The latest medical research on Rheumatology

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about rheumatology gathered by our medical AI research bot.

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Stratifying management of rheumatic disease for pregnancy and breastfeeding.

Nature Reviews Rheumatology

The management of inflammatory rheumatic diseases during pregnancy and breastfeeding has undergone considerable change in the past few years. Moder...

New therapies for systemic lupus erythematosus - past imperfect, future tense.

Nature Reviews Rheumatology

The failure of many new, mostly biologic, drugs to meet their primary end points in double-blind clinical trials in patients with systemic lupus er...

Association of Pain Centralization and Patient-Reported Pain in Active Rheumatoid Arthritis.

Arthritis Care Res

Pain is a significant burden for rheumatoid arthritis (RA) patients despite advancements in treatment. We examined the independent contribution of pain centralization to the pain experience of patients with active RA.

Two hundred and sixty-three RA patients with active disease underwent quantitative sensory testing (QST) including assessment of extra-articular pressure pain thresholds (PPTs), temporal summation (TS), and conditioned pain modulation (CPM). The pain experience was assessed by a pain intensity numeric rating scale and the Patient-Reported Outcomes Measurement Information System (PROMIS® ) Pain Interference computerized adaptive test. We examined associations between QST measures and pain intensity and pain interference. Multiple linear regression models were adjusted for demographic and clinical variables, including swollen joint count and C-reactive protein.

Patients with the lowest PPTs (most central dysregulation) reported higher pain intensity than patients with the highest PPTs (adjusted mean difference (95% CI) 1.02 (0.37, 1.67)). Patients with the highest TS (most central dysregulation) had higher pain intensity than those with the lowest TS (adjusted mean difference (95% CI) 1.19 (0.54, 1.84)). CPM was not associated with differences in pain intensity. PPT and TS were not associated with pain interference. Patients with the lowest CPM (most centrally dysregulated) had lower pain interference than patients with the highest CPM (adjusted mean difference (95% CI) -2.35 (-4.25, -0.44)).

Pain centralization, manifested by low PPTs and high TS, was associated with more intense pain. Clinicians should consider pain centralization as a contributor to pain intensity, independent of inflammation. This article is protected by copyright. All rights reserved.

Stability of measures of pain catastrophizing and widespread pain following total knee replacement (TKR).

Arthritis Care Res

Pain catastrophizing and widespread pain (WP) are predictors of pain chronicity/severity. Gaps remain in our understanding of the extent to which each is a stable (trait) or dynamic (state) variable. We assess a) the stability of each variable from before to after total knee replacement (TKR), and b) whether changes are explained by pain improvements.

We used data from a prospective study of TKR recipients ages 40+. Questionnaires included body pain diagrams assessing WP, the Pain Catastrophizing Scale (PCS), and WOMAC Pain. We divided subjects into WP groups (0 vs. 1-2 vs. ≥3 pain regions) and into low and high PCS groups (<16 vs. ≥16). We assessed changes in group membership from pre- to 12 months post-TKR, then compared these changes between subjects with most and least WOMAC pain improvement.

176 subjects completed scales at both timepoints; 64% were female, mean age was 66, and baseline median WOMAC pain was 40. 71% of subjects in the high PCS group improved to join the low PCS group at follow-up. While 73 subjects (41%) changed WP group, they were similarly likely to worsen and to improve. We found a statistically significant positive association of improvement in WOMAC pain with improvement in PCS (r=0.31), but not WP (r=-0.004).

The PCS reflects state-like aspects of catastrophizing that diminish along with pain. In contrast, WP scores worsened and improved equally often, regardless of knee pain relief. The findings urge caution in interpreting PCS and WP as trait measures in musculoskeletal research. This article is protected by copyright. All rights reserved.

Canakinumab provides rapid and sustained long-term efficacy and safety in patients with cryopyrin-associated periodic syndrome aged ≤5 years.

Arthritis Rheumatol

To assess longer-term efficacy and safety of canakinumab and the response to vaccination in children aged ≤5 years with cryopyrin-associated periodic syndrome (CAPS).

CAPS patients (aged ≤5 years) received 2mg/kg canakinumab subcutaneously every 8 weeks; patients with neonatal onset multisystem inflammatory disease (NOMID), received a starting dose of 4 mg/kg in this open-label trial. Efficacy was evaluated using physician's global assessment (PGA), and serum levels of C-reactive protein (CRP) and amyloid A (SAA). Adverse events (AEs) were collected. Vaccination response was evaluated using post-vaccination antibody titers at 4 and 8 weeks after immunization.

Of the 17 patients enrolled, 12 (71%) had Muckle-Wells syndrome, 4 (24%) had NOMID, and 1 (6%) had familial cold autoinflammatory syndrome. All patients (17/17) were complete responders to canakinumab. PGA improved, and 65% of patients had absent auto-inflammatory disease at the end of study. Median CRP levels decreased over time. No such change was evident in SAA levels. During the extension study, post-vaccination antibody titers increased above protective levels in 16/17 (94%) assessable vaccinations. Ten (59%) patients had AEs suspected to be related to canakinumab; 8 (47%) experienced at least 1 serious AE. None of the AEs/SAEs required interruption of canakinumab therapy.

Canakinumab effectively maintained efficacy through 152 weeks and appears to have no effect on the ability to produce antibodies against standard childhood killed vaccines. Safety profile of canakinumab was consistent with previous studies, supporting long-term use of canakinumab for CAPS in children < 5 years of age. This article is protected by copyright. All rights reserved.

Associations of gout and baseline serum urate with cardiovascular outcomes: analysis of the Coronary Disease Cohort Study.

Arthritis Rheumatol

To determine whether gout and serum urate (SU) are associated with increased risk of death, time to first readmission for any cardiovascular event or incident heart failure in people with cardiovascular disease.

People presenting with an acute coronary syndrome (ACS) were enrolled in the Coronary Disease Cohort Study. Clinical data were collected from the index hospital admission, and clinical, echocardiographic, and biochemical data were collected post-discharge. Gout was defined by self-report or use of urate lowering therapy or use of colchicine with evidence of gout on review of the medical records. The primary end-points were all-cause mortality, time to readmission for a cardiac ischaemic event or heart failure.

Data from 1514 participants were available. During the follow-up period, 53/160 (33.1%) of those with gout and 298/1354 (22.1%) of those without gout died. After adjusting for other factors known to be associated with mortality there was no gout-specific increase in risk of mortality (adjusted HR 0.98 (95%CI 0.69-1.38). Time to readmission for heart failure was significantly briefer in those with, compared to those without, gout (adjusted HR 1.46 42 (95%CI 1.02 - 1.97. Irrespective of gout, as SU increased there was an increased risk of death, and readmission for either a cardiovascular event or heart failure CONCLUSIONS: Survival post-ACS is similar in those with and without gout. People with gout are at an increased risk of readmission for heart failure and have more days in hospital. Risk of these events increases in parallel with SU. This article is protected by copyright. All rights reserved.

Disease Activity, ANCA-Type, and Lipid Levels in ANCA-Associated Vasculitis.

Arthritis Rheumatol

Patients with ANCA-associated vasculitis (AAV) are at elevated risk for cardiovascular disease (CVD). A clearer understanding of the association between changes in disease activity and lipid levels in AAV would inform CVD risk stratification in this population.

Lipid levels were assessed using baseline and month 6 stored serum samples from the Rituximab for ANCA-associated Vasculitis (RAVE) trial which randomized subjects to rituximab or cyclophosphamide followed by azathioprine. Paired t tests and multivariable linear regression were used to assess changes in lipid levels.

Of the 142 subjects with samples available, the mean age was 52.3 (±14.7) years, 72 (51%) were male, 95 (67%) were proteinase (PR3)-ANCA+, 72 (51%) had a new diagnosis of AAV, and 75 (53%) were treated with rituximab. Levels of several lipid levels increased between baseline and month 6, including total cholesterol (+12.4mg/dL, [+7.1, +21.0]), low-density lipoprotein (+10.3 mg/dL, [+6.1, +17.1]), and apolipoprotein B (+3.5 mg/dL, [+1.0, +8.3]). These changes were observed among newly-diagnosed and PR3-ANCA+ subjects but not among those with relapsing disease or myeloperoxidase (MPO)-ANCA+ subjects. There was no difference in changes in lipid levels between rituximab- and cyclophosphamide-treated patients. Changes in lipids correlated with changes in ESR, but not with other inflammatory markers or glucocorticoid exposure.

Lipid levels increase during remission induction among patients with AAV with newly-diagnosed disease and those who are PR3-ANCA+. Disease activity and ANCA type should be considered when assessing lipid profiles to stratify CVD risk in patients with AAV. This article is protected by copyright. All rights reserved.

Osteoclast-derived Autotaxin, a distinguishing factor for inflammatory bone loss.

Arthritis Rheumatol

The severity of rheumatoid arthritis (RA) correlates directly with bone erosions due to osteoclast (OC) hyperactivity. Despite controlled inflammation, RA patients in sustained clinical remission or low disease activity may continue to accrue erosions urging the need for treatments suitable for long-lasting inhibition of OC activity without altering their physiological function in bone remodeling. Autotaxin (ATX) contributes to inflammation but its role in bone erosion is unknown.

ATX was targeted by both treatments with pharmacological drugs and conditional inactivation of Ennp2 (ATX gene) in OC (ΔATXCtsk mice). Arthritic and erosive diseases were studied in human tumor necrosis factor transgenic (hTNF+/- ) and K/BxN serum-transfer arthritis mice. Systemic bone loss was also analyzed in the Lipopolysaccharide (LPS)-induced inflammation and estrogen deprivation models. Joint inflammation and bone erosion were assessed by histology and microcomputed tomography. The role of ATX was examined in murine OC differentiation and activity assays.

OC present at inflammatory sites overexpressed ATX. Pharmacological inhibition of ATX significantly mitigated focal (36% amelioration; p<0.05) and systemic bone loss (43% amelioration; p<0.05) in hTNF+/- mice without affecting synovial inflammation. OC-derived ATX revealed instrumental in OC bone resorptive activity and was upregulated under inflammation elicited by TNF or LPS. Specific loss of ATX in OC significantly protected against systemic bone loss and erosion after LPS and K/BxN-treatment (30% in systemic bone loss; p<0.01 and 55% in erosion; p<0,001) without bone protective property following ovariectomy.

Our results identify ATX as a novel OC factor that specifically controls inflammation-induced bone erosions and systemic bone loss. Therefore, ATX inhibition offers a novel therapeutic approach for preventing bone erosion in RA. This article is protected by copyright. All rights reserved.

The value of carotid ultrasound in cardiovascular risk stratification in patients with psoriatic disease.

Arthritis Rheumatol

This study aimed to assess whether subclinical atherosclerosis, as evaluated by carotid ultrasound, could predict incident cardiovascular events (CVE) in patients with psoriatic disease (PsD) and determine whether incorporation of imaging data could improve cardiovascular risk prediction by the Framingham Risk Score (FRS).

In this cohort analysis, patients with PsD underwent ultrasound assessment of the carotid arteries at baseline. The extent of atherosclerosis was assessed using carotid intima media thickness (cIMT) and total plaque area (TPA). Incident CVE (new or recurrent) that occurred following the ultrasound assessment were identified. The association between measures of carotid atherosclerosis and the risk of developing incident CVE was evaluated using Cox proportional hazard models after adjusting for FRS.

559 patients with PsD were assessed of whom 23 had incident CVE ascertained. The calculated rate of developing first CVE during the study period was 1.11 events per 100 patient years (95% 0.74, 1.67). When analyzed separately, TPA (Hazard Ratio (HR) 3.74, 95% Confidence Interval (CI) 1.55, 8.85; p=0.003), mean cIMT (HR 1.21, 95% CI 1.03, 1.42; p=0.02), max cIMT (HR 1.11, 95% CI 1.01, 1.22; p=0.03), and high TPA category (HR 3.25, 95% 1.18, 8.95, p=0.02) predicted incident CVE after controlling for FRS.

The burden of carotid atherosclerosis is associated with an increased risk of developing future CVE. Combining vascular imaging data with information on traditional cardiovascular risk factors could improve the accuracy of cardiovascular risk stratification in patients with PsD. This article is protected by copyright. All rights reserved.

Cause-Specific Mortality in Gout: Novel Findings of Elevated Risk of Non-Cardiovascular Related Deaths.

Arthritis Rheumatol

To examine cause-specific mortality beyond cardiovascular (CV) diseases in patients with gout compared to the general population.

We included all residents of Skåne (Sweden) aged 18+ in the year 2002. Using the Skåne Healthcare Register, we identified subjects with new diagnosis of gout (2003-2013) and matched each person with gout with 10 comparators free of gout by age and sex. Using information on the underlying cause of death from the Causes of Death Register (until 31st Dec 2014), we estimated hazard ratios (HR) of mortality for specific causes of death in a multi-state Cox model, adjusting for potential confounders.

Among 832,258 persons, 19,497 had a new diagnosis of gout (32% women) and were matched with 194,947 comparators. Persons with gout had higher prevalence of chronic kidney disease, metabolic and CV comorbidities. Gout was associated with 17% increased hazard of all-cause mortality (HR 1.17, 95% confidence interval 1.14-1.21) overall, and 23% (HR 1.23, 1.17-1.30) in women and 15% (HR 1.15, 1.10-1.19) in men. In terms of cause-specific mortality, the strongest associations were seen for the relation of gout to risk of death due to renal disease (HR of 1.78, 1.34-2.35), diseases of digestive system (HR 1.56, 1.34-1.83), CV diseases (HR 1.27, 1.22-1.33), infections (HR 1.20, 1.06-1.35), dementia (HR 0.83, 0.72-0.97).

Several non-CV causes of mortality are increased in persons with gout, highlighting the need for improved management of comorbidities.

Blockade of the CX3CL1-CX3CR1 Pathway Inhibits the Progress of Skin Inflammation, Fibrosis, and Vascular Injury in an Experimental Mouse Model of Systemic Sclerosis.

Arthritis Rheumatol

To assess the preclinical efficacy and mechanism of action of an anti-CX3CL1 monoclonal antibody (mAb) in systemic sclerosis (SSc).

Cultured human dermal fibroblasts were used to evaluate the direct effect of anti-CX3CL1mAb on fibroblasts. In addition, bleomycin and growth factor-induced SSc models were used to investigate the effect of anti-CX3CL1mAb on leukocyte infiltration, collagen deposition, and vascular damage in the skin.

Anti-CX3CL1mAb treatment significantly inhibited Smad3 phosphorylation (p<0.05) and expression of collagen I and fibronectin 1 (p<0.01) in dermal fibroblasts stimulated with TGF-β1. In the bleomycin model, daily subcutaneous bleomycin injection increased serum CX3CL1 levels (p<0.05) and augmented lesional CX3CL1 expression. Simultaneous administration of anti-CX3CL1mAb or CX3CR1 deficiency significantly suppressed the dermal thickness, collagen content, and capillary loss caused by bleomycin (p<0.05). Injection of bleomycin induced expression of phosphorylated Smad3 and TGF-β1 in the skin, which was inhibited by anti-CX3CL1mAb. Further, the dermal infiltration of CX3CR1+ cells, macrophages (inflammatory and M2-like subsets), and CD3+ cells significantly decreased following anti-CX3CL1mAb therapy (p<0.05), as did the enhanced skin expression of fibrogenic molecules, such as thymic stromal lymphopoietin and secreted phosphoprotein-1 (p<0.05). However, the treatment did not significantly reduce the established skin fibrosis. In the second model, simultaneous anti-mCX3CL1mAb therapy significantly diminished the skin fibrosis induced by serial subcutaneous injection of transforming growth factor-β and connective tissue growth factor (p<0.01).

Anti-CX3CL1mAb therapy may be a novel approach for early skin fibrosis in inflammation-driven fibrotic skin disorders such as SSc. This article is protected by copyright. All rights reserved.

Tracheobronchial cobblestone in relapsing polychondritis.

Arthritis Rheumatol

A previously healthy 30-year-old man suffered from high fever, hoarseness, joint pain in the left hand, and red eyes for 2 months. Chest computed t...