StemCell Therapy

GRAND RAPIDS, Mich.--(BUSINESS WIRE)--Tetra Therapeutics, a clinical-stage biopharmaceutical company developing novel treatments for patients with cognitive impairment and memory loss, today announced a poster presentation at the 12th Clinical Trials on Alzheimers Disease Meeting (CTAD) being held in San Diego, from December 4 7.

The poster, titled Tumor Necrosis Factor (TNF) Blocking Agents Reduce Risk for Alzheimers Disease in Patients with Rheumatoid Arthritis and Psoriasis, highlights data from a retrospective population-based study of 56 million patients in which inflammatory disease in the body is shown to increase risk for Alzheimers disease and that risk can be reduced in these patients by treatment with a TNF blocking drug. The study was conducted in conjunction with Case Western Reserve University.

Our analysis demonstrates the value of a large, population-based database covering 20% of the entire US population. We find that inflammation in the body increases risk for Alzheimers disease across multiple diseases involving the joints, the gut and the skin, said Mark E. Gurney, Ph.D., Chairman and Chief Executive Officer of Tetra Therapeutics and co-author of the study. The study further indicates that the risk for Alzheimers disease can be reduced in patients with rheumatoid arthritis and psoriasis by treatment with TNF blocking agents such as etanercept, adalimumab, and infliximab. The results of our retrospective study need to be validated by well-controlled, prospective studies, but offer the hope that Alzheimers disease can be prevented in some patients in whom an inflammatory disease is a risk factor for developing Alzheimers disease.

The study used the de-identified population-level, electronic health records of 56 million unique patients collected by the IBM Watson Health Explorys Cohort Discovery platform from 360 hospitals and 317,000 providers. The study evaluated patients with inflammatory diseases (including rheumatoid arthritis, ankylosing spondylitis, psoriasis, psoriatic arthritis, inflammatory bowel disease, ulcerative colitis, and Crohn's disease). The study examined whether these systemic inflammatory diseases - which in part are mediated by tumor necrosis factor (TNF) - increased the risk for Alzheimers disease and whether or not risk could be mitigated by an FDA-approved, TNF blocking biologic drug.

The study findings are exciting in that we clearly see that TNF blocking agents reduce the risk for co-morbid Alzheimers disease in real-world patients diagnosed with rheumatoid arthritis or psoriasis, said Rong Xu, Ph.D., Associate Professor, Department of Population and Quantitative Health Sciences, School of Medicine at Case Western Reserve University and co-author of the study. Given that anti-TNF biologics are powerful drugs, we believe further prospective studies are necessary to understand their potential in treating or preventing Alzheimer's disease.

The analysis compared a diagnosis of Alzheimer's disease as an outcome measure in patients who received at least one prescription for a TNF blocking agent (etanercept, adalimumab, and infliximab) or for methotrexate.

Alzheimer's risk was increased in adults with the following diagnoses (all P<0.0001):

Key findings:

About Alzheimers Disease and Tumor Necrosis Factor (TNF)

Alzheimers disease (AD) is the most common cause of dementia. Multiple lines of evidence indicate that TNF may trigger or amplify aberrant microglia signaling in the brain and thereby contribute to AD pathogenesis. Systemic inflammatory diseases affecting the joints, skin and gut are caused in part by the production of TNF by activated macrophages and these diseases can be treated effectively with a TNF blocking agent. Furthermore, systemic TNF can access the brain through receptor-mediated transcytosis. In the brain, elevation of tumor necrosis factor (TNF) in cerebrospinal fluid collected from subjects with mild cognitive impairment is associated with progression to AD at 6 months follow up.

About Tetra Therapeutics

Tetra Therapeutics is a clinical stage biotechnology company developing a portfolio of therapeutic products that will bring clarity of thought to people suffering from Alzheimers disease, Fragile X Syndrome, traumatic brain injury, and other brain disorders. Tetra uses structure-guided drug design to discover mechanistically novel, allosteric inhibitors of phosphodiesterase 4 (PDE4), an enzyme family that plays key roles in memory formation, learning, neuroinflammation, and traumatic brain injury. Tetra Therapeutics is headquartered in Grand Rapids, Michigan. For more information, please visit tetratherapeutics.com.

Link:
Tetra Therapeutics Announces Presentation of Data from Retrospective Population-Based Study of 56 Million Patients at the 12th Clinical Trials on...

A research team led by biomedical scientists at the University of California, Riverside, has found that a drug approved by the FDA to treat rheumatoid arthritis and ulcerative colitis can repair permeability defects in the guts epithelium.

Affecting roughly 1 million Americans, ulcerative colitis is a chronic inflammatory bowel disease of the large intestine in which the lining of the colon becomes inflamed and leaky. Affecting more than 2 million Americans, rheumatoid arthritis is an autoimmune disease in which the bodys immune system attacks the joints.

The study is the first to show the drug, tofacitinib, also called Xeljanz, has a direct effect on cells lining the gut by correcting defects that occur in inflammation. Until now, the effects of tofacitinib on intestinal epithelial cell functions were largely unknown.

Our work increases our understanding of how this drug is useful for treating ulcerative colitis, said Declan McCole, a professor of biomedical sciences in the UCR School of Medicine, and the lead author of the study that appears in the journal Inflammatory Bowel Diseases. We now better understand where in the gut the drug is working, and how.

McCole explained that increased intestinal permeability or leakiness is a feature of ulcerative colitis and plays a critical role in promoting inflammation. His team tested tofacitinib in human intestinal epithelial cell lines, as well as in organoids, or colonoids, that were derived from primary human colonic stem cells isolated from human subjects primarily patients undergoing elective colonoscopy for colon cancer screening and found tofacitinib repaired inflammation-induced permeability defects in both.

The epithelium is a thin layer that lines the alimentary canal. The gastrointestinal epithelium is comprised of cells that have gaps between them, making them selectively permeable and providing a barrier that keeps out pathogens, toxins, and antigens from entering the gut, while allowing the absorption of nutrients. In ulcerative colitis, this epithelial permeability becomes leaky, allowing bacterial products to cross into the gut and nutrients and water to leak out. This, in turn, triggers immune responses, resulting in fluid loss and diarrhea.

We found tofacitinib fixes the leakiness in the intestinal barrier, McCole said. Specifically, it fixes intestinal epithelial permeability defects caused by interferon-gamma, an inflammatory cytokine involved in autoimmune diseases such as ulcerative colitis and rheumatoid arthritis.

By targeting specific molecules, the drug inhibits a pathway that is activated by inflammation, said Anica Sayoc-Becerra, a graduate student in the Biomedical Sciences Graduate Program, a member of McColes lab, and the first author of the research paper. Our study shows tofacitinib is not just acting on immune cells, as was first thought, but can have a direct effect on the epithelial cells that are the key factor in maintaining gut barrier function.

A major focus of McColes lab is PTPN2, a protein-coding gene associated with autoimmune diseases such as Crohns disease, ulcerative colitis, and rheumatoid arthritis. Individuals with mutations in this gene that cause it to lose function have an increased risk of getting these diseases. McColes research group was the first to identify PTPN2 normally helps to protect the barrier function of the epithelial cells that line the gut.

A patient that has a PTPN2 loss-of-function mutation is predicted to have a leakier gut, McCole said. Rather than trying to repair PTPN2, my lab was successful in inhibiting some of the consequences of the loss-of-function mutation in this gene.

Sayoc-Becerra explained PTPN2 deactivates the same signaling pathway as tofacitinib.

We thought tofacitinib might be a very effective way of correcting the defects that occur from the loss-of-function mutations of PTPN2 without having to introduce new genes into a cell, animal, or patient, she said.

McCole and Sayoc-Becerra were joined in the study by UC Riversides Moorthy Krishnan, Jossue Jimenez, Rebecca Hernandez, Kyle Gibson, and Reyna Preciado; as well as Shujun Fan and Grant Butt of the University of Otago in New Zealand. Sayoc-Becerra expects to graduate with her doctoral degree in December 2019. This is her first paper as first author.

Next, the researchers plan to identify specific patients who may derive the greatest benefit from the drug. This will allow more targeted treatment of patients likely to be good responders to tofacitinib in a personalized medicine approach to treating this disease.

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health, as well as inflammatory bowel disease research awards from Pfizer Inc., the maker of tofacitinib.

Go here to read the rest:
Drug decreases gut leakiness associated with ulcerative colitis - UC Riverside

Certain levels of plasma protein adenosine deaminase 2 (ADA2) are sensitive and specific, and can be used as a novel biomarker of macrophage activation syndrome in patients with systemic juvenile idiopathic arthritis (JIA), according to research results published in the Annals of the Rheumatic Diseases.

Researchers sought to evaluate the role and function of ADA2 as a novel biomarker of macrophage activation syndrome because of the overlapping clinical features between macrophage activation syndrome and active systemic JIA.

A reference range for plasma ADA2 activity was first established using samples from 324 healthy individuals (174 children and 150 adults). Spectrophotometric assays showed that patients with biallelic ADA2 mutations had a near absence of ADA2 activity compared with carriers who had approximately half-normal plasma ADA2 activity.

After establishing the reference range, the researchers compared ADA2 levels in children with Kawasaki disease, pediatric systemic lupus erythematosus, and juvenile dermatomyositis with age-matched healthy controls. Investigators established that ADA2 levels did not correlate with markers of disease activity and were not a general marker of systemic inflammation in any of the 3 disorders.

Among the JIA population, most patients showed plasma ADA2 activity levels that were comparable with age-matched healthy controls; however, a small subset had levels well above the upper limit of normal. After stratification by JIA category, investigators found that ADA2 activity was present in children with oligoarticular and polyarticular JIA, enthesitis-related arthritis, and psoriatic arthritis.

Using multiple macrophage activation syndrome biomarkers, researchers compared ADA2 activity in patients with JIA and created a correlation matrix based on Spearman rank correlation r values. The comparisons demonstrated that ADA2 levels correlated with ferritin, interleukin-18, and C-X-C Motif Chemokine Ligand 9. ADA2 activity also correlated well with increased aspartate aminotransferase levels in macrophage activation syndrome, but not with conventional markers of inflammation.

Although the patterns displayed by these markers were different, all the markers were sensitive and specific in discriminating macrophage activation syndrome from systemic JIA using the upper limit of normal as a cutoff.

Seven patients with macrophage activation syndrome had available serum samples. Consistent with previous analyses, investigators found that ADA2 levels were generally higher during a confirmed episode of macrophage activation syndrome compared with other time points. Researchers noted that patients who experienced recurrent episodes of macrophage activation syndrome exhibited ADA2 levels near the upper limit of normal even when macrophage activation syndrome was absent.

Whether ADA2 contributes to the pathophysiology of [macrophage activation syndrome] is not clear, the researchers concluded. The [physiologic] function of ADA2 remains to be determined.

Reference

Lee PY, Schulert GS, Canna SW, et al. Adenosine deaminase 2 as a biomarker of macrophage activation syndrome in systemic juvenile idiopathic arthritis [published online November 9, 2019]. Ann Rheum Dis. doi: 10.1136/annrheumdis-2019-216030

Read the original post:
Novel Biomarker of Macrophage Activation Syndrome Identified in Juvenile Idiopathic Arthritis - Rheumatology Advisor

CHICAGO - About 54 million adults have doctor-diagnosed arthritis, according to The Arthritis Foundation. Almost 300,000 babies and children have arthritis or a rheumatic condition

For Chelsea May, those numbers hit too close to home. Her 14-year-old daughter, Jenna, suffers from Juvenile Psoriatic Arthritis and Uveitis. She was diagnosed four years ago.

To help fight spread awareness of the debilitating disease and raise money for research, Jenna's family will host their third annual bake sale on Dec. 6. The bake sale will take place at the Mt. Greenwood Holiday Stroll from 4 p.m. to 7 p.m.

"We are also looking for donations of baked goods as well," May said.

The donations and money received from the bake sale will be donated to the Arthritis Foundation's Jingle Bell Run which will take place on Dec. 14.

The Arthritis Foundation's Jingle Bell Run is the original festive race for charity, bringing people from all walks of life together to champion arthritis research and resources.

Less than a week after the bake sale, Jenna's family will gear up for the Jingle Bell Run in Chicago. If you would like to donate or join Jenna's run team, click here.

Visit link:
Jingle Bake Sale To Benefit The Arthritis Foundation - Beverly, IL Patch

ATLANTA There is no significant difference in the rate of serious infections in patients with rheumatoid arthritis (RA) receiving upadacitinib 15 mg or adalimumab, according to study results presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals (ACR/ARP) Annual Meeting, held November 8 to 13, 2019, in Atlanta, Georgia.

However, the results indicated that patients receiving upadacitinib 15 mg and 30 mg had higher rates of herpes zoster compared with patients receiving adalimumab or methotrexate.

The study included data from 5 randomized double-blind, placebo- or active-controlled phase 3 trials of upadacitinib 15 mg (included in all 5 trials) or 30 mg daily (included in 4 trials) in patients with RA.

Researchers calculated the exposure adjusted event rates (EAERs; events/100 patientyears [PY]) of treatment-emergent adverse events (AEs) for the integrated placebo (3 trials; 12/14 weeks), the integrated methotrexate (2 trials; mean exposure, 36 weeks), the originator adalimumab (mean exposure, 42 weeks), upadacitinib 15 mg (mean exposure, 53 weeks), and upadacitinib 30 mg (mean exposure, 59 weeks) groups.

In all 5 phase 3 trials, 3834 patients received 1 dose of upadacitinib 15 mg (n=2630) or 30 mg (n=1204) with no option to switch doses, for a total of 4020.1 PY of upadacitinib exposure.

Similar to patients who received adalimumab, patients who received upadacitinib 15 mg had EAERs of overall serious adverse events (SAEs) and AEs that led to discontinuation. Compared with methotrexate, upadacitinib 15 mg and 30 mg had higher EAERs of both SAEs and AEs.

The most commonly reported AEs were upper respiratory tract infection, nasopharyngitis, and urinary tract infections, all of which occurred more frequently among patients in the upadacitinib groups compared with the placebo group.

Patients in the upadacitinib 15 mg and adalimumab groups had comparable rates of serious infection events (SIEs); however, rates of SIEs were higher among patients receiving upadacitinib compared with methotrexate. Compared with patients receiving methotrexate and adalimumab, patients receiving either dose of upadacitinib had higher rates of herpes zoster.

Among patients receiving upadacitinib, those in the 15-mg group had lower rates of SIEs and herpes zoster compared with the 30-mg group.

All treatment groups had similar rates of malignancies, excluding non-melanoma skin cancer, and adjudicated major adverse cardiovascular events and venous thromboembolic events. In addition, all treatment groups had comparable rates of death.

Compared with the other treatment groups, upadacitinib 30 mg had a higher rate of non-melanoma skin cancer; however, the rates of non-melanoma skin cancer for both the upadacitinib groups fell within the range reported for patients with RA treated with disease-modifying antirheumatic drugs.

Visit Rheumatology Advisor for live coverage and more news from the 2019 ACR/ARP Annual Meeting.

Reference

Cohen S, van Vollenhoven R, Winthrop K, et al. Safety profile of upadacitinib in rheumatoid arthritis: integrated analysis from the SELECT phase 3 clinical program. Presented at: 2019 ACR/ARP Annual Meeting; November 8-13, 2019; Atlanta, GA. Abstract 509.

Read more from the original source:
Rates of Serious Infection Events Similar With Upadacitinib, Adalimumab in Rheumatoid Arthritis - Rheumatology Advisor

In September, the world of entertainment news buzzed with word that Kim Kardashian West tested positive for lupus and rheumatoid arthritis. The star underwent further tests, however, resulting in a diagnosis of psoriatic arthritis instead. While all three autoimmune disorders share some signs and symptoms, psoriatic arthritis is generally considered to have a better prognosis than lupus. That said, the conditions can co-exist and lupus has gotten a reputation for being difficult to diagnose, especially in the absence of the butterfly-shaped rash on ones cheeks and nose.

Im so relieved. The pain is going to come and go sometimes, but I can manage it and this is not going to stop me, Kardashian said in an article in response to receiving her psoriatic arthritis diagnosis. Her relief at not having lupus is understandable, given that lupus can affect a greater number of organs and systems in the body and is considered to be life-threatening.

Lupus, rheumatoid arthritis and psoriatic arthritis are examples of some conditions that are often considered when an individual is undergoing diagnosis for certain autoimmune diseases, because they share several symptoms and can trigger positive results in the same diagnostic tests. Kim Kardashian received the initial news that she had lupus or rheumatoid arthritis likely due to positive antinuclear antibody (ANA) test results.

An ANA is a blood test ordered when a doctor, usually a rheumatologist, suspects that a patient has a particular kind of autoimmune disorder. This test checks for the existence of autoantibodies, which are produced when a persons body is, in effect, attacking itself and several areas of the body are affected. A positive ANA test usually indicates that the doctors suspicions are confirmed, and then other factors (like medical and family history) need to be considered and more tests done to arrive at a diagnosis.

Psoriatic arthritis is usually diagnosed between the ages of 20 and 50, and occurs in women and men equally. While there is no cure, appropriate and early treatment can help prevent major damage to affected parts of the body.

Psoriatic arthritis appears in a minority of individuals who have already been diagnosed with psoriasis, an autoimmune skin condition with which Kim Kardashian and her mother, Kris Jenner, had already been diagnosed. Psoriatic arthritis affects around 520,000 individuals in the United States alone.

The autoimmune condition is believed to be caused by a combination of genetic factors and environmental triggers. So while some people inherit psoriatic arthritis-related genes, only a subset of those individuals will go on to develop the condition. In these cases, the disease could be triggered by other illnesses or infections, various forms of extreme stress, poor diet, smoking, and so on.

Around 40 percent of psoriatic arthritis patients have one or more close family members with psoriasis or psoriatic arthritis diagnosis, which strongly indicates that the disease is hereditary. Interestingly, recent research has suggested that psoriasis patients who go on to develop psoriatic arthritis have a different genetic profile than those who do not. And the most well-studied of the psoriatic arthritis genes belong to a family of genes called the human leukocyte antigen (HLA) complex, which help the body tell the difference between its own proteins and viral or bacterial proteins.

According to Genetics Home Reference by the U.S. National Library of Medicine, Variations of several HLA genes seem to affect the risk of developing psoriatic arthritis, as well as the type, severity, and progression of the condition.

Ive been feeling so tired, so nauseous, and my hands are really getting swollen. I feel like I literally am falling apart. My hands are numb, Kardashian said on a recent episode of Keeping Up with the Kardashians.

These kinds of descriptions are common in all three conditions lupus, rheumatoid arthritis, and psoriatic arthritis though each patient presents with a different array of symptoms, and all with varying degrees of severity. The main symptoms of psoriatic arthritis are pain, stiffness, and swelling in affected joints, along with chronic fatigue. Joints near the end of the fingertips and tips of the toes are often affected, as are bones in the spine.

The symptoms of psoriatic arthritis tend to worsen over time, though some patients experience periods of remission when symptoms temporarily improve. Compared to rheumatoid arthritis, psoriatic arthritis is more likely to cause swelling in the smallest joints of the fingers and toes, foot pain (in the heel and/or sole of the foot), and lower back pain caused by inflammation in vertebral joints. Patients with psoriatic arthritis are also more likely to experience symptoms on one side of the body or in different appendages on each side (in other words, it tends to be an asymmetric disease), whereas patients with rheumatoid arthritis are more likely to experience symptoms that affect both sides of the body equally (symmetric disease).

Most if not all patients with psoriatic arthritis also have psoriasis, an autoimmune condition that causes red, scaly patches of skin that can be itchy, painful and embarrassing. Psoriasis usually precedes the onset of psoriatic arthritis by several years. People with psoriatic arthritis commonly experience fingernail changes, too, such as the formation of a pitted or ridged nail surface, or the nails become separated from the nail beds.

There are several treatment options for psoriatic arthritis, which include nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation and pain, immunosuppressants to suppress the immune system, disease-modifying antirheumatic drugs (DMARDs) to slow the progression of the disease, and newer medications that minimize the activity of certain enzymes involved in the inflammatory process. Treatment plans may also involve steroid injections administered directly into affected joints, or joint replacement surgery in cases where the disease has significantly progressed.

Kristen Hovet covers genetics, medical innovations and the intersection of sociology and culture. The North Dakota native is based in Vancouver, Canada, where she is working on a masters degree in health communication at Washington State University. Follow her on her website or Twitter @kristenhovet

See the original post here:
Kim Kardashian West's battle with psoriatic arthritis: Will understanding the genetics of the autoimmune disorder point to a cure? - Genetic Literacy...

While theres no cure for knee osteoarthritis, a combination of strategies can help relieve your pain and keep you active.

Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services.Policy

Although the cornerstones of treatment are exercise and physical therapy and pain medications and steroid injections are also options you can also try knee braces, shoe inserts or simply wearing more supportive shoes.

Knee braces can be helpful for managing your pain, says physical therapist Dawn Lorring, PT, MPT. The location and severity of your symptoms will drive which brace works best for you.

Osteoarthritis is caused by the breakdown of cartilage (thats the cushioning material that covers the ends of bones in joints.) This causes pain and stiffness.

In the knee joint, arthritis can occur at any of three points where the bones come in contact:

Sleeve braces. People who have mild pain or stiffness that limits their activities can try a sleeve-type brace. These provide compression, which can reduce swelling and warm the joint. This might relieve the stiffness.

These braces also provide added support. If your knee feels unsteady or wobbly, a compression-type brace can be helpful, Lorring says. Some of them have plastic stays or a hinge on the side, which provides a little more support. She recommends getting one that has an opening at the knee cap.

Sleeve braces arent covered by insurance, but they are relatively inexpensive, ranging from $10 to 100.

Web brace. A more advanced brace is a sleeve with silicone webbing over the front. As you bend and straighten your knee, the webbing tightens in certain areas. This provides extra support to the knee.

A regular sleeve brace provides compression all over. The brace with the webbing also provides guidance for how the knee cap moves, Lorring says.

This type of brace might be the most helpful for someone with osteoarthritis beneath the knee cap. A web brace costs about $100.

Unloader brace. When arthritic changes are between the femur and tibia, a device called an unloader knee brace may help, especially if one side is more arthritic than the other. These have a metal band that goes around the thigh and another one around the calf, connected by a hinged bar. This creates a frame that can be adjusted to shift pressure (unload) from one side of the knee to the other.

If the inside of your knee hurts, the brace can be adjusted to put more force on the outside of your knee, unloading weight off the inside, Lorring explains.

These are less beneficial if your arthritis symptoms are similar on both the inside and outside of the joint.

Unloader knee braces are expensive ($500 to $1,000), but they can be covered by insurance. Youll need a doctors prescription and documentation that it is medically necessary.

Shoes and inserts. Various foot problems (like high arches or flat feet) or just the particular way you walk can affect the alignment of your body. That might be putting more pressure on your knee joints. You may get some relief by choosing better shoes or wearing shoe inserts (also called orthotics).

Because everyone is different, theres no universal advice for shoes or inserts. Lorring recommends consulting a physical therapist or an expert in foot mechanics who can observe how you walk and help you pick out shoes or shoe inserts that match your needs. I encourage people to look at running shoes because there are more support options, she says.

The goal with orthotics is to make sure your foot is moving in the best way it can so your knee isnt getting more force than it should, Lorring says. There are a wide variety of shoe inserts and heel wedges that you can buy in a drug store or online. You can also get them custom made or save some money and get semi-custom ones. Like with shoes, you need to get inserts and wedges that are specific to your needs.

You can have an insert that doesnt add much arch support but it adds cushion, which can be beneficial if you walk on the outside of your foot, Lorring says. However, if your foot rolls inward too much, you may need more arch support.

You can get heel wedges that are sloped in one direction or the other, which is similar to the action of an unloader brace. It shifts pressure from one side of the knee to the other.

Ultimately, you have to find what works for you, Lorring says.

This article originally appeared in Cleveland Clinic Arthritis Advisor.

See more here:
Could a Knee Brace Help Ease Your Osteoarthritis Pain? - Health Essentials from Cleveland Clinic

AbbVie's (ABBV - Get Report) fledgling rheumatoid arthritis treatment Rinvoq is showing promise and appears to be tracking "meaningfully ahead of expectations," according to analysts at Piper Jaffray.

Analyst Christopher Raymond reiterated the firm's overweight rating on theNorth Chicago biopharma while increasing its price target to $92 from $90.

At last check Tuesday AbbVie was trading down 1.2% at $86.

Piper Jaffray's bullish outlook on Rinvoq is fueled by the results of a new survey of 100 rheumatologists, who provided mostly positive feedback about the drug. A rival treatment still enjoys success, but Rinvoq could soon be on its heels, the analyst wrote.

"While indications of Xeljanz (PFE - Get Report) entrenchment do exist, fully 33% of doctors indicate they would be early Rinvoq adopters, just because of AbbVie's involvement," Raymond wrote.

"And in terms of reported sales contact," AbbVie's rheumatology focus on Rinvoq appears to rival that "of its Humira effort, and then finally, when compared to the prior two rheumatoid arthritis launches (Olumiant and Kevzara), unaided awareness, brand familiarity and initial user base are all head-and-shoulders above."

"[Just] months post-launch, ... Rinvoq registers 1% patient share," Raymond wrote. But "asked to delineate most recent scripts, doctors give Rinvoq 8% share. When asked to projectshare in six months, rheumatologists indicate Rinvoq's share will grow to 6%."

"In that Rinvoq largely takes a back seat to [AbbVie treatment] Skyrizi as a key growth driver in the minds of most investors we speak with, we see this feedback as a welcome source of upside in coming quarters," Raymond wrote.

AbbVie is a holding in Jim Cramer's Action Alerts PLUS Charitable Trust Portfolio. Want to be alerted before Cramer buys or sells ABBV? Learn more now.

Read the original post:
AbbVie Affirmed Overweight at Piper Jaffray on Potential of Arthritis Drug - TheStreet.com

Study Assesses Risk of Infections, Cancer With Interleukin Inhibitors in Rheumatic Disease

According to the study, the risks may be comparable to those reported for other biologics approved for the treatment of rheumatic diseases.

A number of IL-1, IL-6, IL-12/23, and IL-17 inhibitors are used as therapy options in rheumatologic diseases. Although IL inhibitors have demonstrated efficacy, there are limited data regarding their safety profile and it is unknown to what extent IL inhibitors may increase the risk of serious infections and cancer.

To assess this risk, researchers conducted a systematic review and meta-analysis using data from clinical trials that evaluated IL inhibitor therapies and reported safety data. The meta-analysis included 74 studies including 29,214 patients. The studies included tocilizumab, secukinumab, anakinra, ixekizumab, rilonacept, sarilumab, sirukumab, ustekinumab, brodalumab, guselkumab, clazakizumab, canakizumab, and olokizumab.

Diseases in the study included rheumatoid arthritis (RA), psoriatic arthritis, ankylosing spondylitis, gout, juvenile idiopathic arthritis, giant call arteritis, systemic lupus erythematosus, primary Sjogren syndrome, systemic sclerosis, familial Mediterranean fever, and osteoarthritis.

Overall, 69 studies included data for serious infections across all rheumatic diseases, comprising a total of 24,236 patients. The pooled analysis showed an increased risk of serious infections with the use of IL inhibitors compared with placebo.

Fourteen of the studies reported the incidence of opportunistic infection, with 9998 patients in these trials. Oral candidiasis was the most commonly reported opportunistic infection, according to the analysis. Others included herpes zoster, esophageal candidiasis, Mycobacterium tuberculosis, atypical mycobacterial infections, and histoplasmosis. Overall, the results showed an increased risk of opportunistic infections with the use of IL inhibitors compared with placebo.

A total of 46 studies with approximately 21,000 patients had data on the incidence and type of cancers across all rheumatic diseases. A total of 141 cases of cancer reported in the treatment groups and 28 in the control groups. The analysis found that, overall, there was an increased risk for cancer with IL inhibitors compared with placebo.

The researchers noted that, although the review suggest that the risk of cancer may be increased with longer IL inhibitor therapy, the results are not conclusive and should be further investigated by long-term data.

This analysis provides estimates of toxic effects for infections and cancer associated with the use of IL inhibitors that can inform shared decision-making when patients and clinicians are contemplating the use of IL inhibitors for rheumatologic diseases, they concluded.

References

Bilal J, Berlinberg A, Riaz IB, et al. Risk of infections and cancer in patients with rheumatologic diseases receiving interleukin inhibitors: a systematic review and meta-analysis. JAMA Network Open. 2019. Doi: 10.1001/jamanetworkopen.2019.13102.

Read more here:
Study Assesses Risk of Infections, Cancer With Interleukin Inhibitors in Rheumatic Disease - Pharmacy Times

BACKGROUNDS:

Rheumatoid arthritis (RA) is a systemic autoimmune disease that confers one of the strongest risks for cardiovascular disease (CVD) morbidity and mortality than in general population. Pulse wave velocity (PWV) and augmentation index (AIx) are composite measures of arterial stiffness (AS) and associated with CV risk.

The aim of this study was to systemically review the evidence regarding the relationship between PWV, AIx and RA, as well as underlying influential factors.

Eligible literatures were searched in PubMed, EMBASE and The Cochrane Library published up to February 28, 2019 in English. The pooled weight mean difference (WMD) with its 95% confidence interval (CI) was calculated using random-effect model analysis.

A total of 38 studies were finally incorporated in the meta-analysis. The results indicated that, compared to controls, RA patients had significantly increased levels of carotid-femoral (cf)-PWV (WMD=1.10m/s, 95% CI: 0.84-1.35), brachial-ankle (ba)-PWV (WMD=0.20m/s, 95% CI: 0.12-0.28), cartoid-radial (cr)-PWV (WMD=0.51m/s, 95% CI: 0.23-0.79), AIx (WMD=4.79%, 95% CI: 1.34-8.24) and AIx normalized to a 75 beats/minute heart rate ([emailprotected]) (WMD=5.78%, 95% CI: 3.82-7.74) (all p <0.001). Meta-regression and subgroup analysis demonstrated significant association of cf-PWV with age, disease duration and erythrocyte sedimentation rate (ESR) in RA.

Overall, there is increased PWV level in patients with RA, and this alteration is associated with age, disease duration and ESR.

The rest is here:
Assessment of Aortic Stiffness in Patients With Rheumatoid Arthritis Using Pulse Wave Velocity: An Update Meta-analysis - DocWire News

As we begin the final month of 2019, the U.S. Food and Drug Administration (FDA) has several PDUFA dates to approve drug applications. Heres a look at those scheduled for the first two weeks of the month.

Celgenes Luspatercept for Beta-thalassemia-associated Anemia

Celgene had a target action date of December 4, 2019 for its Biologics License Application (BLA) for luspatercept. Luspatercept is an investigational erythroid maturation agent for adults with very low to intermediate-risk myelodysplastic syndromes (MDS)-associated anemia who have ring sideroblasts and require red blood cell (RBC) transfusions, and for the treatment of adults with beta-thalassemia-associated anemia who require RBC transfusionsit is this second indication for which the company had the December 4 PDUFA date.

Luspatercept is also being reviewed by the European Medicines Agency (EMA). It is a first-in-class erythroid maturation agent (EMA) that regulates late-stage red blood cell maturation. The therapy was jointly developed by Celgene and Acceleron. The application was built on the results from the Phase III COMMANDS trial in ESA-nave, lower-risk MDS patients and the Phase II BEYOND trial in non-transfusion-dependent beta-thalassemia.

The FDA approved luspatercept-aamt under the brand name of Reblozyl on November 8 for anemia in adults with beta-thalassemia. Beta-thalassemia is a rare, inherited blood disorder caused by a genetic defect in hemoglobin. The target action date for luspatercept for erythroid maturation agent for adults with very low to intermediate-risk myelodysplastic syndromes (MDS)-associated anemia who have ring sideroblasts and require red blood cell (RBC) transfusions is April 4, 2020.

Amgens Biosimilar to Janssens Remicade

Amgen has a target action date of December 14 for its BLA of ABP 710, a biosimilar candidate to Janssen Pharmaceuticals Remicade (infliximab), a drug for various inflammatory diseases such as Crohns disease, ulcerative colitis, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis and plaque psoriasis.

ABP 710 (and infliximab) are anti-tumor necrosis factor alpha (anti-TNF) monoclonal antibodies. The BLA submission includes analytical, pharmacokinetic and clinical data in addition to pharmacology and toxicology data. A Phase III study comparing efficacy, safety and immunogenicity was run in patients with moderate-to-severe rheumatoid arthritis and confirmed no clinically meaningful differences between ABP 710 and infliximab.

Avadels FT218 for Narcolepsy

Avadel Pharma has a target action date of December 15 for AV001. The New Drug Application (NDA) was originally accepted in May 2019 under the FDAs Priority Review program, which gives it a statutory six-month review. It was then extended by three months as the result of FDA requests for additional analytical information and Avadels resultant additional submissions.

FT218 is an investigational drug designed to be administered in one single dose, before bedtime, to treat excessive daytime sleepiness (EDS) and cataplexy in patients suffering from narcolepsy. It was granted orphan-drug designation by the FDA on January 8, 2018 on the theory that is may be clinically superior to the currently marketed, twice-nightly sodium oxybate product.

On November 25, 2019, Avadel announced it had completed patient enrollment of 205 patients in the REST-ON Phase III clinical trial for FT218. The enrollment target was 205 patients. Additional patients may be enrolled if they meet eligibility criteria. Topline data is expected in the second quarter of 2020.

The company says that if the drug is approved, it has the potential to capture a significant share of the twice-nightly sodium oxybate market, which is currently valued at $1.7 billion per year.

The REST-ON trial is a double-blind, randomized, placebo-controlled Phase III study to evaluate the efficacy and safety of once-nightly FT218. It is under a Special Protocol Assessment agreement with FDA.

Read the original here:
FDA Action Alert: Celgene, Amgen and Avadel - BioSpace

OBJECTIVE:

To determine the prevalence of comorbidities in rheumatoid arthritis (RA), discover which comorbidities might predispose to developing RA, and identify which comorbidities are more likely to develop after RA.

We performed a case-control study using a single-center biobank, identifying 821 cases of RA (143 incident RA) between January 1, 2009, and February 28, 2018, defined as 2 diagnosis codes plus a disease-modifying antirheumatic drug. We matched each case to 3 controls based on age and sex. Participants self-reported the presence and onset of 74 comorbidities. Logistic regression models adjusted for race, body mass index, education, smoking, and Charlson comorbidity index.

After adjustment for confounders and multiple comparisons, 11 comorbidities were associated with RA, including epilepsy (odds ratio [OR], 2.13; P=.009), obstructive sleep apnea (OR, 1.49; P=.001), and pulmonary fibrosis (OR, 4.63; P<.001), but cancer was not. Inflammatory bowel disease (OR, 3.82; P<.001), type 1 diabetes (OR, 3.07; P=.01), and venous thromboembolism (VTE; OR, 1.80; P<.001) occurred more often before RA diagnosis compared with controls. In contrast, myocardial infarction (OR, 3.09; P<.001) and VTE (OR, 1.84; P<.001) occurred more often after RA diagnosis compared with controls. Analyses restricted to incident RA cases and their matched controls mirrored these results.

Inflammatory bowel disease, type 1 diabetes, and VTE might predispose to RA development, whereas cardiovascular disease, VTE, and obstructive sleep apnea can result from RA. These findings have important implications for RA pathogenesis, early detection, and recommended screening.

The rest is here:
Comorbidities As Risk Factors for Rheumatoid Arthritis and Their Accrual After Diagnosis - DocWire News

The 2019 annual meeting of the American College of Rheumatology (ACR) had an abundance of sessions dedicated to the management of rheumatoid arthritis (RA).

Novel TreatmentModalities

A large focus of the novel RA treatment sessions were the Janus kinase (JAK) inhibitors. Multiple abstracts regarding upadacitinib, an oral JAK-1 selective inhibitor, were presented. Josef Smolen, MD, of the University of Vienna in Austria, discussed 48-week results of the SELECT-MONOTHERAPY trial (A Study Comparing Upadacitinib [ABT-494] Monotherapy to Methotrexate [MTX] Monotherapy in Adults With Rheumatoid Arthritis [RA] Who Have an Inadequate Response to MTX; ClinicalTrials.gov Identifier: NCT02706951). For patients continuing upadacitinib 15 mg/d, ACR20, ACR50, and ACR70 response was 87%, 70%, and 46%, respectively; ACR20, ACR50, and ACR70 response for upadacitinib 30 mg/d was 87%, 72%, and 54%, respectively. The most frequent treatment-emergent adverse events were infection, particularly herpes zoster, and elevations in creatine phosphokinase and alanine aminotransferase levels.

Efficacy and safety data on filgotinib, another JAK-1 selective inhibitor, were presented by Bernard Combe, MD, of Montpellier University in France. The FINCH1 (Filgotinib in Combination With Methotrexate in Adults With Moderately to Severely Active Rheumatoid Arthritis Who Have an Inadequate Response to Methotrexate; ClinicalTrials.gov Identifier: NCT02889796) study was a phase 3 randomized controlled trial comparing filgotinib 100 mg/d and 200 mg/d with the active comparator, adalimumab 40 mg every 2 weeks, or placebo in addition to a stable dose of methotrexate. The efficacy of filgotinib 200 mg/d was found to be noninferior to adalimumab, achieving a Disease Activity Score in 28 joints/C-reactive protein (DAS28-CRP) score of 3.2 in 60% of participants at week 24.

Updates onPharmacotherapy Safety Data

Several important abstracts regarding pharmacologic safety data in RA were presented at the meeting. Daniel H. Solomon, MD, of Brigham and Womens Hospital in Boston, Massachusetts, presented safety data on methotrexate based on his prespecified secondary analyses of CIRT (Cardiovascular Inflammation Reduction Trial Inflammation Imaging Study; ClinicalTrials.gov Identifier: NCT02576067), which was a randomized controlled trial that included adults with cardiovascular disease and diabetes or metabolic syndrome. Participants were randomly selected to receive low-dose methotrexate (<20 mg/wk) or placebo and were followed for a mean of 27 months. Relative rates of gastrointestinal, infectious, pulmonary, and hematologic adverse events were increased in patients receiving methotrexate compared with participants who were receiving placebo. Notably, there were no differences in the relative rates of malignant, mucocutaneous, neuropsychiatric, musculoskeletal, or renal adverse events.

In addition to upadacitinib as previously mentioned, safetyprofiles of other JAK inhibitors were also presented. Tofacitinib has beenassociated with blood clots in patients who have additional risk factors forthromboembolism. High-dose tofacitinib 10 mg twice daily should not be used inthe treatment of RA. Risk factors for thromboembolism include previouscardiovascular events, cancer, clotting disorders, use of hormonalcontraceptives, and pending major surgery or prolonged immobilization. Datafrom phase 3b/4 trials evaluating tofacitinib 11 mg/d with methotrexate werepresented by Stanley B. Cohen, MD, of the Metroplex Clinical Research Center inDallas, Texas. Importantly, no new safety risks were observed, which wassimilar to that seen with the tofacitinib immediate-release 5 mg twice dailydosage.

A very important and potentially practice-changing updatewas presented by Michael George, MD, of the University of Pennsylvania inPhiladelphia. Dr George analyzed the risk for serious infection associated withlong-term use of glucocorticoids for the treatment of RA. Medicare claims dataon more than 170,000 individuals were used for the analysis. Among older patientswith RA on stable treatment with conventional synthetic and biologic disease-modifyingantirheumatic drugs (DMARDs), prednisone at dosages <5 mg/d weresignificantly associated with increased risk for serious infections. Seriousinfections included urinary infections, pneumonia, bacteremia, and skin or softtissue infections. This study has important management implications forrheumatologists as long-term use of glucocorticoids should be minimized.

Updates onEpidemiology Research in RA

In terms of epidemiology and RA disease trajectory, datafrom the Risk RA Prospective Study were presented by Aase Hensvold of theKarolinska Institute in Stockholm, Sweden. This study followed patients whowere referred to the rheumatology clinic from the primary care setting becauseof positive anti-cyclic citrullinated antibodies but who lacked arthritis uponexamination. A detailed ultrasound evaluation was performed at baseline andfollow-up. Slightly less than half of the enrolled individuals with anti-cycliccitrullinated antibodies developed ultrasound-detectable arthritis at a medianfollow-up time of 11 months. However, participants who had tenosynovitisdetected by ultrasound at baseline were more likely to progress to RA at follow-up.The study highlights the utility of a baseline ultrasound evaluation for thepurpose of prognostication in patients with early or preclinical RA.

Data presented by Elena Myasoedova, MD, PhD, of the MayoClinic College of Medicine and Science in Rochester, Minnesota, explored thechanging epidemiology of RA from a population-based incidence cohort. She foundthat although the incidence of RA has been constant over the past approximately24 years, there has been a decrease in the number of patients with RA withpositive rheumatoid factor and an increase in patients with seronegativedisease. When comparing patients who met the 2010 European League AgainstRheumatism (EULAR)/ACR criteria with those who met the 1987 ACR criteria only,patients in the former group had higher joint counts and were more likely to beever smokers. However, overall the prevalence of smoking declined during the 30-yearstudy period.

Several sessions at the ACR annual meeting featuredcomorbidities in RA. Joshua F. Baker, MD, of the University of Pennsylvania,performed a cross-sectional analysis of diabetes and RA using the VeteransAffairs RA registry. Type 2 diabetes mellitus was present in 26% of patients atenrollment. Multivariable analysis noted that high baseline disease activitywas associated with a greater risk of incident diabetes; prednisone use wascontrolled for in analysis. Interestingly, tumor necrosis factor inhibitor usewas associated with a significantly lower risk for diabetes. This study impliesthat better disease control may lower the risk for subsequent metaboliccomplications such as type 2 diabetes mellitus in patients with RA.

Cardiovascular risk was discussed by Jon T. Giles, MD, ofColumbia University in New York City. Dr Giles presented information about indicatorsof actionable levels of atherosclerosis in patients with RA who traditionallyare labeled as having low or intermediate cardiovascular risk that is based onstandard risk algorithms. Dr Giles found that actionable levels of coronaryartery calcium determined by traditional risk factors such as older age, eversmoking, antihypertensive use, and aspirin use may not necessarily be adequatefor individuals with RA. Particularly, RA disease activity should be anadditional component of the risk algorithm. Using his modified risk algorithm, DrGiles found that a large proportion of patients with RA who were traditionallycategorized as having lower cardiovascular risk may benefit from additionalscreening and prevention strategies. Similarly, Bryant England, MD, of theUniversity of Nebraska, presented data on multimorbidity in RA from acommercial claims database. Compared with baseline enrollment and one-yearfollow-up, the percentage of patients with multimorbidity considerablyincreased for patients with RA compared with those without RA. Therefore, screeningfor and management of chronic conditions in patients with RA is necessary atthe initial visit to prevent the progression of multimorbidity.

The epidemiology of inflammatory arthritis related to immunecheckpoint inhibitors (ICI) that are used in the treatment of cancer waspresented by Tawnie Braaten, MD, of Johns Hopkins School of Medicine in Baltimore,Maryland. Patients with ICI-induced inflammatory arthritis were found to have ratesof seropositivity and persistent disease activity at 3 and 6 months aftercessation of ICIs. Longer duration of ICI use and combination ICIs wereassociated with persistent inflammatory arthritis. Three-quarters of patientsunderwent immunosuppression, which did not appear to affect tumor response.This study is important because the use of ICIs continues to grow in cancertherapy, and patients with resultant inflammatory arthritis will increasinglybe referred to rheumatology practices.

Practice-Changing Updates

Several abstracts related to tapering both conventionalsynthetic and biologic DMARDs were presented at the meeting. In a late-breakingabstract presented by Siri Lillegraven, PhD, of Diakonhjemmet Hospital in Oslo,Norway, patients with RA who were in sustained remission during treatment with conventionalsynthetic DMARDs and who continued therapy tended to have flares less often andwith less radiographic joint progression than patients whose therapy wastapered. The risk of adverse events related to continued therapy on biologicDMARDs and JAK inhibitors was further explored in a meta-analysis presented by DorotheVinson, of Assistance Publique Hospital of Marseille in France. She reportedthat tapering biologic DMARDs and JAK inhibitors did not lead to a decreasedrisk for serious infections, serious adverse events, or malignancy compared withcontinuing treatment.

While the efficacy and safety of pharmacotherapies tend toshape our practice as rheumatologists, Alexis Ogdie-Beatty, MD, of the PerelmanSchool Medicine at the University of Pennsylvania, along with Ben Nowell, PhD,of the Global Healthy Living Foundation in New York City, highlighted thegrowing use of smartphone applications in clinical and research practice. Theirinteresting session titled, Doctor, Should I Get this App? explored therapidly expanding collection of smartphone apps geared toward behavior changes suchas lifestyle improvement with a focus on weight loss, stress, and sleep. Withfurther review by the rheumatology community, these apps may be recommended to patientswith RA to improve certain issues affecting quality of life that may not beamenable to pharmacologic therapies.

Conclusion

There were many interesting and ground-breaking abstractsrelated to RA at this years ACR annual meeting. Data on the safety andefficacy of JAK inhibitors were widely discussed and will continue to be animportant topic of continued research. The decision to taper vs continue conventionalsynthetic and biologic DMARDs in light of important safety data will needfurther investigation. Perhaps with increasing use of mobile technology,monitoring patients between appointments will allow for accelerated research onthe treatment of RA.

See the rest here:
Expert Insights on Rheumatoid Arthritis From the ACR/ARP 2019 Annual Meeting - Rheumatology Advisor

While guidelines for psoriatic arthritis recommend a treatment target of remission or low disease activity, consensus is lacking on how to define either. Disease activity is most often measured by DAPSA (Disease Activity index for Psoriatic Arthritis) scorebased mainly on jointsor VLDA/MDA (very low disease activity/minimal disease activity) criteriabased on assessment of joints, skin, and entheses. Previous research indicates that remission/low disease activity rates are higher with the use of DAPSA than with VLDA/MDA, according to Laure Gossec, MD, PhD, but what measurements with either test mean to patients is not well known.

For a study published in Annals of the Rheumatic Diseases, Dr. Gossec and colleagues surveyed patients with psoriatic arthritis of more than 2 years and compared their perceptions of remissions with those of their physicians and VLDA, LDA, and DAPSA scores.

In these patients not selected for good disease control and with usually long disease duration, remission or low disease activity were attained by more than 50% of patients, says Dr. Gossec. Patient-perceived remission/low disease activity was frequent (65.4%). Patient-perceived remission was as frequent as remission based on DAPSA, whereas good status according to VLDA/MDA was reached less frequently. DAPSA-based status appeared to correctly reflect patient-perceived low disease activity, which is an argument to use this score to assess psoriatic arthritis.

As the first to compare treatment targets using composite scores and patient questions on assessment of status, the cross-sectional study used a patient questionnaire developed for this study with patient research partners, but not externally validated. Dr. Gossec also notes that whether the findings would be replicated in patients over time is unknown. She adds, though, that physicians now have more information on patient perceptions of remission, and comparison with composite scores to follow-up patients; DAPSA appeared to agree more with patients assessments, though both scores have strengths and weaknesses.

Comparing patient-perceived and physician-perceived remission and low disease activity in psoriatic arthritis: an analysis of 410 patients from 14 countrieshttps://ard.bmj.com/content/78/2/201

Excerpt from:
Comparing Perceptions of Psoriatic Arthritis Disease Activity - Physician's Weekly

When I was a little girl, I had high-flying dreams and they had very little to do with my juvenile arthritis, a childhood illness similar to rheumatoid arthritis (RA). First, I wanted to be a ballerina and practiced dance moves on my parents' Persian rug. Then I watched Jacques Cousteau and his crew of marine biologists diving in waters all over the world and scuttled the dancing dream in favor of serving on his ship, the Calypso, and spending much of my life under water. But at age 16, I went home after a two-year hospital stay in a power wheelchair, trailing recommendations from my then-medical team to lower my expectations of life to those resembling a turnip's. Because of the disease, y'know.

It would be easy to dismiss this as a function of attitudes in a land and time far away from now. But these perceptions persist, if not in others, then certainly in ourselves. Its a strange thing, this shift in assumption and expectation. The minute you get a diagnosis of chronic illness, its as if the rug is pulled out from under you. Your future, which had just shone with possibility, now seems dull, hopeless, and framed in less-than.

Do you really have to give it all up and accept a life of sitting on the sidelines? No. Not by a long shot. The key is to adapt and change your approach. But more on that in a bit. First, lets take a look at the obstacles.

I've lived with RA for more than half a century and have learned that the only predictable thing about this condition is that you never know what it'll do next. Sometimes, you're lucky and find a medication that works, suppressing the symptoms so you can get back to your life. At other times, its all you can do to get dressed in the morning. And, of course, all the stages in between.

Fifty years ago, an American psychologist by the name of Martin Seligman did a study that led to a classic theory of depression. He divided dogs into two groups. Both would receive shocks, but one group of dogs would be able to escape, the other not. The dogs that had no control over the situation curled up in a ball, whimpering. Seligman developed a theory called learned helplessness, stating that when people have no agency (that is, no control), they are more likely to develop depression.

When you have no ability to predict how your RA will feel in the morningand therefore what you will be able to doyou can feel helpless. If youre feeling that kind of helplessness for weeks or months, it spreads into other areas of your life, making you feel depressed. It may even be accompanied by its bratty cousin, "Feel Like Giving Up." And that's OK. Because RA affects every part of your life and it's hard to re-learn how to be you. There's nothing wrong with having a moment (or 10) of intense frustration. But what's really important is to make sure it doesn't stick around.

So much of living with RA is about kicking that cousin out of your psyche. Again, your doctor can help, as can therapy, family and friends, and a community of others like you. Having support will help you fight back and find other ways of taking up the reins of your life.

The great thing about life is that there is no one way to do anything. Whether it's opening a jar, having a family, or building your own business, there are ways around that big boulder called RA in the middle of your path. These tips can help:

Talk to your doctor. Your rheumatologist is one of the most important members on your team. If your RA is getting in the way of you creating a life, call them. You might need to adjust your treatment so you can start the journey back to living first, with RA just muttering in the background. Many people also include diet, exercise, supplements, and alternative treatments in how they approach living with RA.

Give yourself extra time to achieve your goals. Maybe your RA diagnosis won't require a complete change in direction for your life. You might be able to stay on your current career path or even keep training for that big race you've been wanting to tackle, but it's probably going to take a little extra time to get there. Getting the right treatment working for you can take time, and flares don't respect your "to-do" list.

Don't expect to follow "normal" timelines when it comes to working toward big goalsRA is bound to get in the way. When it comes to dreams, pursuing them is what matters, not how you go about it. You are free to create your own path, one that respects and accommodates your RA. For instance, I used to work as a policy analyst, frequently working from home four days a week on research and writing tasks. This enabled me to work much more effectively, with fewer sick days.

When RA brings physical limitations, use your mental muscle instead. I will forever be grateful to my parents for the way they dealt with the lost teenager who came home from the hospital. They told me that although my body might not work very well, there was nothing wrong with my mind and they expected me to use it. This meant working hard in school so I could get to college. By then, I had realized the importance of focusing on what I was able to do (and not just because I couldn't swim, so working with Cousteau was a wash).

Finding alternate routes to getting where I wanted to go eventually became a bit of a hobby and by now, I can almost always find a way around an obstacle. Remember that although your condition might get in the way of you becoming a trapeze artist, you can absolutely find another way to be in the circus.

Go easy on yourself, but not too easy. Frustration about struggling with RA might get misdirected toward yourself. Try not to be angry at yourself or your body. It'll get you nowhere, except derailed, and it isnt something you would tolerate for anyone else. Be kind and understanding to yourself.

Human beings have a gift of adaptation, being able to live in almost any climate, under any conditions, and changing their approach to survive. Use that gift to create your life. Yes, with RA, but a life in which you tear down limits of low expectations.

Following your dreams is a process, sometimes a long one, with side tracks and pauses, and often infuriatingly so. But persevering, accommodating your own needs to move slower, to take pauses, but then reassessing and getting back to your path is possible. The only way to live with RA is to become as stubborn as a goat and refuse to stay down. You learn to withstand long periods of having to put your dream (and your life) on hold while you deal with your condition and its nonsense. During those times of flares and pain, you hone a single-minded focus by getting through each day. When it is over, when you are better and get your life back, you use that focus to pick up your dream and work on it some more.

After many years of attending university, with many challenges, I graduated with my masters degree in social work. After immigrating to Canada from Denmark, and with the offer of a government job in human rights, I thought of those doctors who'd had zero expectations of the girl with a chronic illness and disability. In that moment, I wanted very much to write them a letter, telling them how their assumptions of my inability had had the exact opposite effect: They had only spurred me on.

In my family, that's called the "Show the Bastards" gene. I'll bet you have one, too.

Read this article:
Rheumatoid Arthritis Will Change Your Life. It Doesn't Have to Ruin It. - HealthCentral.com

Genetics and weather are coming against Newfoundlanders and Labradorians who have the highest incidence of arthritis in Canada.

One in four Newfoundlanders and Labradorians suffer from one form of arthritis or another.

That from the Arthritis Societys Jennifer Henning. She says arthritis is an inflammation of the joint, but there are some 100 different types of the disease which is split into two major categories, inflammatory and degenerative.

Rheumatoid arthritis is an autoimmune attack on the joints by the bodys own immune system. It can happen at any time, and affect the entire body.

Osteoarthritis is the most common form and comes as the result of wear and tear, injury or the general aging process. It involves a degeneration of the cartilage between the bones of the joint.

Both types of arthritis result in significant pain and loss of mobility.

Henning says unfortunately, weather doesnt help.

She says in laymans terms, the body is tighter because its cold, and when its wet the tissues swell, causing a greater amount of pain and inflammation.

She says genetics also play a strong role especially in the inflammatory type of arthritis.

Rheumatoid arthritis is more common in women and is often triggered by a traumatic event like childbirth, injury or illness.

Originally posted here:
Genetics and Weather in NL Producing Highest Incidence of Arthritis in Canada - VOCM

Dear Doctor: Im a 66-year-old man whose right knee really hurts from arthritis. My sister keeps talking about something called prolotherapy. What is it, and can it help?

Dear Reader: Prolotherapy is an injection-based approach to treating pain in the soft tissues of the joint. Specifically, a small amount of a liquid irritant is introduced at the site where a tendon or ligament attaches to the bone. The idea is that the irritant will set off a localized inflammation reaction, which will then trigger the release of growth factors that promote the healing of soft tissues.

The roots of prolotherapy date back to the ancient Greeks, who believed that deliberately causing inflammation in a certain area of the body could stimulate the tissues to repair themselves. In the 1930s and 1940s, several physicians expanded on the concept. They experimented with various solutions and developed techniques sometimes referred to as needle surgery to target connective tissue in the joints.

Today, prolotherapy injections typically consist of sugar- or salt-based solutions to which a local anesthetic, such as lidocaine, is added. Patients seek the treatment to help with joint pain and stiffness resulting from injury, overuse or inflammatory conditions such as arthritis and degenerative disc disease. Areas of the body targeted by the practice include the knees, back, hips, ankles, shoulders and hands.

Treatment protocols usually consist of a series of three to eight injections given over weeks or months, depending on the specific case. The injections can be moderately painful, and patients often use Tylenol or stronger medications to manage localized aches and tenderness. Patients are advised to limit activity for several days after each injection, and they may be asked to supplement the therapy with specific exercises that focus on range of motion.

Since creating inflammation is the point of prolotherapy, the use of NSAIDs, or non-steroidal anti-inflammatories, to address the resulting pain and discomfort is not recommended. Possible side effects of the procedure include bleeding, bruising or swelling at the injection site. These can last for a week or more. Allergic reactions to the injected solution, infection and nerve damage are possible, but rare.

Does prolotherapy work? In some case studies, patients report improvement in pain and strength in the affected areas. But studies of the treatment have yielded mixed results. Some have argued that the studies showing benefit have been too small and not scientifically rigorous. The one area of agreement appears to be the need for large and scientifically rigorous studies.

Although prolotherapy is gaining in popularity, the National Institutes of Health identify it as a complementary and alternative medical treatment. And since its considered an experimental therapy, many insurance companies wont cover it. Costs can range from $400 to $1,000 per treatment, depending on the provider.

As with all alternative therapies, we think its wise for you to check with your doctor to see whether prolotherapy may be helpful for you.

Send your questions to askthedoctors@mednet.ucla.edu.

Originally posted here:
Ask the doctors: Arthritis pain may be relieved by prolotherapy - The Spokesman-Review

", "", "" ] }, { "position": "bottom", "content": [ "Follow us ", "", "" ] } ] }, { offCanvas: { pageSelector: "#mm-off-canvas-content" } }); var mmenuapi = $("#mm-menu").data( "mmenu" ); $("#menuFlyOutLogInPopUp").click(function() { mmenuapi.close(); displayLogInPopUp();});checkStatus(); /*var loginDivTemp = document.getElementById("loginDiv"); var subscribeDivTemp = document.getElementById("subscribeDiv"); var loginDivClone = loginDivTemp.cloneNode(true); var subscribeDivClone = subscribeDivTemp.cloneNode(true); var loginPlaceholder = document.getElementById("loginDivPlaceholder"); var subscribePlaceholder = document.getElementById("subscribeDivPlaceholder"); loginPlaceholder.appendChild(loginDivClone); subscribePlaceholder.appendChild(subscribeDivClone); $("#fade").click(function () { closeSplashAndSetCookie(); });*/ }); function displayLogInPopUp() { document.getElementById('fade').style.display='block'; document.getElementById('logInPopUpForm').style.display='block'; } function getParameterByName(name) { var match = RegExp('[?&]' + name + '=([^&]*)').exec(window.location.search); return match && decodeURIComponent(match[1].replace(/+/g, ' ')); } //what-input.js !function (e, t) { "object" == typeof exports && "object" == typeof module ? module.exports = t() : "function" == typeof define && define.amd ? define("whatInput", [], t) : "object" == typeof exports ? exports.whatInput = t() : e.whatInput = t() }(this, function () { return function (e) { function t(o) { if (n[o]) return n[o].exports; var i = n[o] = { exports: {}, id: o, loaded: !1 }; return e[o].call(i.exports, i, i.exports, t), i.loaded = !0, i.exports } var n = {}; return t.m = e, t.c = n, t.p = "", t(0) }([function (e, t) { e.exports = function () { var e = document.documentElement, t = "initial", n = null, o = ["input", "select", "textarea"], i = [16, 17, 18, 91, 93], r = { keyup: "keyboard", mousedown: "mouse", mousemove: "mouse", MSPointerDown: "pointer", MSPointerMove: "pointer", pointerdown: "pointer", pointermove: "pointer", touchstart: "touch" }, u = [], d = !1, a = { 2: "touch", 3: "touch", 4: "mouse" }, s = null, p = function () { window.PointerEvent ? (e.addEventListener("pointerdown", c), e.addEventListener("pointermove", m)) : window.MSPointerEvent ? (e.addEventListener("MSPointerDown", c), e.addEventListener("MSPointerMove", m)) : (e.addEventListener("mousedown", c), e.addEventListener("mousemove", m), "ontouchstart" in window && e.addEventListener("touchstart", v)); var t = !1; try { var n = Object.defineProperty({}, "passive", { get: function () { t = !0 } }); window.addEventListener("test", null, n) } catch (e) { } e.addEventListener(l(), m, !!t && { passive: !0 }), e.addEventListener("keydown", c), e.addEventListener("keyup", c) }, c = function (e) { if (!d) { var u = e.which, a = r[e.type]; if ("pointer" === a && (a = w(e)), t !== a || n !== a) { var s = !(!document.activeElement || -1 !== o.indexOf(document.activeElement.nodeName.toLowerCase())); ("touch" === a || "mouse" === a && -1 === i.indexOf(u) || "keyboard" === a && s) && (t = n = a, f()) } } }, f = function () { e.setAttribute("data-whatinput", t), e.setAttribute("data-whatintent", t), -1 === u.indexOf(t) && (u.push(t), e.className += " whatinput-types-" + t) }, m = function (t) { if (!d) { var o = r[t.type]; "pointer" === o && (o = w(t)), n !== o && (n = o, e.setAttribute("data-whatintent", n)) } }, v = function (e) { window.clearTimeout(s), c(e), d = !0, s = window.setTimeout(function () { d = !1 }, 200) }, w = function (e) { return "number" == typeof e.pointerType ? a[e.pointerType] : "pen" === e.pointerType ? "touch" : e.pointerType }, l = function () { return "onwheel" in document.createElement("div") ? "wheel" : void 0 !== document.onmousewheel ? "mousewheel" : "DOMMouseScroll" }; return "addEventListener" in window && Array.prototype.indexOf && (r[l()] = "mouse", p(), f()), { ask: function (e) { return "loose" === e ? n : t }, types: function () { return u } } }() }]) }); //headerweatericon.js if (window.matchMedia("(min-width: 39.9375em)").matches) { var weatherScript = document.createElement("script"); weatherScript.src = "/js/min/weatherbug.min.js"; document.head.appendChild(weatherScript); } $(document).foundation(); function getCookie(cname) { var name = cname + "="; var decodedCookie = decodeURIComponent(document.cookie); var ca = decodedCookie.split(';'); for(var i = 0; i

See the original post here:
Arthritis treatment safe for cats with kidney disease [Ask the Vet's Pets] - Reading Eagle

Millions of patients in England will be stopped from having an X-ray on their sore back, hernia repair surgery or scan of their knee to detect arthritis under controversial plans from NHS and doctors to ration unnecessary treatment.

The Guardian has seen a list of 34 diagnostic tests and treatments that in future patients will only be able to get in exceptional circumstances as part of a drive to save money and relieve the pressure on the NHS.

The sweeping changes they are set to propose include many forms of surgery, as well as ways of detecting illness including CT and MRI scans, and blood tests, for cancer, arthritis, back problems, kidney stones, sinus infections and depression. Three of the procedures have since been dropped from the list.

If implemented, the clampdown would involve an unprecedentedly radical restriction on patients right to access and doctors ability to recommend procedures, some of which have been used routinely for decades.

It would also see patients told to use physiotherapy or painkillers to dull the pain of an arthritic knee rather than undergo an exploratory operation called an arthroscopy. Kidney stones would no longer be removed in an operating theatre and instead would be treated with sound wave therapy to reduce the pain.

Similarly, in future adenoids would not be removed because evidence now shows that it is not necessary, doesnt work well and can cause problems like bleeding and infection, according to the rationale set out in the document for curtailing that procedure.

Disclosure of the list prompted fears that the move amounts to a major escalation of NHS rationing.

An NHS spokesperson said the document was out of date and had not been approved or implemented. They added there was strong support from senior doctors in the Academy of Medical Royal Colleges for action to eliminate wasteful interventions that dont benefit patients.

The Patients Association warned that if implemented the changes would force patients to either endure the pain of their condition or pay for private care to tackle it.

Putting barriers in the way of people expecting to have so many previously commonplace tests and treatments would lead to harm and distress, said Rachel Power, the associations chief executive.

Patients have seen the range of treatments offered by the NHS cut back over recent years, and the NHS has been upfront about this being to save cash. Often there are good reasons for not using these low value treatments as a first choice, but they are appropriate for some patients.

We are unhappy at any new barriers being erected between patients and the treatments they need.

This is of a piece with the restrictions on prescribing over the counter medicines [which NHS England brought in last year], and patients have told us of the harm and distress this broad programme of restrictions has caused them, she added.

As a result of this rationing, we know that patients who can afford to pay privately are doing so, while those who cant are going without and suffering. This is exactly what having an NHS is supposed to prevent.

The 50-page document is the result of months of detailed and until now secret discussions between four key medical and NHS bodies involved in the NHSs evidence-based interventions programme, which aims to identify procedures that do not work.

They are NHS England; the Academy of Medical Royal Colleges (AOMRC), which represents the UKs 220,000 doctors professionally; NHS Clinical Commissioners, which speaks for GP-led clinical commissioning groups; and the National Institute for Health and Care Excellence (Nice), which advises the government and NHS which treatments are effective and represent value for money.

They believe many of the interventions should be scrapped, or at most used very sparingly, because they could make patients anxious or even put them in danger. For example, they are suggesting that the prostate-specific antigen test, which is used to detect prostate cancer the commonest form of cancer in men is used much less often.

The document says: Blood tests to check your prostate are not needed except for very specific cases. Blood tests can lead to further investigation that may also be unnecessary and can cause anxiety.

The four medical bodies planned to put the proposals out to public consultation this month but had to delay because of general election purdah rules.

Hospitals would be told not to operate on patients to try to slow the progress of osteoporosis (brittle bone disease), or if they have sinusitis, or to remove a disc from the spine of someone suffering from crippling pain.

Dr Richard Vautrey, chair of the British Medical Associations GPs committee, said any changes should be based on the best available evidence and not cost-cutting.

In the current climate, NHS resources must be used wisely but any restriction on treatments must be based on up to date clinical evidence and not solely on cost.

Doctors must always be able to provide the best care possible and use their clinical expertise to refer patients for the most appropriate treatments when that is needed.

Prof Carrie MacEwan, chair of the AOMRC, defended the planned restrictions. Medicine continually evolves and its right that we dont carry out tests, treatments or procedures when the evidence tells us they are inappropriate or ineffective and which, in some cases, can do more harm than good.

The list is drawn up by medical experts and senior specialist clinicians who have reviewed the latest evidence from around the world and its absolutely right we act on that evidence in the best interests of patients and so that we can focus our resources on things that we know do work, she added.

Read more:
Revealed: NHS plans to ration 34 everyday tests and treatments - The Guardian

(Photo : pixabay)

Theresearchprovided by the Oregon State University provided the first complete cellular-level look at what goes on in joints that are affected by osteoarthritis, which is considered as a costly and debilitating condition that affects almost one-quarter of adults in America.

The study was published inNature Biomedical Engineering, and it gave an insight into how factors like drugs, diet, and exercise can affect the joint's cells, which is important because cells do the work of maintaining, developing and repairing the tissue.

Arthritis treatment

Theresearchdone by the OSU College of Engineering's Brian Bay and the scientists from the Royal Veterinary College in London and University College London created a sophisticated scanning technique to view joints of mice that have arthritis and joints of healthy mice.

Brian Bay said that the techniques for quantifying changes in arthritic joints had been constrained by a lot of factors. Restrictions on the length of scanning time and the sample size are two of them, and the level of radiation used in some of the techniques ultimately damages or destroys the samples that are being scanned. The nanoscale resolution of intact, loaded joints had been considered unattainable.

Brain Bay and scientists from 3Dmagination Ltd, the University of Manchester, Edinburgh Napier University, the Diamond Light Source, and the Research Complex at Harwell created a way to conduct nanoscale by capturing the images of bones and whole joints under precisely controlled loads.

The scientists enhanced the resolution without compromising the study's field of view, decrease the total radiation exposure to preserve the tissue mechanics, and to prevent movement during the scanning.

Brian Bay stated that with a low-dose of pink-beam synchrotron X-ray tomography and mechanical loading with nanometric precision, scientists could measure the structural organization simultaneously and functional response of the tissues. That means that scientists can look at the joints of the patient from the tissue layers down to the cellular level with a large field of view and high resolution without having to cut out the samples.

He also stated that the two features of the study make it helpful in advancing the study of osteoarthritis. By using intact joints and bones, all of the functional aspects of the complex tissue that is layering are preserved. The small size of the mouse bones leads to imaging that is seen on the scale of the cells that maintain, develop, and repair the tissues.

The effect of osteoarthritis on health

Osteoarthritis is the degeneration of joints, and according to the Centers for Disease Control and Prevention, it affects more than50 million American adults. Around 18% of men and 25% of women suffer from osteoarthritis.

As the senior population in America increases, the prevalence of arthritis will likely rise in the coming years. The CDC estimates that by 2040 there will be 78 million arthritis patients, more than one-quarter of the projected total adult population, two-thirds of those with arthritis are expected to be women. By 2040, 34 million adults in America will have limits in the activities that they do because of arthritis.

Brian Bay said that osteoarthritis will affect most of the adults during their lifetime to the point where a hip joint or a knee joint needs replacement with a difficult and costly surgery after years of pain and disability. This new treatment that OSU has to develop can prevent any severe arthritis from forming that could save millions of adults from having to go through the difficulties of arthritis.

See more here:
Oregon State University Has Provided a New Treatment for Athritis - Science Times