Obesity and Rheumatoid Arthritis. A bad association


– A new study offers a double message about the potential impact of obesity on systemic lupus erythematosus (SLE) in women: Excess pounds are linked to a higher risk of patient-reported outcomes such as pain and fatigue, and body mass index may be an appropriate tool to study weight issues in this population.


For the new study, Dr. Patterson and her colleagues analyzed findings from surveys of 148 participants in the Arthritis Body Composition and Disability study. All participants were women with a verified SLE diagnosis.

About two-thirds of the sample were white, 14% were Asian, and 13% were African American. The average age was 48 years, the average disease duration was 16 years, and 45% took glucocorticoids.

Researchers used two measurements of obesity: BMI of 30 kg/m2 or greater and fat mass index (FMI) of 13 kg/m2 or greater.

They calculated FMI with data collected via whole dual x-ray absorptiometry. Of the participants, 32% and 30% met criteria for obesity under FMI and BMI definitions, respectively.

Researchers also collected survey data regarding measurements of disease activity, depressive symptoms, pain and fatigue.

The study authors controlled their results to account for factors such as age, race, and prednisone use. They found that those defined as obese via FMI had more disease activity and depression than did nonobese women: 14.8 versus 11.5, P = .010, on the Systemic Lupus Activity Questionnaire scale, and 19.8 versus 13.1, P = .004, on the Center for Epidemiologic Studies Depression scale.

On two other scales of pain and fatigue, obese patients scored lower – a sign of worse status – compared with nonobese women: 38.7 versus 44.2, P = .004, on the Short Form 36 (SF-36) Health Survey pain subscale and 39.6 versus 45.2, P= .010, on the SF-36 vitality subscale. The researchers reported similar findings when using BMI to assess obesity.

It’s not clear why obesity and lupus may be linked, Dr. Patterson said, though she noted that inflammation is a shared factor. “People with lupus have arthritis and chronic pain, so there may be this vicious feedback cycle with hindrances to be able to live healthy lifestyles,” she added.

The study has limitations, including that the sample is largely white, while lupus is more common among minority women. In addition, the study does not include underweight patients or track patients over time. “It will be important to look at obesity and patient-reported outcomes to determine whether weight loss results in better outcomes,” Dr. Patterson said.

The study does provide an extra benefit by suggesting that BMI is not an inferior tool to measure the effects of obesity in the SLE population, Dr. Patterson said. BMI has been criticized as a misleading measurement of obesity. But the BMI and FMI measures produced similar results in this study. “That’s really good news in a way for the practicalities of using this information,” she said.

But FMI may still be a better measurement of obesity in the general population, where BMI may be more likely to be thrown off by high muscle mass.

It may seem obvious that obesity is linked to worse lupus outcomes, but rheumatologist Bryant England, MD, of the University of Nebraska, Omaha, said that this research is noteworthy because it highlights the importance of focusing on obesity in the clinic.

Rheumatologists shouldn’t leave obesity to primary care physicians but instead confront it themselves, said Dr. England, who moderated a discussion of new research at an ACR annual meeting press conference. But he cautioned that prudence is especially important when talking about obesity with lupus patients because they may be sensitive about medication-related weight gain.

Dr. Patterson and the other study authors reported having no relevant disclosures. Dr. England also reported no relevant disclosures. The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update


J. Smolen et al.


Recent insights in rheumatoid arthritis (RA) necessitated updating the European League Against Rheumatism (EULAR) RA management recommendations. A large international Task Force based decisions on evidence from 3 systematic literature reviews, developing 4 overarching principles and 12 recommendations (vs 3 and 14, respectively, in 2013). The recommendations address conventional synthetic (cs) disease-modifying antirheumatic drugs (DMARDs) (methotrexate (MTX), leflunomide, sulfasalazine); glucocorticoids (GC); biological (b) DMARDs (tumour necrosis factor (TNF)-inhibitors (adalimumab, certolizumab pegol, etanercept, golimumab, infliximab), abatacept, rituximab, tocilizumab, clazakizumab, sarilumab and sirukumab and biosimilar (bs) DMARDs) and targeted synthetic (ts) DMARDs (Janus kinase (Jak) inhibitors tofacitinib, baricitinib). Monotherapy, combination therapy, treatment strategies (treat-to-target) and the targets of sustained clinical remission (as defined by the American College of Rheumatology-(ACR)-EULAR Boolean or index criteria) or low disease activity are discussed. Cost aspects were taken into consideration. As first strategy, the Task Force recommends MTX (rapid escalation to 25 mg/week) plus short-term GC, aiming at >50% improvement within 3 and target attainment within 6 months. If this fails stratification is recommended. Without unfavourable prognostic markers, switching to—or adding—another csDMARDs (plus short-term GC) is suggested. In the presence of unfavourable prognostic markers (autoantibodies, high disease activity, early erosions, failure of 2 csDMARDs), any bDMARD (current practice) or Jak-inhibitor should be added to the csDMARD. If this fails, any other bDMARD or tsDMARD is recommended. If a patient is in sustained remission, bDMARDs can be tapered. For each recommendation, levels of evidence and Task Force agreement are provided, both mostly very high. These recommendations intend informing rheumatologists, patients, national rheumatology societies, hospital officials, social security agencies and regulators about EULAR’s most recent consensus on the management of RA, aimed at attaining best outcomes with current therapies.


In RA, When to Stop Anti-TNF Therapy


Kevin D. Deane, MD, PhD

Stopping Tumor Necrosis Factor Inhibitor Therapy in Patients With Established Rheumatoid Arthritis in Remission or With Stable Low Disease Activity: A Pragmatic Multicenter, Open-Label Randomized Controlled Trial

Ghiti Moghadam M, Vonkeman HE, Ten Klooster PM, et al; Dutch National POET Collaboration
Arthritis Rheumatol. 2016;68:1810-1817

Study Summary

In this study, Ghiti Moghadam and colleagues from The Netherlands used a pragmatic trial design to investigate rates of rheumatoid arthritis (RA) flare after cessation of anti-tumor necrosis factor (anti-TNF) therapy. They analyzed 817 patients, all of whom had a Disease Activity Score in 28 joints (DAS28) < 3.2 for 6 months before inclusion.

Individuals with RA were randomized in a 2:1 ratio to stop or continue anti-TNF therapy (531 and 286 patients, respectively). The primary outcome was flare of disease, as determined by a DAS28 ≥ 3.2 over 12 months of follow-up or an increase in score ≥ 0.6.

At 12 months, the anti-TNF discontinuation group had more flares (approximately 51% vs 18%; P < .001) and a higher mean DAS28 (P < .001). Of the 195 patients who restarted anti-TNF therapy, around 85% regained a DAS28 < 3.2 after 6 months. Besides stopping anti-TNF therapy, predictors of time to a flare were a higher baseline DAS28 and disease duration > 10 years at the time of study entry. In terms of safety, there was one death due to an infection in the continuation group, and 34 hospitalizations in the discontinuation group compared with seven in the continuation group (P = .012)


Increasing numbers of studies have been investigating the possibility that individuals with RA can decrease therapy and yet continue to have excellent disease control. These studies were reviewed in an outstanding article by Schett and colleagues[1] that was published in the May 2016 edition of the Annals of Rheumatic Diseases. Results have been variable, although there has been substantial heterogeneity across the studies.

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Mechanistic, Epidemiologic Clues Suggest Possible Link Between Obesity, Inflammation in Rheumatoid Arthritis


The Rheumatologist

October 11, 2016 • By

Obesity has an established systemic inflammatory component. Could that be a trigger for the inflammation seen inrheumatoid arthritis (RA) and other rheumatic diseases? Although there is no direct scientific evidence, both mechanistic and epidemiologic clues do give some intriguing suggestions of a possible link.

“At first, we thought that fat was involved only in energy storage and helping insulate the body from cold,” says Michael B. Brenner, MD, chief of the Division of Rheumatology, Immunology and Allergy at Brigham and Women’s Hospital in Boston. “We now realize that there is an entire immune system within adipose tissue [AT] that switches from a Type 2 anti-inflammatory state to a pro-inflammatory state characterized by many of the same cytokines and cells that we see in RA.”

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Be vigilant for restrictive lung disease in RA


Publish date: October 4, 2016

Author(s): Kari Oakes

– Patients with rheumatoid arthritis who have pulmonary symptoms and a restrictive pulmonary function test pattern have a high likelihood for a diagnosis of interstitial lung disease, making it necessary to put it high on the differential and to begin working collaboratively with pulmonologists, according to Jon T. Giles, MD.

Overall, 8%-15% of RA patients will develop clinically significant interstitial lung disease (ILD), although radiographic evidence of ILD can be seen in up to half of RA patients, and in one study about one in four patients had evidence of ILD on CT scanning within 2 years of RA diagnosis. The overall risk for RA patients to develop ILD has been shown to be nine times higher than for matched controls (Arthritis Rheum. 2010 Jun;62[6]:1583-91), Dr. Giles said at the annual Perspectives in Rheumatic Diseases held by Global Academy for Medical Education.

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A combination of cellular biomarkers predicts failure to respond to rituximab in rheumatoid arthritis: a 24-week observational study


Martin H. Stradner, Christian Dejaco, Kerstin Brickmann, Winfried B. Graninger and Hans Peter BrezinschekEmail authorView ORCID ID profile
Arthritis Research & Therapy201618:190
DOI: 10.1186/s13075-016-1091-1© The Author(s). 2016
Received: 14 May 2016Accepted: 8 August 2016Published: 24 August 2016



Although B cell depletion with rituximab (RTX) is an effective treatment strategy in rheumatoid arthritis (RA), one third of patients do not achieve remission or low disease activity (LDA). Thus, identifying patients who will benefit from RTX is highly desirable. In the present study we investigated whether lymphocyte subsets other than B cells are predictors of a clinical response to RTX treatment.


Patients with RA who were receiving RTX for the first time were included in an observatory registry. Clinical assessments, complete blood count and flow cytometry of lymphocyte subsets were obtained at baseline and at week 24 after RTX. Complete data were available for 44 patients. Logistic regression and receiver operating characteristic curve analyses were computed to analyze the predictive value of lymphocyte subsets for European League Against Rheumatism (EULAR) response and LDA (defined as disease activity score in 28 joints (DAS28) ≤3.2) at week 24.


EULAR responders had lower total lymphocyte counts (LC), T cells and CD4 + T cells at baseline. Although these parameters were independent predictors of EULAR response they failed in determining who would reach LDA. In contrast, LC >2910/μl or plasmablast frequency >2.85 % at baseline predicted a significantly higher DAS28 at week 24 after RTX and identified patients not achieving LDA at week 24 with sensitivity of 93.3 % and specificity of 44.8 %.


A combination of LC and plasmablast frequency identifies patients with RA who will not benefit from RTX with high probability.


Rheumatoid arthritis Biomarker Rituximab T cells Plasmablasts Lymphocytes

Periodontal Infection May Determine Best Treatment for Patients with RA


July 4, 2016 • By

The Rheumatologist

The pathology of rheumatoid arthritis (RA) includes a breach in self-tolerance, chronic synovial inflammation and joint destruction. As the disease progresses, patients are increasingly likely to have high serum levels of anti-cyclic citrullinated peptide (CCP) antibody. A search for the source of anti-CCP antibodies has led researchers to suggest that infection with a common periodontal pathogen, Porphyromonas gingivalis, may play an important role in the generation of the anti-CCP antibodies. Porphyromonas gingivalis produces an enzyme known as peptidularginine deiminase (PPAD), which modifies peptidylarginine residues to citrulline, thereby creating the antigen that is the target of the anti-CCP antibody. This connection between RA and Porphyromonas gingivalis infection has also led investigators to question whether the relationship can be leveraged to improve the treatment of RA.

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