Search

Background Pneumocystis pneumonia (PCP) is increasingly being diagnosed in patients with systemic lupus erythematosus (SLE), and hydroxychloroquine (HCQ) has been found to possess antifungal activities. We hence aimed to investigate the association between HCQ and PCP risk among patients with SLE. Methods Using the 1997–2013 nationwide claim data, we identified 24,343 newly-diagnosed SLE patients. We then identified 58 PCP cases and selected 348 non-PCP controls matching (1:6) by age, sex, disease duration and the year of PCP diagnosis date. The risk of PCP was assessed by determing odds ratios (ORs) with 95% confidence intervals (CIs) by using multivariable conditional logistic regression. Results The risk of PCP was associated with moderate to severe renal disease (OR 6.73, 95% CI 1.98–22.92), higher doses of glucocorticoids (≤5 mg/day, reference; 5–10 mg/day, OR 25.88, 95% CI 2.97–225.33; > 10 mg/day, OR 286.58, 95% CI 28.58–> 999), higher 3-month cumulative dose of cyclophosphamide (not use, reference; ≤1.4 g, OR 0.64, 95% CI 0.14–3.01; > 1.4 g, OR 11.52, 95% CI 1.97–67.39) and use of mycophenolate mofetil/mycophenolic acid (OR 50.79, 95% CI 5.32–484.77), whereas 3-month cumulative dose of HCQ was associated with a reduced risk of PCP among patients with SLE (not use, reference; ≤14 g, OR 0.69, 95% CI 0.21–2.24; > 14 g, OR 0.20, 95% CI 0.05–0.71). Conclusions This study demonstrated incident PCP was associated with mycophenolate mofetil/mycophenolic acid use and higher doses of cyclophosphamide or glucocorticoid, whereas the use of a higher dose of HCQ was associated with a reduced risk of PCP in lupus patients.

With galectin-3 playing an important role in inflammatory responses, elevated galectin-3 levels have been shown in patients with autoimmune diseases. However, there are limited data regarding galectin-3 expression in patients with autoinflammatory diseases such as adult-onset Still's disease (AOSD). This study aimed to investigate the extracellular galectin-3 expression and examine its association with activity parameters and disease outcome in AOSD patients.Plasma levels of galectin-3 and inflammasome downstream cytokines including interleukin (IL)-1β and IL-18 were determined by ELISA in 42 active AOSD patients and 20 healthy controls (HC). The protein levels of galectin-3 and cytokines were determined using immunoblotting.Plasma levels of galectin-3 and inflammasome downstream cytokines including IL-1β and IL-18 were significantly higher in AOSD patients (median 5.02 ng/ml, interquartile range [IQR] 3.12-7.88 ng/ml; 3.42 pg/ml, IQR 1.48-6.70 pg/ml; and 5758 pg/ml, IQR 859-11,895 pg/ml, respectively) compared with HC (1.86 ng/ml, IQR 1.09-2.89 ng/ml; 0.99 pg/ml, IQR 0.62-1.35 pg/ml; and 129 pg/ml, IQR 71-155 pg/ml, respectively, all p 0.001). Plasma galectin-3 levels were positively correlated with clinical activity scores, inflammatory parameters values, and the levels of IL-1β and IL-18 in AOSD patients. AOSD patients with systemic pattern had significantly higher galectin-3 levels (median 6.08 ng/ml, IQR 4.01-9.54 ng/ml) compared with those with chronic articular pattern (3.56 ng/ml, IQR 3.04-4.98 ng/ml, p 0.05). After 6-month therapy, galectin-3 levels significantly declined, paralleling the decreases in clinical activity scores and plasma levels of IL-1β and IL-18.Elevated galectin-3 levels and their positive correlation with disease activity scores, inflammatory parameter, and inflammasome downstream cytokines suggest the involvement of galectin-3 in AOSD pathogenesis.Key Points• We revealed for the first time the association of plasma galectin-3 levels with AOSD activity parameters.• We explored the link between galectin-3 levels and NLRP3-inflammasome downstream cytokines in AOSD disease.

Aim To assess the effects of celecoxib and sulfasalazine on cardiovascular risk in patients with ankylosing spondylitis (AS). Methods We performed a 10-year population-based retrospective cohort study. A total of 1208 AS patients and 19 328 non-AS patients were sampled from the Taiwan National Health Insurance (NHI) database. We compared these two groups of patients to identify the differences in the exposure of non-steroidal anti-inflammatory drugs and sulfasalazine and their effects on cardiovascular risk. Univariate analyses were performed using Chi-squared tests for dichotomous variables and t-tests for continuous variables. Cox proportional hazard models were conducted to investigate the risk of developing cardiovascular diseases (CVD). Results AS patients had an adjusted hazard ratio (HR) of 1.72 (CI = 1.46–2.02, P < 0.01) for CVD compared with non-AS controls. The risk increased significantly with the progression of the disease. The use of celecoxib and sulfasalazine provided protective effects against CVD in both groups of patients. Both drugs at high cumulative defined daily doses (DDD) and celecoxib alone at high cumulative DDD showed significant protective effects against CVD in AS patients and the control group, respectively. Sulfasalazine at ≥ 0.5 DDD (1000 mg/day) reduced CVD risk in patients with AS (HR = 0.65, CI = 0.43–0.998, P < 0.05). Conclusions In this population-based retrospective cohort study, sulfasalazine at its optimal dose reduced CVD risk in patients with AS. Celecoxib was neutral regarding CVD risk in AS patients.

Both cardiovascular diseases (CVD) and osteoporosis are common comorbidities in rheumatoid arthritis (RA) patients. Although accumulating evidence indicates a link between CVD and osteoporotic fracture, whether CVD contributes to osteoporotic fracture risk in RA has yet to be explored. We examined the incidence rate and risk factors of osteoporotic vertebral fracture in RA patients with new-onset CVD (RA-CVD) and evaluated the effects of medications on such fracture risk. A retrospective study was conducted using a nationwide database from 2000 to 2010: 1267 RA-CVD and 1267 non-CVD patients were enrolled from 30,507 patients with newly diagnosed RA. The main outcome was the development of osteoporotic vertebral fracture. After being adjusted for age, gender, and comorbidities, the Cox proportional hazard model was used to identify independent factors contributing to osteoporotic vertebral fracture. The adjusted hazard ratio (aHR) of developing osteoporotic vertebral fracture was 1.47-fold greater in RA-CVD group than in non-CVD group (95% confidence interval 1.19–1.81, p

Aim To establish guidelines for the clinical management of axial spondyloarthritis that take into account local issues and clinical practice concerns for Taiwan. Method Overarching principles and recommendations were established by consensus among a panel of rheumatology and rehabilitation experts, based on analysis of the most up‐to‐date clinical evidence and the clinical experience of panelists. All Overarching Principles and Recommendations were graded according to the standards developed by the Oxford Centre for Evidence Based Medicine, and further evaluated and modified using the Delphi method. Results The guidelines specifically address issues such as local medical considerations, National Health Insurance reimbursement, and management of extra‐articular manifestations. Conclusion It is hoped that this will help to optimize clinical management outcomes for axial spondyloarthritis in Taiwan.

This study aimed to determine the safety and efficacy of tramadol 37.5 mg/acetaminophen 325 mg combination tablets (Ultracet®) in patients with ankylosing spondylitis (AS). This was a 12-week, randomized, double-blind, placebo-controlled study. Sixty patients with active AS according to the Modified New York Criteria were enrolled. Active disease was defined by Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) for more than 3 at randomization. Subjects were randomized equally into two groups: the treatment group received aceclofenac plus Ultracet® one tablet twice a day, and the control group received aceclofenac plus placebo for 12 weeks. The primary endpoint was a difference of Assessment in Ankylosing Spondylitis (ASAS20) response criteria between two groups at week 12. At week 12, ASAS20 was achieved by 53.3 % of the aceclofenac plus Ultracet group and 31 % of the aceclofenac alone group (p = 0.047). For the pain visual analogue scale at week 12, there was a reduction of 45.6 % in aceclofenac plus Ultracet group and 25.7 % in the aceclofenac alone group (p = 0.087). There was no statistically significant difference between two groups in BASDAI, Bath Ankylosing Spondylitis Functional Index, Bath Ankylosing Spondylitis Global Index, Physician Global Assessment, spinal mobility, ESR, hs-CRP, and Ankylosing Spondylitis Quality of Life Questionnaire. A slight increase in total adverse events was noted with dizziness (7.5 vs 1.5 %), vertigo (4.5 vs 1.5 %), and nausea/vomiting (6 vs 0 %) in the Ultracet arm compared to placebo. The tramadol 37.5 mg/acetaminophen 325 mg combination tablet (Ultracet®) might has additional effect to nonsteroidal anti-inflammatory drugs in the treatment of patients with ankylosing spondylitis. It showed marginal benefit in pain and disease activity. However, a slight increase in minor adverse events was noted.

Immunogenicity influences adalimumab levels and therefore clinical response in patients with rheumatic diseases. To study the relationship between clinical response, adalimumab levels and antidrug antibodies (ADAb) in ankylosing spondylitis (AS). Observational cohort study of 115 consecutive AS patients treated with adalimumab in the Netherlands (n=85) and Taiwan (n=30), monitored during 24 weeks. Adalimumab levels and ADAb titres were determined using an ELISA and an antigen binding test (ABT), respectively, designed by Sanquin Research, Amsterdam. Response to adalimumab treatment was defined as a Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) response, and disease activity was measured using the Ankylosing Spondylitis Disease Activity Score using C-reactive protein (CRP) (ASDAS). At baseline, median BASDAI (IQR) was 6.4 (4.5-7.6) and mean ASDAS (SD) was 3.5 (1.0). After 24 weeks, 49 (42.6%) patients were BASDAI50 responders and mean ASDAS (SD) for responders was 1.5 (1.0) vs 2.6 (1.0) for non-responders (p 100 AU/mL). In these patients, CRP and erythrocyte sedimentation rate remained elevated during treatment. Adalimumab levels are related to clinical response in AS patients measured with ASDAS and are influenced by ADAb detectable with an ABT

Acute motor axonal neuropathy (AMAN), a variant of Guillain Barre syndrome (GBS), is frequently induced by the antecedent infection of some atypical pathogen, such as Campylobacter jejuni, Mycoplasma pneumonia and some virus. It is generally accepted that corticosteroids and immunosuppressants are not recommended in patients with GBS including AMAN. However, if systemic autoimmune reaction developed, the principle of management might be changed.We report a young man who rapidly developed acute motor axonal neuropathy. Although plasma exchange had been given, the violent immunological reaction was unable to be controlled, prolonged leukemoid reaction and high level of autoimmunological titers, including C-reactive protein (CRP), rheumatoid factor (Rf), and antineutrophil cytoplasmic autoantibody (ANCA) persisted. Consequently, two months later, this patient developed acute respiratory distress syndrome (ARDS) and type 3 of rapidly progressive glomerulonephritis (RPGN) with rapid decline of renal function until immunosuppressants were given.AMAN combined with the violent systemic autoimmune reaction strongly indicated an uneven disease course and implied that only standard plasmapheresis is not sufficient and corticosteroids with immunosuppressant should be added in early stage.