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There is a high co-morbidity between chronic inflammatory disorders and depression. Proinflammatory cytokines like TNF-α seem to play a central role in the pathogenesis of these disorders, and its neutralization provides a potent treatment for inflammatory disorders. Few studies showed that TNF-α blockers also caused an improvement in depressive symptoms associated with these chronic inflammatory disorders. To evaluate the effectiveness of TNF-α blockers on symptoms of ankylosing spondylitis (AS), depression, anxiety and quality of life, 9 AS patients resistant to classical therapy were enrolled and followed-up at 2nd and 6th weeks after a TNF-α blocker was started. Hamilton Depression and Anxiety Scales (HAM-D, HAM-A), Hospital Depression and Anxiety Questionnaire (HAD), Quality of Life Scale (SF36) and AS severity index (BASDAI) were applied to the patients at weeks 0, 2 and 6. ESR and CRP were evaluated to monitor biological disease activity. There was a significant reduction in HAM-D ( p = 0.00), HAM-A ( p = 0.00), HAD anxiety scores ( p = 0.02) and a significant improvement in SF36 physical function ( p = 0.00), physical role limitations ( p = 0.00), bodily pain ( p = 0.05), general health ( p = 0.01), vitality ( p = 0.03) and emotional role limitations ( p = 0.00) subscales, BASDAI scores ( p = 0.00), ESR ( p = 0.00) and CRP ( p = 0.00). Change in clinical disease activity (BASDAI) was not correlated with change in depression-anxiety scores, while change in biological disease activity (CRP) was correlated with change in depression-anxiety scores. TNFα blockers may have a potential antidepressant effect besides its anti-inflammatory effect that seems to be independent of its clinical effect. [ABSTRACT FROM AUTHOR]

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The aims of this study were to determine the association and potential mechanisms between TNF-antagonists and increased cardiovascular risk in rheumatoid arthritis (RA) patients. Three groups of RA patients were studied; ten treated with TNF-antagonists, 13 with methotrexate, and 14 were naïve to treatment. Mean age: 47.2 (SD 11.3), 52.3 (SD 16.6), and 51.2 (SD 13.3) years; mean disease duration 102 (SD 90.4), 72.9 (SD 67.3), and 71.3 (SD 87.1) months, and treatment duration 24.2 (SD 18.5), 34.7 (SD 32.2), and 0 months for each group. Clinical data: systolic and diastolic blood pressure and body mass index were assessed. Disease activity was determined by DAS-28 index. An ELISA assay for IL-6, sIL-6 R, IFN-gamma, TNF-alpha, sTNFRI, sTNFRII, IGF I, and adiponectin were performed. Fasting glucose, insulin, lipid profile, CRP, and ESR were also done. HOMA-IR and QUICKI indexes were calculated. Statistically significant differences observed between the TNF group and the other two groups were: TNF-alpha levels ( p, 0.0014), soluble TNF RII ( p, 0.0432), IFN-gamma ( p, 0.008), and DAS-28 <2.6 ( p, 0.033). Finding of elevated levels of sTNFRII and IFN-gamma in patients with RA on anti-TNF suggests that this therapy does not completely suppress the inflammatory process and may promote atherogenesis. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor (TNF)-alpha antagonists successfully modulate the pathogenesis of rheumatoid arthritis (RA). However, little is known about the effect of TNF-alpha blockade on the histology of chronic viral hepatitis. We describe the cases of two patients with RA, one with concurrent chronic hepatitis B virus and the other with hepatitis C virus infection who, as part of their evaluation, underwent liver biopsies while undergoing treatment with a TNF-alpha antagonist. [ABSTRACT FROM AUTHOR]