Background: The present study aimed to evaluate microbial diversity, taxonomic profiles, and fecal short chain fatty acid (SCFA) in female patients with fibromyalgia syndrome (FMS). Methods: Forty participants (19 patients with FMS and 21 controls) were included in the study, and the diagnosis of FMS was made based on the revised American College of Rheumatology criteria. DNA extraction from fecal samples and 16S rRNA gene sequencing were conducted to estimate microbial composition. To compare alpha diversity, the Shannon index accounting for both evenness and richness, Pielou’s evenness, and Faith’s phylogenetic diversity (PD) were calculated. Unweighted and weighted UniFrac distances, Jaccard distance, and Bray–Curtis dissimilarity were used to calculate beta diversity. Furthermore, stool metabolites were analyzed using gas chromatography-mass spectrometry, and a generalized regression model was used to compare the SCFA of stools between FMS and healthy controls. Results: Compared with the control, patients with FMS had lower observed OTU (p = 0.048), Shannon’s index (p = 0.044), and evenness (p < 0.001). Although patients with FMS had a lower PD than did controls, statistical significance was not reached. We observed significant differences in unweighted (p = 0.007), weighted UniFrac-based diversity (p < 0.005), Jaccard distance (p < 0.001), and Bray–Curtis dissimilarity (p < 0.001) between the two groups. Although the FMS groups showed lower propionate levels compared with those of the control group, only marginal significance was observed (0.82 [0.051] mg/g in FMS vs. 1.16 [0.077] mg/g in the control group, p = 0.069). Conclusions: The diversity of the microbiome in the FMS group was lower than that in the control group, and the reduced stool propionate levels could be associated with the decreased abundance of propionate-producing bacteria.

Osteoporosis is a systemic skeletal disorder that causes vulnerability of bones to fracture owing to reduction in bone density and deterioration of the bone tissue microstructure. The prevalence of osteoporosis is higher in patients with autoimmune inflammatory rheumatic diseases, including rheumatoid arthritis (RA), than in those of the general population. In this autoimmune inflammatory rheumatic disease, in addition to known risk factors for osteoporosis, various factors such as chronic inflammation, autoantibodies, metabolic disorders, drugs, and decreased physical activity contribute to additional risk. In RA, disease-related inflammation plays an important role in local or systemic bone loss, and active treatment for inflammation can help prevent osteoporosis. In addition to conventional synthetic disease-modifying anti-rheumatic drugs that have been traditionally used for treatment of RA, biologic DMARDs and targeted synthetic DMARDs have been widely used. These agents can be employed more selectively and precisely based on disease pathogenesis. It has been reported that these drugs can inhibit bone loss by not only reducing inflammation in RA, but also by inhibiting bone resorption and promoting bone formation. In this review, the pathogenesis and research results of the increase in osteoporosis in RA are reviewed, and the effects of biological agents on osteoporosis are discussed.

Background: This study explores the association of neutrophil-to-lymphocyte (NLR), monocyte-to-lymphocyte (MLR), and platelet-to-lymphocyte (PLR) ratios with the 3-month treatment response and persistence of tumor necrosis factor-alpha (TNF-α) blockers in patients with ankylosing spondylitis (AS). Methods: This retrospective cohort study investigated 279 AS patients who were newly initiated on TNF-α blockers between April 2004 and October 2019 and 171 sex- and age-matched healthy controls. Response to TNF-α blockers was defined as a reduction in the Bath AS Disease Activity Index of ≥50% or 20 mm, and persistence referred to the time interval from the initiation to discontinuation of TNF-α blockers. Results: Patients with AS had significantly increased NLR, MLR, and PLR ratios as compared to controls. The frequency of non-response at 3 months was 3.7%, and TNF-α blockers’ discontinuation occurred in 113 (40.5%) patients during the follow-up period. A high baseline NLR but not high baseline MLR and PLR showed an independently significant association with a higher risk of non-response at 3 months (OR = 12.3, p = 0.025) and non-persistence with TNF-α blockers (HR = 1.66, p = 0.01). Conclusions: NLR may be a potential marker for predicting the clinical response and persistence of TNF-α blockers in AS patients.