TNF-.38 Nevertheless, no reduction in the levels of the theoretically targeted inflammatory markers was observed in the active medication arm compared to placebo during the study period.

Higher median hsCRP levels in CANTOS at baseline compared to the corresponding values in CIRT which ranged within normal limits (4.2 vs 1.6 mg/L), may account for the contrasting outcomes of these trials, indicating that targeting inflammation may prevent recurrence of cardiovascular events only in those patients with signs of a persistent inflammatory response.39 It may also be assumed that blockade of the central interleukin-1 to interleukin-6 signaling pathway may be more effective than alternative anti-inflammatory approaches, but there is still a long distance to be covered before this theory can be confirmed.

Aiming to further test the inflammatory hypothesis of atherosclerosis, the Colchicine Cardiovascular Outcomes Trial (COLCOT) evaluated the impact of colchicine on cardiovascular outcomes, recruiting approximately 4500 patients with recent myocardial infarction, assigned to receive either colchicine at a daily dose of 0.5 mg or placebo.40 The anti-inflammatory properties of colchicine are attributed to the ability of the drug to inhibit microtubule polymerization, thereby preventing cytokine release and leukocyte migration. More specifically, the suppression of Nod-Like Receptor Protein 3 inflammasome by colchicine seems to be responsible for a down-regulation of interleukin-1 and interleukin-18 production leading to subsequent reductions in interleukin-6 and CRP.41 In COLCOT, treatment with colchicine over a 2-year period led to a 23% reduction in the recurrence of major cardiovascular events, including death from cardiovascular causes, myocardial infarction, stroke and unstable angina resulting in coronary interventions, compared to placebo.40

Severe reduction in coronary artery blood supply results in acute myocardial ischemia and myocardial necrosis. In the current era, reperfusion strategies aiming to timely restore blood flow within the ischemic region, have revolutionized the treatment of acute myocardial infarction by reducing the loss of vital myocardium, thus resulting in significantly improved outcomes. Despite prompt reperfusion treatments, cardiac injury and myocardial cell death following the ischemic event trigger local and systemic inflammatory responses promoted by intracellular cytokines, such as interleukin-1a. The activation of the inflammatory cascade, despite complete restoration of coronary flow, leads to further loss of cardiomyocytes, impairs myocardial healing and affects myocardial remodeling.42 The intensity of this inflammatory response seems to be associated with worse clinical outcomes, including mechanical complications of myocardial infarction and heart failure.43 Inhibition of the IL-1 pathway for 2 weeks with Anakinra, a recombinant human IL-1 receptor antagonist, in 40 patients with stable STEMI, was found to reduce CRP levels and prevent new-onset heart failure long-term after STEMI but had a neutral effect on recurrent ischemic events compared to placebo in the VCU-ART pilot studies.44,45

The MRC-ILA Heart Study recruited 182 patients with NSTEMI presenting in the first 48 hours after onset of chest pain, randomized to either anakinra treatment or placebo for 2 weeks. Despite a significant suppression in CRP levels in the anakinra arm, the incidence of hard cardiovascular endpoints was similar between the two groups at 30 days and 3 months of follow-up.46

On the other hand, chronic heart failure is considered as a condition of systemic inflammation, characterized by high circulating levels of inflammatory cytokines in response to hypoxia, hemodynamic overload and low-grade cell death.47 IL-1 has been identified as one of the soluble cardiodepressant factors, demonstrating negative inotropic effects on the myocardial cells by impairing -adrenergic receptor signaling downstream in multiple ways.48 The blockade of IL-1 pathways with anakinra has been shown to improve peak oxygen consumption and reduce inflammatory markers in patients with chronic heart failure.49,50 In 60 patients with acute decompensation of heart failure and elevated CRP levels randomized to receive anakinra for 2 weeks, 12 weeks or placebo within 14 days after hospital discharge, an improvement was observed regarding peak oxygen consumption, heart failure biomarkers and quality of life in patients in whom anakinra was continued for 12 weeks.51 In the DHART2 trial, however, among 31 patients with heart failure and preserved ejection fraction randomized to receive either anakinra or placebo, treatment with anakinra for 12 weeks reduced high sensitivity CRP and NT-pro-BNP levels but showed no impact on peak oxygen consumption.52

Recurrent pericarditis is a condition that poses therapeutic challenges because it is corticosteroid dependent and is resistant to treatment with colchicine. The AIRTRIP trial has proposed IL-1 inhibition with anakinra as a promising therapy for recurrent pericarditis, while its efficacy remains to be confirmed in large scale clinical trials.53

Although the management of traditional CVD risk factors has constituted for decades the cornerstone of CVD risk prevention strategies, targeting low and/or high grade chronic systemic inflammation emerges as a novel, challenging therapeutic approach for ameliorating the burden of atherosclerotic disease. The rationale for such interventions has been provided by observational and population-based studies in systemic rheumatic diseases, exploring whether antirheumatic treatment has a beneficial impact on vascular injury and CVD outcomes. Particularly for bDMARDs, a number of studies have tried to address this question by examining the effect of treatment on lipid profile, surrogate markers of atherosclerosis and CVD-related outcomes, as summarized in Table 1.

Table 1 Summary of the Effects of Biologic DMARDs on Cardiovascular Outcomes and Surrogate Markers

Findings should generally be interpreted with caution for several reasons: (a) early studies included mixed populations consisting of patients with various types of inflammatory arthritis;54,55 (b) the overwhelming majority of studies with hard end-points are observational, thus causation cannot be ascertained; (c) there are enormous variations in the type, number and disease state of patients included, the main methods used to assess biomarkers and surrogates and even the ascertainment of cardiovascular events. In this review, we focus on studies recruiting individuals with a specific type of arthritis; however it should be acknowledged that studies examining the cardiovascular effect of bDMARDs in patients with SpA are less robust. For studies examining surrogate markers, it is important to bear in mind, at which time points assessments were made. For example, just after administration of a tumor necrosis factor inhibitor (TNFi) or after a specific time interval like 3-, 6-, or 12-months.56,57 Thirdly, disease duration might also play some role in the influence that bDMARDs have on CVD-surrogate markers.58

Results for TNFi are somehow conflicting for total cholesterol (TC), HDL and triglycerides (TG) which appear to be stabilized or increased upon treatment with these drugs. A meta-analysis has shown that even if TC and HDL are increased, the TC/HDL ratio remains stable.59 In contrast, more consistent results exist for LDL which seems to be unaffected.60 On the other hand, there is a general agreement that IL-6 blockade with tocilizumab results in an increase in most components of the lipid profile.60 Data from systematic reviews and meta-analysis support that such treatment led to increased levels of TC, HDL and LDL.61 However, as shown in a Phase III study evaluating the effect of tocilizumab after 24 weeks of treatment, on CVD risk in RA, despite the increase in TC, LDL and TG, IL-6 inhibition led to an alteration of HDL composition towards an anti-inflammatory phenotype with less serum amyloid-A content.62,63 Data for B-cells depletion treatment, with rituximab are few and sometimes contradictory especially for TC and HDL which appear to be increased or stable,5,64 in contrast to LDL and TG which remain stable.5 Finally, in a study assessing the effect of bDMARDs in various CVD-related biomarkers, it was found that leptin/adipokine ratio was more improved for other biologics (including rituximab, tocilizumab and CTLA-4 inhibitor abatacept) compared to TNFi. In the same study, after 24 weeks, Lipoprotein-a was also more improved when tocilizumab was compared with TNFi.65

A number of observations and systematic reviews suggest that treatment with TNFi improves insulin resistance in RA patients.66,67 However, it remains unknown whether the TNFi exert their beneficial effects directly by normalizing beta cell function and insulin signaling or through other mechanisms independent of TNF- or systemic inflammation.68 In this respect a longitudinal study indicated that IL-1 inhibition with anakinra resulted in more effective control of patients with type-2 diabetes mellitus compared to TNF- after six months of treatment.69 The better outcomes were linked with a favorable shift of the adipokineprofile in the anakinra group suggesting a crucial role of IL-1 in metabolic dysregulation in diabetic RA patients. More importantly such observations provide evidence for a tailored approach in RA subjects with specific metabolic characteristics.

Although there are some disagreements, it seems that treatment with TNFi in RA leads to favorable outcomes in arterial stiffness as assessed by pulse-wave velocity (PWV) but not with the augmentation index (AUi), which remained unchanged in most of the studies for RA patients treated with TNFi.7074 Increased CVD risk and a window for improving aortic stiffness, seems to be present also in early RA. In a study enrolling patients with early RA, treatment with TNFi etanercept or with etanercept plus methotrexate, led to improvement in aortic distensibility after one year. Of note, no difference was noticed between treatment arms.75 Endothelial function seems also to be improved7678 as a recent meta-analysis has shown.79 It has to be stressed however that the different methods used for its measurement might limit the generalizability of these results.79 On the other hand, things are less clear for cIMT76,78 An RCT comparing methotrexate alone versus combination treatment with TNFi infliximab plus methotrexate, showed that there was no difference in cIMT between the two groups.80 Data from other studies, however, support that cIMT regressed or at least remained stable upon treatment with TNFi.74

Not many data are available for the other bDMARDs. In an open-label RCT, after 24 weeks, tocilizumab had the same effect with etanercept or adalimumab in arterial stiffness, as assessed by cardio-ankle vascular index and aortic augmentation index.81 As for rituximab, in a small study, 6 patients resistant to TNFi treatment, received rituximab and displayed significant improvement of flow-mediated dilation (FMD), as early as week 2, being also maintained up to week 6.82 Finally, another study evaluating 38 RA patients showed that FMD was improved at week 24 after rituximab infusion.83 On the other hand, no major effects were seen for cIMT, although longer follow-up period might be needed to assess the atheroprotective effect, if any.64,83 For Abatacept, data are too few to draw a definite conclusion.84 In a study with 45 RA patients, it has been shown that after 12 months of treatment cIMT and FMD remained stable.85

Several lines of evidence support the hypothesis that TNFi are indeed associated with lower risk for CVD events. Data from the British Society of Rheumatology Biologics Registry for RA patients treated with TNFi or bDMARDs-nave patients receiving conventional DMARDs were recorded for the 20012009 time period and linked with the national registry for myocardial infarctions (MI). It was shown that the former (median follow-up per person: 5.3 years) compared to the latter (median follow-up per person: 3.5 years) had less risk for MI.86 In a similar setting, no association was found between exposure to TNFi in RA patients and ischemic stroke.87 Data from about 4000 patients included in the QUEST-RA study an international multicentre crosssectional study selecting data from RA persons in three or more rheumatology clinics in several countries showed that prolonged exposure to TNFi was combined with lower risk for all CVD events including MI and stroke.88 Finally, in a large prospective study examining data from about 20,000 patients-years, derived from the database of the Australian rheumatology association, it was found that treatment with TNFi or other biologics in patients with inflammatory arthritis (including those with psoriatic arthritis or ankylosing spondylitis) was associated with less CVD events.89 In concert with these studies, a meta-analysis, published in 2011 showed that RA patients treated with TNFi compared to those receiving conventional DMARDs, had lower risk for MI and strokes in data derived from observational cohorts but not from RCTs.78,90 Finally, in the largest meta-analysis so far, Roubille et al found that TNFi treatment lead to reduction in the risk for MI and strokes but not heart failure in RA patients.91

Despite the unfavorable alterations observed in the lipid profile, tocilizumab does not exhibit higher risk for CVD compared to other biologics.92,93 Besides, a study examining single nucleotide polymorphisms (SNP) in the IL-6 receptor gene, found that a specific SNP was associated with altered odds of coronary heart disease in RA patients.94 In a recent RCT enrolling about 3000 patients and comparing tocilizumab vs etanercept, major adverse cardiovascular events were comparable between the two groups, after a mean follow-up of 3.2 years.95 In fact, the most recent meta-analysis has shown IL-6 inhibition with tocilizumab had a lower risk for major adverse cardiovascular events compared to TNFi but not with abatacept.96 With regards to rituximab, data are less robust. The results from the global clinical trial programme (n = 3595 patients, followed up for about 11 years), showed that rates for MI and CVD events were comparable to the general population.97 Of note, a handful of reports raise the possibility of acute MI after rituximab infusion in RA and lymphoma patients98,99 Finally, for abatacept, in a study using data from Marketscan and Medicare, having as a composite primary endpoint the occurrence of MI, transient ischemic attack and coronary revascularization, it was found that during the 31,733 years of follow-up, this regime was better than TNFi in RA patients with diabetes mellitus.100 In a study of a similar setting, RA patients treated with abatacept had 20% lower risk for CVD compared to those who received TNFi, regardless of their baseline CVD status.101 Of note, similar results were reported for older (>65 years-old) patients treated with abatacept. These, analyzing data from 47,193 patients, displayed lower risk for MI, than individuals with RA who received TNFi.102

Overall, one could say that the lipid alterations observed are of limited significance and do not seem to affect cardiovascular outcomes. Surrogate markers, like FMD are found to be improved or at least remain stable, upon treatment with bDMARDs, while hard outcomes like myocardial infarction and stroke are reduced. Results seems to be comparable across different bDMARDs classes, but data are more robust for TNFi.

Evidence about the association between treatment with biologic drugs and cardiovascular effect, is much less for SpA than for RA. It seems, however, that changes in the lipid profile are similar in both groups of patients.5 Complexity in the interpretation of the results derives also from the different diseases, like ankylosing spondylitis (AS) and psoriatic arthritis (PsA) classified under the umbrella of SpA. In fact, although they have many similarities, especially in terms of clinical manifestations and treatment options, it seems that regarding the underlying pathogenic mechanisms and comorbidities, there are some important differences between these conditions such as distribution of joint involvement predominantly spinal in AS and peripheral in PsA- unfavorable metabolic profile in PsA, skin disease in PsA and others. Additionally, data are missing for drugs that recently have been added in the rheumatologists armamentarium, like anti-IL-17 and anti-IL-23 regimes.

In AS patients, treatment with etanercept led to increase in HDL and TC over the first 3 months. Noteworthy, TC/HDL ratio was better, as were the qualitative changes in HDL. In fact, serum-amyloid A (SAA) disappeared, leading thus to a more atheroprotective HDL.103 In another study examining the effect of anti-TNF treatment in the lipid profile of AS patients, it was found that after 14 weeks of treatment, TC and HDL were increased while TC/HDL ratio, TG and LDL remained unchanged.104 Interestingly, a large study with more than 200 patients with axial SpA (axSpA the major representative of which is AS) showed that compared to non-TNFi users, patients who were treated with TNFi had no changes in their lipid profile. When comparisons were made in the latter group between baseline and 2-years follow-up, only a statistically significant increase was seen in TC.105 For PsA, Agca et al in 2017 showed that 5-years treatment with etanercept led to increased TC, HDL and LDL, leaving TC/HDL unchanged, however.106

In general and partially in contrast to what is observed for RA, arterial stiffness appears to remain unchanged for most of the studies regarding AS patients.74,107 A small study examining 28 AS patients did not find changes in arterial stiffness as assessed by PWV after 6 months of treatment with TNFi.108 In concert, similar results were presented by other investigators who reported no significant changes in AuI and PWV in AS patients treated with TNFi for 612 months.109,110

Treatment with TNFi seems to also have a beneficial effect to endothelial dysfunction in SpA. Syngle et al showed that in 12 AS patients treated with infliximab, FMD was improved after 12 weeks.111 Interestingly, it has also been shown that just after infliximab infusion, adhesion molecules used as surrogate markers for endothelial activation like sE-selectin, are significantly reduced in AS non-diabetic patients.112 Treatment with TNFi has also beneficial effects in microvascular function, since endothelium-dependent vasodilation and capillary recruitment was found to be improved in a small cohort of AS patients treated with etanercept for 1 month.113

Atherosclerotic lesions seem to be significantly improved in SpA patients treated with TNFi. In a study enrolling 81 AS patients, 67 of which were treated with TNFi, it was shown that after a mean follow-up of approximately 5 years, cIMT was stable for patients who continued treatment with TNFi but progressed in those who did not.114 Along the same lines, AS patients treated with TNFi for 2 years exhibited lower values of cIMT and number of atherosclerotic plaques compared to healthy individuals.115 Finally, in a randomized placebo controlled study, although treatment with TNFi golimumab left IMT unchanged, patients being in the placebo arm showed significant progression of IMT at 6 months.109

For PsA, in a small study, enrolling 20 PsA patients treated with TNFi, cIMT was significantly decreased at 3 months. After a mean follow-up of 2 years, the significant improvement of cIMT continued only for patients who had continued treatment with TNFi.80 Similarly, Di Minno et al, in a larger study, found that PsA patients treated with TNFi (meanSD treatment duration: 52.3324.11 months) had lower number of plaques and lower cIMT compared to those treated with conventional DMARDs (meanSD treatment duration: 58.2229.21 months).116 Noteworthy, treatment duration with TNFi was inversely correlated with cIMT, implying that effect of treatment on atherosclerotic lesions, at least in these patients is cumulative. It is possible that these effects are more pronounced in specific subgroups of patients. In a recent study, including about 300 patients (mean SD follow up: 2.9 0.7 years) with psoriasis and PsA, it was found that treatment with TNFi reduced the atherosclerotic progression in males but not in females.117 Importantly, measuring vascular inflammation with positron emission tomography (PET), in a subgroup of this cohort, patients treated with TNFi but not those not receiving biologics, had significantly lower target-to-blood pool ratio (TBR) after 1 year.117

Despite psoriasis and PsA having been recognized to be closely linked with CVD risk, not many studies have assessed the effect of immunosuppressives on that. In a relatively recent meta-analysis about the effect of TNFi on CVD risk in patients with inflammatory arthritis, only 6 studies for psoriasis/PsA were included.91 The investigators were able to show that treatment with these regimes was associated with a reduced risk for all CVD, compared to topical therapy. Similarly, in another meta-analysis, it was shown that, compared to Pso/PsA patients receiving topical treatment or methotrexate, those treated with TNFi, had lower risk for CVD or MI.118 Comparing different biologics, a large study (78,162 patients) using data from US commercial databases for patients with psoriasis or PsA, found that the risk for atrial fibrillation or major adverse CVD events did not differ between patients treated with the IL-23 inhibitor ustekinumab or TNFi.119 Data for newer treatment modalities for PsA and AS, like drugs targeting IL-17, are lacking.

Data are less solid for SpA compared to RA. This is more pronounced for newer therapeutic regimes like anti-IL-17 and anti-IL-23 regimes. In general, despite increase in TC and HDL, TC/HDL ratio remains unchanged. Additionally, treatment with TNF inhibitors seems to improve endothelial dysfunction and atherosclerosis, while limited data support the favorable effect of these drugs in hard CVD outcomes.

Inflammatory myocardial disease characterized by immune cell infiltration, degeneration and necrosis of cardiomyocytes is common in systemic autoimmune disorders. From a pathophysiological standpoint, such changes culminate in myocardial oedema the main feature of acute cardiac tissue injury due to autoimmune activation and/or microvascular ischemia which, if untreated, leads to cardiac tissue fibrosis and subsequently to myocardial dysfunction. Cardiac magnetic resonance (CMR) allows the non-invasive visualization and detailed characterization of the various types of myocardial injury, namely oedema, fibrosis, perfusion defects, coronary vessels inflammatory and structural abnormalities,120 all of which occur in patients with systemic diseases and are tightly linked with heightened risk of CV events in this population.121

CMR based studies have demonstrated a substantial degree of myocardial inflammation in systemic autoimmune diseases such as systemic lupus erythematosus, inflammatory myopathies, scleroderma and systemic vasculitis even in individuals without clinical symptoms and normal evaluation of heart function with echocardiography, electrocardiogram and cardiac biomarkers such as troponin.122125 For example a retrospective study including 78 newly diagnosed, treatment nave persons with various systemic autoimmune disorders revealed clinically silent myocardial oedema and fibrosis in the majority of patients.126 Interestingly enough, these abnormalities resolved in follow-up scans after 1 year of treatment for the underlying disease as per physicians choice.

Despite the lack of large prospective studies, there are a few reports indicating that anti-inflammatory regimens have a direct beneficial effect on myocardial oedema assessed by CMR before and after therapeutic intervention. Aggressive treatment with intravenous methylprednisolone followed by immunosuppressives such as cyclophosphamide, azathioprine reduced myocardial contrast enhancement on CMR in patients with autoimmune myositis and such findings were in accordance with clinical improvement.110 Similarly, the prompt initiation of steroids and disease modifying drugs improved cardiovascular outcomes in patients with ANCA-positive vasculitis-related cardiomyopathy, suggesting that antirheumatic drugs of various classes hold a crucial role in ameliorating myocardial inflammation across the whole spectrum of systemic inflammatory diseases.127,128 With regards to bDMARDs a small case-series reported considerable improvement in SLE patients with myocarditis treated with rituximab.129

A number of recent CMR-based studies have provided further insights in the relationship between systemic and myocardial inflammation by indicating significant improvement of heart function after treatment with bDMARDs.130 Ntusi et al showed that treatment with TNFi resulted in considerable attenuation of subclinical myocardial oedema in 32 patients with inflammatory arthritides after 36 months of treatment.131 Reduction of myocardial inflammation was accompanied by improvement in myocardial function and overall disease activity. In line with these observations, IL-6 inhibition with tocilizumab not only improved left ventricular injection fraction but also normalized structural abnormalities such as left ventricular hypertrophy assessed by mass index, confirming the findings of previous echocardiography studies.132134 Taken all together these findings suggest a mechanistic role of TNF- and IL-6 inhibition in modulating myocardial impairment and improving indices of cardiac function in inflammatory diseases. It has been suggested that chronic exposure of the myocardium to pro-inflammatory cytokines mediates amongst others adverse ventricular remodeling leading to diastolic dysfunction and heart failure with preserved ejection fraction, one of the leading causes of death in systemic diseases.135137 Biologic DMARDs may have pleiotropic effects and express their action through suppression of systemic inflammation but also by specific antibody mediated cellular effect on the myocardium. Although some reports suggested an increased frequency of developing heart failure following treatment with bDMARDs,138,139 a systematic review concluded that bDMARDs probably do not increase this risk but in contrast, may have a beneficial effect on morphological and functional parameters of the myocardium highlighting the need for better quality studies.140 To lend more support to the former, treatment with TNFi seems to reduce the levels of N-Terminal probrain natriuretic peptide a well-established biomarker of cardiac performance in patients with RA.141 However, and until future large controlled studies address this question, bDMARDs are generally not recommended in patients with functional class IIIIV heart-failure.

Such observations provide the rationale for large longitudinal studies investigating the results of immunosuppressive treatment on myocardial inflammation and function determined by CMR in systemic rheumatologic diseases in earlier or later stages of the disease.142

Although robust evidence is currently lacking, it appears that treatment with bDMARDs has a positive impact on CVD risk by favorably modifying several aspects of CVD in patients with systemic inflammatory disorders. However, differences in CVD targets should be taken into account when evaluating such data as it is not evident which particular effect and which class of antirheumatic drugs may be responsible for the overall beneficial effect on CVD risk. Apparently, the suppression of systemic inflammation represents the basic mechanism as elevated C-reactive protein has been linked with increased CVD mortality and morbidity in RA patients.143 The increase of lipid levels in these patients following treatment mainly with TNFi and IL-6 inhibitors reflects rather the restoration of lipid metabolism to the level prior the onset of inflammatory disease rather than an atherogenetic process. Furthermore, bDMARDs render atheroprotective effects by improving endothelial function, normalizing coagulation status and alleviating insulin resistance. RA individuals with a higher degree of response to TNFi inhibitors, appear to have a lower incidence of CVD events compared to those with suboptimal control of disease activity supporting the link between inflammation and atherosclerosis.144,145 To lend more support, the results of a secondary analysis of the CANTOS trial suggest that patients achieving the largest reduction in high sensitivity C-reactive protein with canakinumab treatment, had better CVD outcomes.146 On the other hand, the influence of concomitant methotrexate administration with bDMARDs on CVD reduction in patients with inflammatory arthritides has not been investigated complicating the interpretation of the data. Given that patients with longstanding, active disease are more likely to be treated with bDMARDs, only a few studies are adjusted for confounding by indication which is a crucial concern for drawing any definite conclusions regarding the precise impact of these regimens on CVD risk.147

Besides inflammatory burden reduction, drug-specific mechanisms may be responsible for the improved outcome. The CANTOS trial provides evidence that IL-1 inhibition may reduce CVD events suggesting a mechanistic relationship between targeting of the IL-1, IL-6 pathway of innate immunity and treatment of atherosclerosis.148 In this regard, IL-6 blockade may also represent a novel target of vascular therapy as the beneficial effects of canakinumab in CANTOS trial are directly linked with the magnitude of IL-6 inhibition.149 The role of other alternative inflammatory pathways has not been investigated yet. For example NLRP3 inflammasome inhibition reduces atherosclerotic lesions and improves myocardial ischemia in experimental models,150,151 whereas the potential athLRP3-inhibiting properties of colchicine may also be associated with atheroprotective action.152

Taken all together future research agenda in this field may include a shift from traditional atherosclerotic macrovascular disease to other mechanisms which may contribute to increased CVD risk such as silent microvascular myocardial injury in parallel with a personalized medicine based on individual characteristics as well as CVD and disease-related risk profile of the patients. In that respect, the identification of biomarkers and clinical predictors in patients with inflammatory conditions might lead to strategies that support individual patients for specific therapies which in turn may target CVD inflammation more effectively.

The introduction of bDMARDs in the treatment armamentarium has revolutionized the overall management of systemic inflammatory diseases culminating in better long term outcomes and improvement in survival of patients suffering from these conditions.153,154 Modern treatment strategies targeting effective control of inflammation seem to have a positive impact on CVD mortality but it still remains unknown whether such observations reflect a direct effect on vascular pathology or are the results of the suppression of systemic inflammation. Lessons taken from inflammatory arthropathies might have implications in the management of atherosclerosis in the general population as indicated by CANTOS trial. The research in this field is in its infancy and future large studies could determine whether bDMARDs could provide further benefit in the prevention and treatment of atherosclerosis beyond established measures such as management of classical CVD factors and lifestyle changes.

George Fragoulis and Stergios Soulaidopoulos share first authorship. All authors made substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data; took part in drafting the article or revising it critically for important intellectual content; agreed to submit to the current journal; gave final approval of the version to be published; and agree to be accountable for all aspects of the work. All the contributing authors have read and approved the final edition of the manuscript.

The authors report no conflicts of interest in this work.

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2. Tedgui A, Mallat Z. Cytokines in atherosclerosis: pathogenic and regulatory pathways. Physiol Rev. 2006;86(2):515581. doi:10.1152/physrev.00024.2005

3. Arida A, Protogerou AD, Kitas GD, Sfikakis PP. Systemic inflammatory response and atherosclerosis: the paradigm of chronic inflammatory rheumatic diseases. Int J Mol Sci. 2018;19(7):127. doi:10.3390/ijms19071890

4. Gasparyan AY. Cardiovascular risk and inflammation in rheumatic diseases. Rheumatol Int. 2017;37(1):12. doi:10.1007/s00296-016-3619-8

5. Nurmohamed M, Choy E, Lula S, Kola B, DeMasi R, Accossato P. The impact of biologics and tofacitinib on cardiovascular risk factors and outcomes in patients with rheumatic disease: a systematic literature review. Drug Saf. 2018;41(5):473488. doi:10.1007/s40264-017-0628-9

6. Zegkos T, Kitas G, Dimitroulas T. Cardiovascular risk in rheumatoid arthritis: assessment, management and next steps. Ther Adv Musculoskelet Dis. 2016;8(3):86101. doi:10.1177/1759720X16643340

7. Agca R, Heslinga SC, Rollefstad S, et al. EULAR recommendations for cardiovascular disease risk management in patients with rheumatoid arthritis and other forms of inflammatory joint disorders: 2015/2016 update. Ann Rheum Dis. 2017;76(1):1728. doi:10.1136/annrheumdis-2016-209775

8. Arida A, Protogerou AD, Konstantonis G, Fragiadaki K, Kitas GD, Sfikakis PP. Atherosclerosis is not accelerated in rheumatoid arthritis of low activity or remission, regardless of antirheumatic treatment modalities. Rheumatology. 2017;56:934939. doi:10.1093/rheumatology/kew506

9. Jamthikar AD, Gupta D, Puvvula A, et al. Cardiovascular risk assessment in patients with rheumatoid arthritis using carotid ultrasound B-mode imaging. Rheumatol Int. 2020;40(12):19211939. doi:10.1007/s00296-020-04691-5

10. Tousoulis D, Oikonomou E, Economou EK, Crea F, Kaski JC. Inflammatory cytokines in atherosclerosis: current therapeutic approaches. Eur Heart J. 2016;37(22):17231732. doi:10.1093/eurheartj/ehv759

11. Drakopoulou M, Soulaidopoulos S, Oikonomou G, Tousoulis D, Toutouzas K. Cardiovascular effects of biologic disease-modifying anti-rheumatic drugs (DMARDs). Curr Vasc Pharmacol. 2020;18(5):488506. doi:10.2174/1570161118666200214115532

12. Ridker PM, MacFadyen JG, Thuren T, Libby P. Residual inflammatory risk associated with interleukin-18 and interleukin-6 after successful interleukin-1beta inhibition with canakinumab: further rationale for the development of targeted anti-cytokine therapies for the treatment of atherothrombosis. Eur Heart J. 2020;41(23):21532163. doi:10.1093/eurheartj/ehz542

13. Protogerou AD, Zampeli E, Fragiadaki K, Stamatelopoulos K, Papamichael C, Sfikakis PP. A pilot study of endothelial dysfunction and aortic stiffness after interleukin-6 receptor inhibition in rheumatoid arthritis. Atherosclerosis. 2011;219(2):734736. doi:10.1016/j.atherosclerosis.2011.09.015

14. Gasparyan AY, Ayvazyan L, Blackmore H, Kitas GD. Writing a narrative biomedical review: considerations for authors, peer reviewers, and editors. Rheumatol Int. 2011;31(11):14091417. doi:10.1007/s00296-011-1999-3

15. Nurmohamed MT, Heslinga M, Kitas GD. Cardiovascular comorbidity in rheumatic diseases. Nat Rev Rheumatol. 2015;11(12):693704. doi:10.1038/nrrheum.2015.112

16. Kitas GD, Gabriel SE. Cardiovascular disease in rheumatoid arthritis: state of the art and future perspectives. Ann Rheum Dis. 2011;70(1):814. doi:10.1136/ard.2010.142133

17. Hansildaar R, Vedder D, Baniaamam M, Tausche AK, Gerritsen M, Nurmohamed MT. Cardiovascular risk in inflammatory arthritis: rheumatoid arthritis and gout. Lancet Rheumatol. 2020;3(1):e58e70. doi:10.1016/S2665-9913(20)30221-6

18. Kisiel B, Kruszewski R, Juszkiewicz A, et al. Methotrexate, cyclosporine A, and biologics protect against atherosclerosis in rheumatoid arthritis. J Immunol Res. 2015;2015:18. doi:10.1155/2015/759610

19. Steyers CM, Miller FJ. Endothelial dysfunction in chronic inflammatory diseases. Int J Mol Sci. 2014;15(7):1132411349. doi:10.3390/ijms150711324

20. Sitia S, Tomasoni L, Atzeni F, et al. From endothelial dysfunction to atherosclerosis. Autoimmun Rev. 2010;9(12):830834. doi:10.1016/j.autrev.2010.07.016

21. Page MJ, Bester J, Pretorius E. The inflammatory effects of TNF- and complement component 3 on coagulation. Sci Rep. 2018;8(1):19. doi:10.1038/s41598-018-20220-8

22. Bamias G, Stamatelopoulos K, Zampeli E, et al. Circulating levels of TNF-like cytokine 1A correlate with the progression of atheromatous lesions in patients with rheumatoid arthritis. Clin Immunol. 2013;147(2):144150. doi:10.1016/j.clim.2013.03.002

23. Dimitroulas T, Hodson J, Sandoo A, Smith J, Kitas GD. Endothelial injury in rheumatoid arthritis: a crosstalk between dimethylarginines and systemic inflammation. Arthritis Res Ther. 2017;19(1):32. doi:10.1186/s13075-017-1232-1

24. Dimitroulas T, Sandoo A, Douglas K, Kitas G. Symmetric and asymmetric dimethylarginines as biochemical markers of endothelial dysfunction and atherosclerosis in Rheumatoid Arthritis. Mediterr J Rheumatol. 2015;26(2):6275.

25. Dimitroulas T, Douglas KM, Panoulas VF, et al. Derangement of hemostasis in rheumatoid arthritis: association with demographic, inflammatory and metabolic factors. Clin Rheumatol. 2013;32(9):13571364. doi:10.1007/s10067-013-2283-6

26. Gasparyan AY, Stavropoulos-Kalinoglou A, Mikhailidis DP, Douglas KM, Kitas GD. Platelet function in rheumatoid arthritis: arthritic and cardiovascular implications. Rheumatol Int. 2011;31(2):153164. doi:10.1007/s00296-010-1446-x

27. Al-Rawi ZS, Gorial FI, Al-Bayati AA. Red cell distribution width in rheumatoid arthritis. Mediterr J Rheumatol. 2018;29(1):3842. doi:10.31138/mjr.29.1.38

28. Bisoendial RJ, Levi M, Tak PP, Stroes ES. The prothrombotic state in rheumatoid arthritis: an additive risk factor for adverse cardiovascular events. Semin Thromb Hemost. 2010;36(4):452457. doi:10.1055/s-0030-1254054

29. Lopatko I, Sthl A, Mossberg M, et al. Blockade of the kallikrein-kinin system reduces endothelial complement activation in vascular inflammation. EBioMedicine. 2019;47:319328.

30. van Diepen JA, Berbe JFP, Havekes LM, Rensen PCN. Interactions between inflammation and lipid metabolism: relevance for efficacy of anti-inflammatory drugs in the treatment of atherosclerosis. Atherosclerosis. 2013;228(2):306315. doi:10.1016/j.atherosclerosis.2013.02.028

31. E. Toms T, P. Symmons D, D. Kitas G. Dyslipidaemia in rheumatoid arthritis: the role of inflammation, drugs, lifestyle and genetic factors. Curr Vasc Pharmacol. 2010;8(3):301326. doi:10.2174/157016110791112269

32. Myasoedova E, Crowson CS, Kremers HM, et al. Lipid paradox in rheumatoid arthritis: the impact of serum lipid measures and systemic inflammation on the risk of cardiovascular disease. Ann Rheum Dis. 2011;70(3):482487. doi:10.1136/ard.2010.135871

33. Georgiadis AN, Papavasiliou EC, Lourida ES, et al. Atherogenic lipid profile is a feature characteristic of patients with early rheumatoid arthritis: effect of early treatmenta prospective, controlled study. Arthritis Res Ther. 2006;8(3):R82. doi:10.1186/ar1952

34. Sattar N, Kitas GD. Rheumatoid arthritis: testing the inflammation-insulin resistance link in clinical trials. Nat Rev Rheumatol. 2013;9(12):702703. doi:10.1038/nrrheum.2013.178

35. Stavropoulos-Kalinoglou A, Metsios GS, Koutedakis Y, Kitas GD. Body-size phenotypes and cardiometabolic risk in Rheumatoid Arthritis (Short Title: subgroups of obesity in RA). Mediterr J Rheumatol. 2016;27(2):4854. doi:10.31138/mjr.27.2.48

36. Stamatelopoulos KS, Kitas GD, Papamichael CM, et al. Atherosclerosis in rheumatoid arthritis versus diabetes: a comparative study. Arter Thromb Vasc Biol. 2009;29(10):17021708. doi:10.1161/ATVBAHA.109.190108

37. Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017;377(12):11191131. doi:10.1056/NEJMoa1707914

38. Halilova KI, Brown EE, Morgan SL, et al. Markers of treatment response to methotrexate in rheumatoid arthritis: where do we stand? Int J Rheumatol. 2012;2012:17. doi:10.1155/2012/978396

39. Ridker PM. Anti-inflammatory therapy for atherosclerosis: interpreting divergent results from the CANTOS and CIRT clinical trials. J Intern Med. 2019;285(5):503509. doi:10.1111/joim.12862

40. Tardif J-C, Kouz S, Waters DD, et al. Efficacy and safety of low-dose colchicine after myocardial infarction. N Engl J Med. 2019;381(26):24972505. doi:10.1056/NEJMoa1912388

41. Slobodnick A, Shah B, Krasnokutsky S, Pillinger MH. Update on colchicine, 2017. Rheumatology. 2018;57(1):i4i11. doi:10.1093/rheumatology/kex453

42. Abbate A, Toldo S, Marchetti C, Kron J, Van Tassell BW, Dinarello CA. Interleukin-1 and the inflammasome as therapeutic targets in cardiovascular disease. Circ Res. 2020;126:12601280. doi:10.1161/CIRCRESAHA.120.315937

43. Seropian IM, Toldo S, Van Tassell BW, Abbate A. Anti-inflammatory strategies for ventricular remodeling following St-segment elevation acute myocardial infarction. J Am Coll Cardiol. 2014;63(16):15931603. doi:10.1016/j.jacc.2014.01.014

44. Abbate A, Van Tassell BW, Biondi-Zoccai G, et al. Effects of interleukin-1 blockade with anakinra on adverse cardiac remodeling and heart failure after acute myocardial infarction [from the virginia commonwealth university-anakinra remodeling trial (2) (vcu-art2) pilot study]. Am J Cardiol. 2013;111(10):13941400. doi:10.1016/j.amjcard.2013.01.287

45. Abbate A, Kontos MC, Abouzaki NA, et al. Comparative safety of interleukin-1 blockade with anakinra in patients with ST-segment elevation acute myocardial infarction (from the VCU-ART and VCU-ART2 pilot studies). Am J Cardiol. 2015;115(3):288292. doi:10.1016/j.amjcard.2014.11.003

46. Morton AC, Rothman AMK, Greenwood JP, et al. The effect of interleukin-1 receptor antagonist therapy on markers of inflammation in non-ST elevation acute coronary syndromes: the MRC-ILA Heart Study. Eur Heart J. 2015;36(6):377384. doi:10.1093/eurheartj/ehu272

47. Yndestad A, Dams JK, ie E, Ueland T, Gullestad L, Aukrust P. Systemic inflammation in heart failure - The whys and wherefores. Heart Fail Rev. 2006;11(1):8392. doi:10.1007/s10741-006-9196-2

48. Van Tassell BW, Toldo S, Mezzaroma E, Abbate A. Targeting interleukin-1 in heart disease. Circulation. 2013;128(17):19101923. doi:10.1161/CIRCULATIONAHA.113.003199

49. van Tassell BW, Arena RA, Toldo S, et al. Enhanced interleukin-1 activity contributes to exercise intolerance in patients with systolic heart failure. PLoS One. 2012;7(3):e33438. doi:10.1371/journal.pone.0033438

50. Van Tassell BW, Abouzaki NA, Erdle CO, et al. Interleukin-1 blockade in acute decompensated heart failure: a randomized, double-blinded, placebo-controlled pilot study. J Cardiovasc Pharmacol. 2016;67(6):544551. doi:10.1097/FJC.0000000000000378

Read the rest here:
Effect of biologics on cardiovascular inflammation | JIR - Dove Medical Press


Psoriatic Arthritis Pipeline Insight to See Strong Expansion Through 2027 Covid-19 Analysis KSU | The Sentinel Newspaper – KSU | The Sentinel…

Friday, May 14th, 2021

Psoriatic Arthritis Pipeline Insight Market Report defines the business objective to help business owners to avoid contradictory expectations. It provides you customer data along with their demands hence you can accordingly plan for the launching of the product in the market. It presents all the data about whole market scenario. With the help of prominent data provided in the Psoriatic Arthritis Pipeline Insight Market Report, organizations come to know about customers completely and can achieve their goal of selling products in huge quantity and getting huge profits too. Clearly setting the business goal at the beginning will surely help to avoid getting difficulties and set the business easily.

Request sample copy of this report at

DelveInsights, Psoriatic Arthritis Pipeline Insight, 2021, report provides comprehensive insights about 50+ companies and 50+ pipeline drugs in Psoriatic Arthritis pipeline landscape. It covers the pipeline drug profiles, including clinical and nonclinical stage products. It also covers the therapeutics assessment by product type, stage, route of administration, and molecule type. It further highlights the inactive pipeline products in this space.

Geography Covered

Global coverage

Psoriatic Arthritis Understanding

Psoriatic Arthritis: Overview

Psoriatic Arthritis is a chronic inflammatory disease of the joints that can be associated with the psoriasis. It can affect both peripheral joints and axial skeleton causing pain, stiffness, swelling and joint destruction. This joint pathology develops gradually and cause more nuisance than disabling. Psoriatic arthritis is considered as seronegative spondyloarthropathies. The fact that it is Seronegative is that the blood tests negative for some factors that is present in rheumatoid arthritis. Spondyloarthropathy describes a group of conditions that all share common characteristics. First, there is a presence of arthritis that affects the spine. Second, inflammation occurs in ligaments, tendons and sometimes in other organs such as the eye.

Psoriatic Arthritis- Pipeline Insight, 2021 report by DelveInsight outlays comprehensive insights of present scenario and growth prospects across the indication. A detailed picture of the Psoriatic Arthritis pipeline landscape is provided which includes the disease overview and Psoriatic Arthritis treatment guidelines. The assessment part of the report embraces, in depth Psoriatic Arthritis commercial assessment and clinical assessment of the pipeline products under development. In the report, detailed description of the drug is given which includes mechanism of action of the drug, clinical studies, NDA approvals (if any), and product development activities comprising the technology, Psoriatic Arthritis collaborations, licensing, mergers and acquisition, funding, designations and other product related details.

Report Highlights

The companies and academics are working to assess challenges and seek opportunities that could influence Psoriatic Arthritis R&D. The therapies under development are focused on novel approaches to treat/improve Psoriatic Arthritis.

Psoriatic Arthritis Emerging Drugs Chapters

This segment of the Psoriatic Arthritis report encloses its detailed analysis of various drugs in different stages of clinical development, including Phase III, II, I, preclinical and Discovery. It also helps to understand clinical trial details, expressive pharmacological action, agreements and collaborations, and the latest news and press releases.

Psoriatic Arthritis Emerging Drugs

ABT-494: AbbVie

Discovered and developed by AbbVie, RINVOQ is a selective and reversible JAK inhibitor studied in several immune-mediated inflammatory diseases. In August 2019, RINVOQ received U.S. Food and Drug Administration approval for adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate. In December 2019, RINVOQ also received approval by the European Commission for the treatment of adult patients with moderate to severe active rheumatoid arthritis who have responded inadequately to, or who are intolerant to one or more disease-modifying anti-rheumatic drugs. Phase 3 trials of RINVOQ in rheumatoid arthritis, psoriatic arthritis, axial spondyloarthritis, Crohn s disease, atopic dermatitis, ulcerative colitis and giant cell arteritis are ongoing.

Risankizumab: Abbvie

Risankizumab is an interleukin-23 (IL-23) inhibitor that selectively blocks IL-23 by binding to its p19 subunit. IL-23, a cytokine involved in inflammatory processes, is thought to be linked to a number of chronic immune-mediated diseases, including psoriasis.

Further product details are provided in the report ..

Psoriatic Arthritis: Therapeutic Assessment

This segment of the report provides insights about the different Psoriatic Arthritis drugs segregated based on following parameters that define the scope of the report, such as:

Major Players in Psoriatic Arthritis

There are approx. 50+ key companies which are developing the therapies for Psoriatic Arthritis. The companies which have their Psoriatic Arthritis drug candidates in the most advanced stage, i.e. Registered include, Abbvie.


DelveInsight s report covers around 50+ products under different phases of clinical development like

Late stage products (Phase III)

Mid-stage products (Phase II)

Early-stage product (Phase I) along with the details of

Pre-clinical and Discovery stage candidates

Discontinued & Inactive candidates

Route of Administration

Psoriatic Arthritis pipeline report provides the therapeutic assessment of the pipeline drugs by the Route of Administration. Products have been categorized under various ROAs such as






Molecule Type

Products have been categorized under various Molecule types such as

Monoclonal Antibody



Small molecule

Gene therapy

Product Type

Drugs have been categorized under various product types like Mono, Combination and Mono/Combination.

Psoriatic Arthritis: Pipeline Development Activities

The report provides insights into different therapeutic candidates in Phase III, II, I, preclinical and discovery stage. It also analyses Psoriatic Arthritis therapeutic drugs key players involved in developing key drugs.

Pipeline Development Activities

The report covers the detailed information of collaborations, acquisition and merger, licensing along with a thorough therapeutic assessment of emerging Psoriatic Arthritis drugs.

Psoriatic Arthritis Report Insights

Psoriatic Arthritis Pipeline Analysis

Therapeutic Assessment

Unmet Needs

Impact of Drugs

Psoriatic Arthritis Report Assessment

Pipeline Product Profiles

Therapeutic Assessment

Pipeline Assessment

Inactive drugs assessment

Unmet Needs

Key Questions

Current Treatment Scenario and Emerging Therapies:

How many companies are developing Psoriatic Arthritis drugs

How many Psoriatic Arthritis drugs are developed by each company

How many emerging drugs are in mid-stage, and late-stage of development for the treatment of Psoriatic Arthritis

What are the key collaborations (Industry Industry, Industry Academia), Mergers and acquisitions, licensing activities related to the Psoriatic Arthritis therapeutics

What are the recent trends, drug types and novel technologies developed to overcome the limitation of existing therapies

What are the clinical studies going on for Psoriatic Arthritis and their status

What are the key designations that have been granted to the emerging drugs

Key Players



Fresenius Kabi


Fujifilm Kyowa Kirin Biologics


Zydus cadilla


Shanghai Henlius Biotech

Hetero Biopharma


Fresenius Kabi

Torrent Pharmaceuticals





Boehringer Ingelheim

Sun Pharma Global

Gilead Sciences

UCB Biopharma


Bristol-Myers Squibb


Psoriatic Arthritis Pipeline Insight to See Strong Expansion Through 2027 Covid-19 Analysis KSU | The Sentinel Newspaper - KSU | The Sentinel...


Hip pain when walking: Causes and treatment – Medical News Today

Sunday, May 2nd, 2021

Hip pain when walking is a common problem, according to a 2015 study. It is usually caused by problems in the following areas:

Arthritis is a major cause of hip pain when walking. There are over 100 types of arthritis and people of all ages can develop it.

Osteoarthritis (OA) and rheumatoid arthritis (RA) are types of arthritis that affect the joints.

Arthritis typically causes an ache and stiffness in the affected area.

Osteoarthritis is one of the most common types of arthritis. It is caused by cartilage between the bones breaking down, which eventually allows the bones to rub together.

This can cause pain, stiffness and reduced movement. A person with OA in the hip may also feel pain in the groin, buttocks, and sometimes on the inside of the knee or thigh.

Treatments for OA include:

Rheumatoid arthritis (RA) occurs when a persons immune system is not working properly and attacks the joints.

A person with RA in the hip may experience pain, stiffness, and swelling in the hip, thigh, or groin. It usually affects both hips.

Treatments for RA include:

Tendons are the tissues that connect skeletal muscle to bone.

When tendons are inflamed, they can become swollen, irritated, or painful. This condition is called tendinitis, and is often caused by injury or overuse of the tendons.

A person with tendinitis may feel a dull ache where the tendon and bone meet.

Treatments for tendinitis include:

The iliotibial (IT) band is made up of fascia fibers that run from the lateral hip to the top of the shin.

The IT band can tighten if overused, causing inflammation and pain. It most often causes pain in the knee when bending, with referred pain in the hip.

Treatments for IT band tightness include:

Small, fluid-filled sacs called bursae reduce friction between muscles, bones, and tendons around joints. When the bursae become inflamed it is called bursitis.

A person with bursitis will feel pain near the affected joint. A person may develop bursitis if they overuse their muscles.

According to the Arthritis Foundation, bursitis commonly affects the hips, which may be tender and ache during movement.

Treatments for bursitis include:

Labral tears can affect the labrum, which is a ring of cartilage that helps to keep the head (ball) of the femur in place in the acetabulum (socket) of the pelvis.

Labral tears are a major cause of pain in people with symptomatic hip dysplasia. A person with a hip labral tear will feel pain across the entire hip and may experience a clicking sound and locking or a shifty feeling in the joint.

Treatments for labral tears include:

Hip flexor strain can occur when the hip flexor muscles, which connect the femur to the lower back and hip, are injured or strained. This can make it harder to move your knee and thigh upwards to your chest.

A person will usually feel a cramping or pain in the upper leg and a tugging feeling in the thighs and groin.

Treatments for hip flexor strain include:

Sprains or strains can happen when a person overuses the muscles and ligaments in their hips and legs. A person may feel a sharp pain that gets worse with activity.

Treatments for sprains and strains include:

Toxic synovitis is an inflammatory condition of the hip joint that primarily affects children. A person with toxic synovitis may feel pain spreading across the hip area that may increase when bearing weight.

Treatments for toxic synovitis include rest and pain treatment medication, such as an NSAID.

Avascular necrosis, also called osteonecrosis, limits or stops blood flow to the hip joint and other joints. A person with this condition may feel a dull or throbbing ache in the hip that may spread to the groin.

Treatments for avascular necrosis or osteonecrosis include:

According to a 2014 study, most people fracture their hip joint because of a fall. Risk factors for hip fractures include low levels of activity, low bone density, and long-term medication use.

A person with a hip joint fracture will feel pain in the groin and may not be able to put weight on the affected side.

Treatments for a fractured hip joint include:

Osteoporosis condition causes brittle, weak bones. According to a 2002 study, bone fractures can affect almost any bone because of osteoporosis.

A person may feel severe, sudden pain in the hip that worsens with movement.

Treatment of osteoporosis includes:

Joints contain a small amount of fluid. When a joint is affected by arthritis, especially an inflammatory type such as rheumatoid arthritis, fluid can build up in the joint and cause swelling.

A person with joint effusion may feel associated pain that ranges from mild to sharp.

Treatments for joint effusion include:

Hip dislocation happens when the femur slips out of place in the hip socket. According to a 2018 study, a person should seek and receive treatment within 6 hours of the injury to avoid further damage.

A person who has dislocated their hip may feel severe pain, and the hip joint may feel loose and unsteady.

Treatments for dislocation include a closed reduction, which involves a doctor carefully applying force to put the hip back into its socket, or an open reduction, which involves a doctor cutting into the joint, removing excess bone or tissue, and re-positioning bones.

Osteomyelitis of the hip is an inflammatory bone disease typically caused by microorganisms infecting the bone(s) of the hip joint. It leads to progressive bone destruction and loss.

A person may experience related muscle spasms and deep, aching pain in the pelvis and/or upper leg.

The type of treatment a person will have depends on the type of osteomyelitis.

Treatment for acute osteomyelitis includes antibiotics or antifungal medication.

Treatment for sub-acute osteomyelitis, or chronic osteomyelitis, includes:

Nerve problems near the hip joint can also cause pain in the hip when walking.

A pinched (entrapped) nerve can occur in the hip region. A nerve can be pinched by bones, tendons, or ligaments, which causes nerve signals to be irritated by pressure or friction.

A person may experience sharp pain in the thigh, buttocks, groin, and hip, as well as reduced ability in movement, numbness, or tingling.

Treatments include:

Sciatica refers to pain caused by irritation to the sciatic nerve. Sciatica is a symptom rather than a condition. This means a person should work with a doctor to find the cause of sciatica to improve their symptoms.

The sciatic nerve is the longest and widest nerve in the body and runs from the buttock to the feet.

A person may feel mild to severe pain that can be felt in the buttock, hip, and legs.

Treatments for sciatica include:

Sacroiliitis refers to inflammation where the sacral spine joins the pelvis bone, which usually causes pain that may worsen with standing or walking.

Treatments for sacroiliitis includes:

More here:
Hip pain when walking: Causes and treatment - Medical News Today


What can people with arthritis do to manage their pain while waiting for surgery? – Barchester Healthcare

Sunday, May 2nd, 2021

One of the various consequences of the COVID-19 pandemic has been an increase in waiting times for routine surgeries and hospital treatments, as NHS resources have been dedicated to fighting the virus.

This has left many people facing longer waits for procedures that could help them to manage debilitating or painful health conditions, such as joint replacements for those with arthritis.

In response to this situation, Versus Arthritis - the UK's largest charity dedicated to supporting people living with the condition - has offered some advice on managing pain while waiting for surgery.

Arthritis affects people of all ages, but is more common in the elderly. According to the National Institute for Health and Care Excellence, X-ray studies have shown that at least 50 per cent of people over the age of 65 show evidence of osteoarthritis, the most common form of the condition.

Pain, stiffness and restricted movement in the joints are among the main symptoms of arthritis, meaning it can have a particularly significant impact on older people, sometimes leading to a requirement for full-time care.

Family members whose loved ones are struggling to live with arthritis while waiting for surgery could be wondering what they might be able to do to help.

Versus Arthritis offered a number of tips that people can pass on to elderly relatives to help them alleviate or cope with pain in their joints.

As well as painkillers such as paracetamol, ibuprofen and non-steroidal anti-inflammatory drugs, there are options such as using a TENS (transcutaneous electrical nerve stimulation) machine - a small, battery-operated device that relieves pain by administering mild electrical currents to the skin.

Heat pads, hot water bottles, ice pads or cold compresses can also help, as can self-massage to stretch tight muscles. Some people find foam rollers useful to relieve stiffness and tension.

The charity also highlighted the importance of trying to stay in generally good health. Exercising regularly, even if it's only for a short time, can improve mobility, strengthen muscles and ease pain, as well as preparing the body to recover after surgery. If walking is too painful, other activities like swimming or chair yoga can be beneficial.

Maintaining a good diet is also one of the best ways for people to boost their general wellbeing, reduce the strain on their joints and prepare for surgery.

See the article here:
What can people with arthritis do to manage their pain while waiting for surgery? - Barchester Healthcare


COMAQUATICS water workouts are helping people with arthritis –

Sunday, May 2nd, 2021

Members at an aquatic center here in Midland are exercising in the pool to help ease their daily arthritis pains

MIDLAND, Texas More than 54 millions in Americans including 300,000 children live with arthritis everyday and battle the daily challenges that it brings.

COM Aquatics in Midland, water workouts and exercises are taught to members at the center.

Ronald Houdek has been coming to the center for over a year and has noticed a difference.

"I was almost not able to do anything, now I can get out and do errands and walk around somewhat," says Houdek.

Rita Simmons is the director at COM Aquatics and she's noticed great improvement among members.

"The first thing that they see is their balance and their strength, mobility, flexibility, functional movement during the day those are some things our members see," says Simmons.

"An individual may be coming in on a walker or a wheelchair and then getting excited with them when I see them walking on a cane or walking independently it's really neat to see the progress," Simmons says.

Progress is something that Alathea Blischke has seen since starting water walking.

"It was my rheumatologist who sent me here because I have arthritis. When I first came it was about 15, 17 years ago I hobbled into my first class and I went striding out at the end of the semester," says Blischke.

She went on to say, "I step in first it's my ankles, they start to feel good then my legs, my hips, up body, shoulders, I can feel relief coming."

Members continue to make waves of progress and they encourage other to join in on this exercise.

"I definitely advise it for anybody a lot of people have the pains that I do the arthritis and the rheumatism. It's very good it's a lifesaver," says Houdek.

COM Aquatics is partnering with the Arthritis Foundation to host a Water Walk to Cure Arthritis this Friday. at COM Aquatics in Midland from 8AM - 6PM. If you'd like to take part, you can honor the 54 million Americans dealing with arthritis by giving 54 dollars, telling 54 people and moving for 54 minutes. For more information, click here.

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COMAQUATICS water workouts are helping people with arthritis -


Todd McKenney on his big Botox mishap and dancing around his arthritis – Starts at 60

Sunday, May 2nd, 2021

I make sure my mental health is always looked after as well. I think sometimes people forget about it, but I get lots of sleep so I dont just work.

While Todd might have nailed the balancing act that is a busy life in showbiz now, he says he did once cave into the pressures of the industry. Being constantly under the cameras gaze took its toll in 2012 when Todd says he gave in and found himself getting Botox a decision he jokes made him look like an ageing queen from the Gold Coast. Now, he says hes finally learned to embrace the ageing process and is even on a first-name basis with his wrinkles.

I got sucked into it because everyone was getting it and I just went with it, he said. I looked at myself on TV on one episode of Dancing with the Stars and I looked ridiculous.

I had to go on TV every week looking like that! I was like, what have I done. Ill never ever ever do it again. My face set like granite and so when I talk I use my face, I gesticulate, Im a storyteller. Id go on stage and Id be telling these stories and I knew that I wasnt getting the physical facial chaos and so I felt trapped in my own skin. I hated it.

Im now loving my wrinkles, Ive embraced them. I love them and Ive named them. Ive got these two on my forehead, Ada and Elfie. Ive just embraced it.

After a couple of years as a professional dancer, Todd says he quickly learned the importance of diversifying his skill set, after watching many dancers careers cut short because of the harsh toll it took on their body. And so, he added singing to his arsenal and his career began to show the first signs of just how successful he would become.

I always knew that Id do it, I just never knew Id still be doing it at 55, he said. Dancing has been great but Ive got arthritis, so Im now just sort of focusing on the other areas. It became very clear to me that I had to focus on singing and more of an all-round entertaining arsenal if I wanted longevity. Nowadays, I still dance but dance is actually what I do least in my shows. I dont just sit still, its very energetic but I like a chat, I like singing.

Perth in the 1980s didnt offer Todd a lot of opportunities to get into roles as a professional male dancer, but with his mum and grandma being dance teachers he was lucky to essentially grow up at the back of a dance studio, which he joked was cheaper than a babysitter. The early exposure to dance clearly sparked something in him, and by the age of 10 hed gotten into ballroom dancing and eventually would go on to represent Australia at international ballroom dance competitions.

While he always knew he was destined for stardom, his mum was a little more pragmatic and made him get a real job as a backup. When I left school, I was a travel agent. Mum made me have something to fall back on as all good parents do in our industry and I kept saying I dont need anything, Im going to make it, he laughed. I got a job at a travel agency, and then showbiz called.

Todd says the real turning point for his career is one hell be forever indebted to Peter Allen for, and that was his highly successful lead role in The Boy from Oz. He says the role put him on the map and set him up for his future role on Dancing with the Stars and allowed him to do his one-man shows.

Todd McKenney sings Peter Allen and lots more will celebrate his huge debt of gratitude toward the singer-songwriter, but also feature hits from his all-time favourite performers including Bette Midler, Tom Jones, Barry Manilow and Prince. The performer said the cabaret-style show is like a fabulous dinner party with friends. The interactive performance includes lots of chatting with the audience, banter, jokes and stories which Todd says, makes the show incredibly unpredictable and a lot of fun.

When I do these shows, the chat for me is as important as the singing and dancing, he said. So, I think its really important by the end of the show [the audience] get a sense of me, who I am and my humour.

Get your tickets to Todd McKenney sings Peter Allen and lots more here. Todd is only performing his show in Melbourne so get in quick before it sells out!

The rest is here:
Todd McKenney on his big Botox mishap and dancing around his arthritis - Starts at 60


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