International Journal of Rheumatology最新文献

[This corrects the article DOI: 10.1155/2018/1302835.].

Background: The nature and rate of gastric mucosal (GM) damage in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) remain to be among the unsolved problems.

Objective: To define the role of H. pylori and drugs in the development of GM damages in SLE and APS.

Methods: A study was conducted on 85 patients with SLE and APS. All the patients underwent esophagogastroduodenoscopy with targeted biopsy of the mucosa of the gastric body and antrum. The presence of H. pylori in the gastric biopsy specimens was determined using polymerase chain reaction.

Results: Endoscopic examination revealed that the patients with SLE and APS on admission had the following GM changes: antral gastritis (82.4%), erosions (24.7%), hemorrhages (8.2%), and pangastritis (8.2%). SLE and APS patients showed no direct correlation between the found GM damages and the presence of H. pylori. The use of glucocorticoid, low-dose acetylsalicylic acid, nonsteroidal anti-inflammatory drug, and anticoagulant in SLE and APS patients is accompanied by GM damage.

Conclusion: There was no evidence of the role of H. pylori in GM damage in the SLE and APS patients. More frequent detection of H. pylori was observed in anticoagulants or low-dose acetylsalicylic acid users than in glucocorticoids and nonsteroidal anti-inflammatory drugs ones.

Introduction: In Nepal, adalimumab is the most common agent being used, but in a disease activity-based dose tapering to address the economic constraints. Another constraint is the high risk of reactivation of tuberculosis in countries with high burden, especially with the use of tumor necrosis factor blocking agents. Though there are recommendations for screening and treatment of latent tuberculosis infection (LTBI) before using adalimumab, data is not clear regarding the appropriate screening schedule and the timing of initiation of biologic therapy.

Methodology: This retrospective review of prospectively followed cohort of spondyloarthropathy patients aimed to evaluate the efficacy of simultaneous initiation of adalimumab with LTBI treatment. Patients fulfilling either the modified New York criteria for ankylosing spondylitis or Assessment in SpondyloArthritis international Society criteria and who were refractory to oral treatment were screened with Mantoux (≥10mm) and interferon gamma release assay (QuantiFERON) to detected LTBI. Those who tested positive were started on rifampicin/isoniazid combination for 3 months and adalimumab treatment on the same day. The patients were followed up at 2 weeks, 4 weeks, 12 weeks, and then every 3 months for 2 years.

Results: Out of 784 patients diagnosed, 92 were receiving adalimumab. LTBI was detected by positivity of either Mantoux or QuantiFERON in 29.3% patients. None of the patients with LTBI who were started on the 2 drug regime simultaneous with adalimumab developed activation of tuberculosis. However, two patients testing negative for both the tests developed tubercular pleural effusion during treatment.

Conclusions: Our findings indicate that screening for LTBI should be more frequent in patients from high tuberculosis burden countries; treatment of LTBI with rifampicin/isoniazid combination for 3 months is effective in preventing reactivation even when adalimumab is started simultaneously.

Vertebral fractures are one of the most common fractures associated with low bone mineral density. However two-thirds to three-fourths of patients with vertebral fractures are not clinically recognized. The objective of this study was to determine the prevalence of vertebral fractures in patients referred for bone densitometry and the most common site of fracture. The study was carried out in the osteoporosis clinic in Dubai primary health care center. A total of 120 patients were examined using the dual energy X-ray absorptiometry. Of all the patients, 48.3% were osteoporotic and 40.9% were osteopenic. The overall prevalence of vertebral fracture was 14.2%. The result showed that the prevalence of vertebral fracture was higher in female compared to male (15.7% and 9.7%, respectively). It was found that patients aged 80 and above had the highest prevalence of vertebral fracture (54.5%). Undiagnosed vertebral fractures were common. Therefore, it is crucial to prevent vertebral fracture through early diagnosis and appropriate treatment of osteoporosis.

Objectives: The aim of this study was to determine if strategies for coping with illnesses, demographic factors, and clinical factors were associated with medication adherence among patients with rheumatoid arthritis (RA).

Methods: This cross-sectional study was conducted at a Viennese rheumatology outpatient clinic on RA patients. Medication adherence was assessed using the Medication Adherence Report Scale. Strategies for coping with illness were assessed using the Freiburg Questionnaire for Coping with Illness.

Results: Half (N=63, 52.5%) of the 120 patients included in the study were considered completely medication adherent. Female sex (odds ratio [OR]: 4.57, 95% confidence interval [CI]: 1.14 - 18.42), older age (54-65 yr vs. <45 yr OR: 9.2, CI:2.0-40.70; >65 yr vs. <45 yr OR 6.93, CI:1,17 - 40.87), middle average income (middle average income vs. lowest income class OR= 0.06, CI= 0.01-0.43), and shorter disease duration (5-10 yr vs. >10 yr OR= 3.53, CI= 1.04-11.95; 1-4 yr vs. >10 yr OR=3.71, CI= 1.02-13.52) were associated with higher medication adherence. Levels of active coping (15.57 vs. 13.47, p=0.01) or diversion and self-encouragement (16.10 vs. 14.37, p=0.04) were significantly higher among adherent as opposed to less adherent participants. However, in multivariate regression models, coping strategies were not significantly associated with adherence.

Conclusions: Age, sex, monthly net income, and disease duration were found to be associated with an increased risk for medication nonadherence among patients with RA. Coping strategies such as active coping, diversion, and self-encouragement were associated with adherence in univariate models, but not when adjusted for demographic and clinical factors.

Objectives: This observational study was designed to evaluate the impact of a student-led Rheumatology Interest Group on medical student interest in rheumatology.

Methods: The mean numbers of student-rheumatology interactions per six months were assessed for elective enrollment, abstract submissions, and manuscripts, in the pre- and postinterest group period.

Results: Enrollment in the rheumatology elective increased from 2.0 ± 0.36 per six months in the preintervention period to 6.2 ± 1.24 per six months in the postintervention period (p=0.0064). Abstract submissions increased from 0.5 ± 0.34 to 5.86 ± 1.49 (p=0.0077), and manuscript submissions from 0.16 ± 0.16 to 1.57 ± 0.37 (p=0.074).

Conclusion: The Rheumatology Interest Group significantly increased medical student engagement in rheumatology.

We examined whether the cathepsin K inhibitor, ONO-5334, administered alone or in combination with methotrexate (MTX), could ameliorate joint destruction evoked by collagen-induced arthritis (CIA) in female cynomolgus monkeys. CIA was induced by immunizing with bovine type II collagen. ONO-5334 (30 mg/kg/day) was orally administered once daily and MTX (10 mg/body/day) twice weekly for 9 weeks. X-ray (evaluation of joint destruction) and swelling (inflammatory) scores of proximal interphalangeal (PIP), distal interphalangeal (DIP), and metacarpophalangeal (MP) joints were evaluated. Urinary concentrations of C-terminal telopeptide of type I collagen (CTX-I) and type II collagen (CTX-II) were measured. Arthritis, accompanied by bone and cartilage destruction, was successfully induced in this collagen-induced arthritis monkey model. ONO-5334 showed no suppressive effect on joint swelling, while the joint swelling scores in the MTX and combination (ONO-5334 + MTX) groups were less than 50% compared with the control group. ONO-5334 decreased X-ray score by a mean of 64% (p<0.05 vs the control group), and MTX also decreased in X-ray score by a mean of 46% but with no statistical significance. Combination of ONO-5334 and MTX further decreased the X-ray score by 28% over MTX group (74% reduction vs the control group, p<0.01). Maximum increase in CTX-I (10-fold) and CTX-II (7-fold) compared to baseline was observed at 7 and 3 weeks after the first sensitization, respectively. After treatment with ONO-5334 alone or in combination with MTX, concentrations were maintained near baseline for both markers. In conclusion, ONO-5334 prevented joint destruction but not joint inflammation in this monkey CIA model. Concomitant use of ONO-5334 with MTX reduced architectural joint destruction compared to MTX alone; therefore, ONO-5334 may help to prevent joint destruction in combination with MTX for the treatment of rheumatoid arthritis.

Background: Febuxostat is approved in the United States for the management of hyperuricemia in patients with gout. In November 2017 the FDA released a warning alert on a possible link between febuxostat and cardiovascular disease (CVD) reported in a single clinical trial.

Objective: To conduct a systematic review and meta-analysis and assess the risk of major adverse cardiovascular events (MACE) in patients receiving febuxostat compared to a control group.

Methods: We searched the MEDLINE and EMBASE database for studies published up until March 2018. We included randomized clinical trials (RCTs) that compared febuxostat to control groups including placebo and allopurinol. We calculated the pooled relative risk (RR) of MACE and cardiovascular disease (CVD) mortality with the corresponding 95% confidence intervals (CI).

Results: Our search yielded 374 potentially relevant studies. Among the 25 RCTs included in the systematic review, 10 qualified for the meta-analysis. Among the 14,402 subjects included, the median age was 54 years (IQR 52-67) and 90% were male (IQR 82-96); 8602 received febuxostat, 5118 allopurinol, and 643 placebo. The pooled RR of MACE for febuxostat was 0.9; 95% CI 0.6-1.5 (p= 0.96) compared to the control. The RR of CV-related death for febuxostat was 1.29; 95% CI 1.01-1.66 (p=0.03).

Conclusions: Compared with other SU-lowering treatments, febuxostat does not increase or decrease the risk of cardiovascular disease but may increase the risk of CVD death. More RCTs measuring cardiovascular safety as a primary outcome are needed to adequately evaluate the risk of CVD with febuxostat.