Background/Objectives: In Sjögren’s syndrome, exocrine glands are destructed in an autoimmune-mediated process. Obesity is known to influence a wide range of diseases. This study aimed to examine whether obesity has an impact on the disease course of our patients with Sjögren’s syndrome. Methods: Out of the regularly followed-up patients, 125 were grouped based on their body mass index (BMI). Below a BMI of 25, they were listed as “non-obese” (n = 45), whereas above a BMI of 25, they were categorized as “obese” (n = 80). Demographic, laboratory, and immunological parameters; Sjögren’s syndrome disease activity index; certain extraglandular manifestations; and treatment modalities were compared using biostatistical methods. Results: Among the examined cardiovascular and cerebrovascular co-morbidities, type 2 diabetes and hypertension were significantly more frequent in the obese group. Considering the associated further autoimmune disorders and extraglandular manifestations, in our patients, there were no significant differences between the two groups. Among laboratory parameters, gamma glutamil transferase, alanine transaminase, hemoglobin, hematocrit, lymphocyte rate, triglyceride, and c3 and c4 complement levels were significantly higher in the obese group, while the proportion of rheumatoid factor positivity and the neutrophil granulocyte rate were significantly lower. Immunoglobulin G, A, and M levels did not differ significantly between the two subsets. Obese patients needed steroid therapy significantly less frequently; however, statin therapy was remarkably more frequent in that group. Furthermore, the European League Against Rheumatism (EULAR) Sjögren’s syndrome disease activity index (ESSDAI) was significantly lower in the group of overweight patients. Conclusions: Our results suggest that several immunological parameters of obese patients are more favorable compared to those with normal body weight. Behind that, we might suspect either the beneficial effect of statin therapy and/or the obesity paradox.

The aim of the paper was to characterize rheumatoid factor IgA, IgG, and IgM isotypes in patients with Sjögren’s syndrome (SS) subsets, based on the absence or presence of joint complaints of different etiologies. In total, 164 SS patients were grouped based on whether they had polyarthritis as an extraglandular manifestation (n = 73, SS+pa), rheumatoid arthritis as an associated autoimmune disorder (n = 46, SS+RA), or Sjögren’s syndrome without inflammatory joint pain (n = 45, SS). The highest IgA rheumatoid factor isotype levels were detected in SS patients, whereas the lowest levels were found in the SS+RA group, without a significant difference. Neither IgG nor IgM RF differed significantly between the patient subclasses. In addition to other disease-specific markers, seropositive patients who were seropositive for any RF isotype were significantly more frequently anti-Ro/SS-A and anti-La/SS-B positive and had higher ESSDAI levels. In SS and SS+pa patients, a strong negative correlation was observed between IgA RF and age, whereas a strong positive correlation was found between IgA RF and ESSDAI, RF, IgA, IgG, anti-Ro/SS-A, and anti-La/SS-B levels. High total IgG levels together with high IgA RF levels occurred most frequently in SS patients (p = 0.05), whereas the combination of normal IgG and high IgM RF was significantly more frequent in the SS+RA group. The co-occurrence of high total IgG and normal IgM RF did not differ significantly between the patient subsets; however, this was the combination with the highest sensitivity (94.5%) for SS+pa patients. Based on our findings, rheumatoid factor isotypes have an additive value in the differentiation of non-erosive polyarthritis and erosive rheumatoid arthritis during the disease course of patients with Sjögren’s syndrome. All rheumatoid factor isotypes predict a more severe disease course, but IgA RF may serve as a candidate for being an early, poor prognostic factor for SS patients.

Introduction: Sjögren’s disease is characterized by autoimmune destruction of exocrine glands. Obesity generally worsens the course of many diseases; however, earlier observations in our cohort suggested a paradoxically lower disease activity (ESSDAI) in overweight/obese patients. This cross-sectional study aimed to investigate potential mechanisms underlying these findings. Methods: Chemerin and oxidized low-density lipoprotein (oxLDL) levels were measured in a subset of regularly followed patients (n=75). Patients were stratified by body mass index (BMI): BMI <25 kg/m² (“non-obese”, n=27) and BMI ≥25 kg/m² (“overweight/obese”, n=48). Demographic, laboratory, and immunological parameters, disease activity (ESSDAI), extraglandular manifestations, and treatments were compared using biostatistical analyses. Results: Chemerin and oxLDL levels did not differ significantly between groups. ESSDAI was significantly lower in overweight/obese patients (5.04 vs. 2.76; p=0.04), while complement c3 levels were higher (1.20 vs. 1.46 g/L; p<0.001). Across all patients, chemerin positively correlated with BMI, age at diagnosis, c3, c4, CRP, platelet count, and leukocyte count. Hemoglobin and hematocrit were higher in overweight/obese patients, whereas neutrophil ratio was lower and lymphocyte ratio slightly higher. Statin therapy was also more frequent in the overweight/obese group (p=0.04). In this group, BMI and platelet count independently predicted chemerin levels, while platelet count predicted chemerin in normal-weight patients. Conclusion: Despite its positive correlation with BMI, chemerin levels were not significantly higher in overweight/obese patients, suggesting relatively lower levels. This may partly explain their more favorable immunological profile. Increased statin use may also contribute through anti-inflammatory effects.