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Aim of the work: To evaluate the levels of osteoprotegerin (OPG) and receptor activator of the nuclear factor jB ligand (RANKL), in patients with rheumatoid arthritis (RA) and to study the relation between these parameters and bone mineral density (BMD) and disease activity; thus, investigating the possible role of the OPG/RANKL system in RA related bone loss.Patients and methods: Fifty patients with RA and 20 age and sex matched healthy controls were enrolled in the study. BMD of the non-dominant forearm, lumbar spine (L1-4) and proximal femur, including femoral neck, Wards triangle and greater trochanter was assessed using dualenergy X-ray absorptiometry (DEXA). The serum OPG and RANKL were measured by ELISA method.Results: Rheumatoid arthritis patients had a higher incidence of osteoporosis (23/50, 46%) than that in healthy controls (3/20, 15%). They displayed lower BMD values than controls at positions of all detected regions. Compared with healthy controls, RA group showed significantly higher serum levels of RANKL (4.7 ± 3.3 vs. 3.0 ± 3.1 ng/dl, p = 0.001), lower serum levels of OPG (331.2 ± 143.6 vs. 535.8 ± 229.1 pg/ml, p = 0.001) and OPG/RANKL ratio (531.6 ± 149.4 vs. 882.8 ± 148.6, p = 0.001).Conclusions: These data suggest that, in RA patients, changes of the OPG/RANKL system resulting in increased RANKL and decreased OPG in peripheral blood could contribute to the bone loss characteristic and the generation of osteoporosis in these patients.

Resistin levels were found to be higher in the serum and synovial fluid of RA patients than in those with OA. This may suggest a role for resistin in inflammatory rheumatologic diseases. The observed statistically significant correlation between synovial fluid resistin levels and RF, ACPA and Larsen score may suggest that high synovial fluid resistin levels can be considered a poor prognostic factor for RA progression. However, further studies employing a larger cohort of patients are needed to confirm the relevance of resistin as a prognostic marker in RA patients.

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A growing body of evidence suggests that anti-complement-1q (anti-C1q) antibodies are elevated in a variety of autoimmune disease. Therefore, we investigated their prevalence and clinical significance in plasma of patients with hepatitis C virus (HCV) genotype IV in the presence and absence of autoimmune extra hepatic manifestations in comparison to normal healthy individuals. Plasma Anti-C1q Abs levels were assessed by an Enzyme Linked Immunosorbant Assay in 91 chronic HCV-infected patients (51 with and 40 without autoimmune rheumatic manifestations) and 40 healthy volunteers matched for age and gender. Epidemiological, clinical, immunochemical and virological data were prospectively collected. Positive Anti-C1q antibodies were more frequent among HCV patients with extra-hepatic autoimmune involvement, than those without and healthy control subjects. No significant correlations were found between Anti-C1q levels with either the liver activity or the fibrosis scores. In HCV-patients with autoimmune involvements, plasma Anti-C1q levels were significantly higher in patients with positive cryoglobulin, and in those with lymphoma than in those without. These results were confirmed by multivariate analysis. Further large scale longitudinal studies are required to assess and clarify the significance and the pathogenic role of anti-C1q antibodies among HCV infected patients with positive cryoglobulinaemia and lymphoma.

Subclinical atherosclerosis is frequent in SLE patients. Increased disease activity and damage are associated with the occurrence of premature atherosclerosis.

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