Scandinavian Journal of Rheumatology最新文献

Objective: Tumour necrosis factor-α (TNF-α) has been associated with non-alcoholic fatty liver disease (NAFLD) and its severity. This study aimed to evaluate for first time changes in non-invasive indices of hepatic steatosis and fibrosis in patients with ankylosing spondylitis (AS) after treatment with TNF-α inhibitors.

Methods: In this retrospective study, non-invasive indices of steatosis and fibrosis were evaluated in patients with AS treated with TNF-α inhibitors before the initiation of treatment (baseline) and after at least 6 months of treatment (endpoint). Steatosis was evaluated with hepatic steatosis index (HSI) and fibrosis with three indices [fibrosis-4 (FIB-4) index, aspartate aminotransferase to platelet ratio index (APRI), and body mass index (BMI)-aspartate aminotransferase-to-alanine aminotransferase ratio-diabetes mellitus (BARD)]. The efficacy of TNF-α inhibitors was evaluated by serum C-reactive protein (CRP) and Ankylosing Spondylitis Disease Activity Score with CRP.

Results: Fifty-two patients were included in this study and were treated with TNF-α inhibitors for 8.1 months (interquartile range 6.5-11.3 months). There was no change in HSI between baseline and endpoint, whereas FIB-4 (from 0.64 ± 0.23 to 0.83 ± 0.48; p < 0.001) and APRI (from 0.16 ± 0.06 to 0.23 ± 0.13; p < 0.001) increased; BARD was not affected. These results were independent of different TNF-α inhibitors, sex, BMI, and age.

Conclusions: TNF-α inhibitors may have a neutral impact on hepatic steatosis, but a negative impact on hepatic fibrosis indices, findings requiring validation in prospective clinical studies with liver imaging or paired liver biopsies.

Objective: To investigate the validity, reliability, and interpretability of the Danish and Swedish versions of the Bristol Rheumatoid Arthritis Fatigue Multi-Dimensional Questionnaire (BRAF-MDQ) and Bristol Rheumatoid Arthritis Fatigue Numerical Rating Scales (BRAF-NRS V2) (BRAFs) in patients with spondyloarthritis (SpA).

Method: The BRAFs were tested for validity and reliability in an online survey. Participants were identified in the national rheumatology databases.

Results: In Denmark, 234/435 participants (53.8%) completed the first survey (T1), of whom 125 (82.2%) also completed the second survey (T2) (mean ± sd age 59.6 ± 13 years, 52.6% women). In Sweden, 183/420 participants (43.6%) completed T1, of whom 171 (93.4%) also completed T2 (age 54.7 ± 13 years, 62.3% female). In both Denmark and Sweden, the content validity was supported for the BRAFs; regarding structural validity for BRAF-MDQ, explanatory factor analysis identified five factors; Cronbach's α (internal consistency) was 0.94/0.95 for BRAF-MDQ and 0.79-0.93/0.76-0.94 for the four subscales; intraclass correlation coefficients (ICCs) were 0.96/0.93 for BRAF-MDQ and 0.84-0.93/0.86-0.90 for the subscales, and ICCs of the three BRAF-NRS scales were 0.70-0.90/0.71-0.89; and Construct validity: 80% of the hypotheses were fulfilled for the BRAFs.

Conclusions: Good content validity, acceptable construct validity, good reliability, and low degree of measurement error were found for BRAF-MDQ and BRAF-NRS V2. BRAF-MDQ had acceptable structural validity, but five factors were identified, instead of four, suggesting caution in distinguishing dimensions of fatigue. The BRAFs are considered valid and reliable for measuring fatigue in Danish and Swedish patients with SpA.

Objective: To investigate the potential superiority of colchicine prophylaxis twice daily over once daily in preventing gout flares in the first 6 months after initiating xanthine oxidase inhibitors (XOIs).

Method: A retrospective cohort study was conducted in three rheumatology centres in the Netherlands. Gout flare incidence densities were calculated for patients using colchicine once or twice daily in the first 6 months after starting XOIs. The incidence rate ratios (IRRs) between groups were analysed using Poisson regression, adjusted for confounders. The proportion of patients reaching a serum urate of <0.36 mmol/L within the first 6 months was compared between groups.

Results: In total, 808 gout patients started XOIs (allopurinol in 99.7%) with colchicine prophylaxis: 192 on twice-daily and 616 on once-daily colchicine 0.5 mg. The incidence densities of gout flares were 3.3 and 2.8 per patient-year, resulting in an IRR of 0.93 [95% confidence interval (CI) 0.80-1.09] for twice-daily compared to once-daily colchicine, adjusted for renal function (estimated glomerular filtration rate), serum urate at baseline, duration of colchicine prophylaxis, C-reactive protein, age, duration of illness, fast dose titration, tophi, gouty bone erosions, and monosodium urate crystal confirmation. Within 6 months, 59.8% and 68.6% in the colchicine twice-daily and once-daily groups, respectively, reached the serum urate target (difference -8.8%, 95% CI 1.1% to -18.7%).

Conclusions: Colchicine prophylaxis 0.5 mg twice daily was not superior to colchicine once daily regarding flare prophylaxis after starting an XOI. As colchicine twice daily is associated with higher intolerability and costs, once-daily dosing should be preferred.

Objective: To evaluate whether rapid and sustained suppression of inflammation, using the NEO-RACo treatment, including prednisolone 7.5 mg/day for 2 years, in patients with early active rheumatoid arthritis (RA) can prevent the reduction of bone mineral density (BMD) in a 10 year follow-up.

Method: In the NEO-RACo study, 99 patients, aged 18-60 years, with early RA and without earlier use of disease-modifying anti-rheumatic drugs (DMARDs), were treated with a triple combination of conventional synthetic DMARDs and 7.5 mg prednisolone daily for 2 years and double blindly randomized to receive either placebo or infliximab infusions for the first 6 months. After 2 years, the therapies could be modified, always aiming for strict remission. All patients also received 1000 mg calcium and 800 IU vitamin D₃ daily. BMD was measured by dual-energy X-ray absorptiometry at baseline, 2 years, 5 years, and 10 years. BMD Z-score ≤ -2.0 was considered to be below the expected value.

Results: At baseline, two patients (2%) had a Z-score ≤ -2.0, including one patient with osteoporosis. At the time of the last BMD measurement, five patients (5%) had a Z-score ≤ -2.0, and no new-onset osteoporosis cases occurred. No significant differences emerged between the randomization groups.

Conclusions: Both randomization groups were treated early and aggressively, and the decrease in BMD was low throughout the 10 year follow-up. The use of infliximab during the first 6 months provided no extra benefit regarding bone loss.Trial Registration: http://www.clintrials.gov (NCT00908089).

Objective: To evaluate the causal effect of genetically predicted serum urate (SU) levels on the risk of overall and major site-specific cancers in individuals of European ancestry, using Mendelian randomization (MR) analysis.

Method: Data from two population-based cohorts from southern Sweden, the Malmö Diet and Cancer Study (MDCS) and Malmö Preventive Project (MPP), and summary-statistics data from the Global Urate Genetic Consortium (GUGC) and UK Biobank cohort were used. A set of 26 SU-related variants was used as instrumental variables to perform a range of one- (using MDCS-MPP) and two-sample (using GUGC and UK Biobank) MR analyses. Causal relationships were assessed between genetically determined SU and 13 site-specific cancers (bladder, breast, color ectal, gastric, hepatic, lung, pancreatic, prostate, renal, skin, lymphatic, haematopoietic, and gynaecological cancers, and brain tumour) and 'any cancer'. We also performed epidemiological association analyses on individual-level data to determine SU-cancer relationships.

Results: There was some suggestive evidence of an association between higher levels of genetically predicted SU and lower risk of brain (p = 0.04; one-sample MR) and colorectal (p = 0.02; two-sample MR) cancers, although these findings were not consistent across both MR approaches. No significant associations were observed between SU levels and the risk of other cancers (all p > 0.05).

Conclusion: Our MR study found no consistent evidence of a causal effect of genetically predicted SU on overall or Q3 common site-specific cancers in European individuals.

Rheumatoid arthritis (RA) is an essential cause of secondary sarcopenia, and patients with RA face a higher risk of developing sarcopenia. In the literature, there is a lack of reviews on animal models of RA-related sarcopenia. This review examines sarcopenia-related changes and mechanisms in induced and immune-mediated arthritis animal models and highlights potential preclinical therapies. The mechanisms for developing sarcopenia in these animal models involved inflammation, protein degradation pathways, protein synthesis, muscle regeneration and differentiation, oxidative stress, energy metabolism, and amino acid metabolism. Some anti-rheumatic drugs, supplements and nutrients, antioxidants, and physical therapy and training have been shown to improve muscle atrophy, maintain muscle mass, and prevent grip strength loss in different RA-related sarcopenia animal models. Overall, this review aims to deepen the mechanistic understanding of RA-related sarcopenia and provide a basis for developing innovative therapies.