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INTRODUCTION: The risk of active tuberculosis is increased in psoriasis patients receiving biologic drug therapy. The QuantiFERON-TB Gold In-Tube assay (QFT) is used for latent tuberculosis screening in these patients. This study presents a retrospective analysis on repeated QFT assays, investigating the influence of biologic drugs and isoniazid therapy on the outcome of the assay. METHODS: Serial QFTs of 58 psoriasis patients, who received biologic drug therapy, were evaluated at baseline and after 12 months of treatment. Patients were retrospectively divided in four groups according to QFT results at baseline and at follow-up: patients having a QFT reversion (from positive to negative results); patients with a conversion (from negative to positive); patients confirming the baseline results, either positive or negative. RESULTS: At the end of the 12-months period, 11.1% of patients with a negative QFT result at baseline presented a conversion, showing low interferon (IFN)-gamma values, whereas 6.9% of positive patients presented a QFT reversion. When the test was repeated after 2-3 months without isoniazid chemoprophylaxis, patients with QFT conversion showed negative results. No patient developed active tuberculosis. CONCLUSIONS: In patients undergoing biologic therapy, a positive QFT assay needs to be further confirmed, as false-positive results may occur after long-term therapy. Repeating QFT tests in patients with low IFN-gamma values could reduce the incidence of false-positive latent tuberculosis infection diagnosis, thus preventing unnecessary tuberculosis chemoprophylaxis. In conclusion, a dynamic QFT response is possible in psoriasis patients undergoing biologic therapy.
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The impact of anti-TNF therapy on systemic immune responses in patients has not been clearly defined. Here, we examined Th1/Th2/Th17 cytokine expression, activation and proliferation of peripheral T cells from patients with psoriasis and inflammatory bowel disease before and during anti-TNF therapy. In parallel, we calculated the correlation with the clinical response and we monitored cytokine expression in biopsies from inflamed tissues. We evidenced a dual role of TNF-blockade. In peripheral blood, it increased the expression of cytokines such as IL-17, IL-10, and IFN-γ, and enhanced the expression of activation markers and the proliferative response of CD4 T cells to TCR stimulation. By contrast, in biopsies from target tissues, TNF-blockade diminished the expression of Th17/Th1 cytokine and early inflammatory genes. Importantly, the enhanced T cell responses to TCR-stimulation did not impair the clinical response to the therapy and, in responder patients, occurred with the concomitant down-regulation of inflammatory genes in the target tissues.