Eradication of Helicobacter pylori may reduce disease severity in rheumatoid arthritis.

BACKGROUND: A triggering infectious agent has long been postulated in rheumatoid arthritis. Data on the possible role of Helicobacter pylori infection are lacking. AIM: To assess the effect of H. pylori eradication in patients with rheumatoid arthritis. METHODS: Fifty-eight adult patients with established rheumatoid arthritis and dyspeptic symptoms were recruited - 28 were H. pylori-positive and 30 were H. pylori-negative on the basis of invasive tests. All infected patients were treated successfully. We evaluated the disease activity using clinical and laboratory parameters at baseline and every 4 months during 2 years, and compared the variations in the two subgroups. RESULTS: H. pylori-eradicated rheumatoid arthritis patients showed progressive improvement over time (P < 0.0001) of all clinical indices compared with baseline, whereas H. pylori-negative rheumatoid arthritis patients remained substantially unchanged. After 2 years, H. pylori-eradicated rheumatoid arthritis patients differed significantly (P < 0.04-0.0001) from patients without H. pylori infection in terms of improvement of all clinical parameters. At the same time point, several laboratory indices (erythrocyte sedimentation rate, fibrinogen, alpha2-globulins and antinuclear antibody) showed significantly lower values (P < 0.02-0.0003) in the H. pylori-eradicated subgroup compared to the H. pylori-negative subgroup. CONCLUSIONS: Our data suggest that H. pylori infection is implicated in the pathogenesis of rheumatoid arthritis, in that its eradication may induce a significant improvement of disease activity over 24 months. H. pylori eradication seems to be advantageous in infected rheumatoid arthritis patients, but controlled studies are needed.

Homocysteine and antiphospholipid antibodies in rheumatoid arthritis patients: relationships with thrombotic events.

OBJECTIVE: To investigate the possible relationships between plasma homocysteine levels and thrombotic events in a select population of rheumatoid arthritis (RA) patients with or without antiphospholipid (aPL) antibody positivity. METHODS: 168 female RA patients attending the Extra-articular Involvement RA Clinic of University of Genova and 72 female subjects matched for age and vascular diseases as controls were included in the study. 30 of the RA patients showed aPL antibody positivity and 138 aPL antibody negativity on the basis of the concomitant presence or absence of high concentrations of anticardiolipin (aCL) antibodies or the presence of lupus anticoagulant (LA). All subjects were evaluated for plasma homocysteine concentrations and for the occurrence of thrombotic events. RESULTS: Twenty-five RA patients and 5 controls reported a history of thrombotic events. Eleven and 5 of RA patients were found to have been previously affected by venous or arterial thrombosis, respectively. Plasma levels of homocysteine in aPL antibody positive patients with thrombosis were found to be significantly higher than in aPL antibody positive RA patients without thrombosis (p < 0.001). When RA patients with thromboses were analyzed, a significant increase of plasma homocysteine levels was found in aPL antibody-positive RA patients versus aPL antibody-negative RA patients (p < 0.04) and versus related controls (p < 0.003). CONCLUSIONS: The association observed between aPL antibody positivity and high levels of plasma homocysteine in RA patients may represent a possible risk factor for thrombotic events. Therefore, it is suggested that hyperhomocysteinemia might be involved in the vascular-related mortality observed in RA patients with a history of thrombosis.

Anticardiolipin antibodies, free protein S levels and thrombosis: a survey in a selected population of rheumatoid arthritis patients.

OBJECTIVE: To investigate plasma levels of natural anticoagulant proteins such as protein S, protein C and antithrombin III in a selected population of patients with rheumatoid arthritis (RA) with and without anticardiolipin antibody (aCL) positivity, and to evaluate the possible relationships with an increased risk of thrombotic events in RA. METHODS: A total of 184 female RA patients attending our Extra-Articular Involvement RA Clinic were evaluated for aCL levels, total and free protein S, protein C and antithrombin III concentrations, and for the occurrence of thrombotic events. Patients were grouped as aCL positive (n = 35) and aCL negative (n = 149). RESULTS: Higher rates of venous and/or arterial thromboses were diagnosed in patients with RA compared to controls (P = 0.01). In particular, lower free protein S levels were found in aCL-positive patients with RA compared to both aCL-negative patients and controls (P = 0.001). Functional assays for protein C, antithrombin III as well as total protein S levels were found to be in the normal range in all patients and controls. CONCLUSION: The association observed between aCL positivity and decreased levels of free protein S in RA patients may represent one of the risk factors for thrombotic events.

Lipoproteins, anticardiolipin antibodies and thrombotic events in rheumatoid arthritis.

OBJECTIVE: To investigate lipoprotein levels in rheumatoid arthritis (RA) patients with and without anticardiolipin antibody (aCL) positivity and to evaluate whether an abnormal lipid profile might be associated with an altered risk of vascular disorders. METHODS: 137 female patients were evaluated for their aCL levels (isotypes IgG and IgM); concentrations of plasma lipids, lipoproteins, and apolipoproteins; and for the occurrence of thrombotic events. The patients were grouped according to their aCL positivity. RESULTS: Higher rates of venous and/or arterial thrombosis were diagnosed in all the RA patients compared to the controls (p = 0.01). Lower levels of the high density lipoprotein cholesterol, apolipoprotein AI, were found in these patients (p = 0.001). Higher levels of lipoprotein (a) were observed in RA patients when compared to controls in both aCL positive and negative RA patients (P = 0.001 and p = 0.01, respectively). CONCLUSION: The presence of aCL and an altered lipid profile may represent an important risk factor for thrombotic events in patients affected by RA.