antituberculosis/necrosis

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Paradoxical response with increased tumor necrosis factor-α levels to anti-tuberculosis treatment in a patient with disseminated tuberculosis.

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It has been reported that tuberculosis (TB) worsens after cessation of tumor necrosis factor-α inhibitors and starting anti-TB treatment. Little is known about the immunological pathogenesis of this paradoxical response (PR). We report the first case of a TB patient in whom PR occurred concurrently

Frequency and tolerance of antituberculosis treatment according to national guidelines for prevention of risk of tuberculosis due to tumor necrosis factor blocker treatment.

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OBJECTIVE Tumor necrosis factor (TNF) blockers increase the risk of tuberculosis infection. National recommendations in France for prevention of latent tuberculosis recommend treatment by rifampicin (RIF) 600 mg/day and isoniazid (INH) 300 mg/day for 3 months. However, its toxicity is unknown in

Inhibition of anti-tuberculosis T-lymphocyte function with tumour necrosis factor antagonists.

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Reactivation of latent Mycobacterium tuberculosis (Mtb) infection is a major complication of anti-tumour necrosis factor (TNF)-alpha treatment, but its mechanism is not fully understood. We evaluated the effect of the TNF antagonists infliximab (Ifx), adalimumab (Ada) and etanercept (Eta) on

Completion rate and compliance of anti-tuberculosis chemoprophylaxis in patients with rheumatic disease receiving tumor necrosis factor antagonists.

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[Recommendations for the diagnosis and treatment of latent and active tuberculosis in patients with inflammatory joint diseases treated with tumour necrosis factor alpha inhibitors].

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The Portuguese Society of Rheumatology (SPR) and the Portuguese Society of Pulmonology (SPP) have developed guidelines for the diagnosis and treatment of latent tuberculosis infection (LTBI) and active tuberculosis (AT) in patients with inflammatory joint diseases (IJD), namely rheumatoid arthritis,

Correlation of serum tumor necrosis factor-alpha, interleukin-4 and soluble interleukin-2 receptor levels with radiologic and clinical manifestations in active pulmonary tuberculosis.

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The precise clinical manifestations of tuberculosis are likely to result from a complex interaction between the host and the pathogen. We took serum samples from a group of patients with a variety of clinical and radiological stages of pulmonary tuberculosis in order to characterize tumor necrosis

[Comparative study of hepatoprotective action of remaxol, reamberin and ademethionine in liver injury induced by antituberculosis drugs (experimental study)].

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The hepatoprotective activity of remaxol, reamberin and ademethionine was studied on a model of the liver injury induced by antituberculosis drugs. The study included 30 male uninbred albino rats. The following antituberculosis drugs were used: isoniazid (50 mg/kg) subcutaneously + rifampicin (250

Clinical efficacy of Baihe Gujin decoction combined with anti-tuberculosis therapy for pulmonary tuberculosis with Yin-deficiency and Fire-hyperactivity syndrome.

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OBJECTIVE

To evaluate the clinical efficacy of Baihe Gujin decoction combined with anti-tuberculosis therapy in mitigating the symptoms of pulmonary tuberculosis and to measure the effect on the CD4+ CD25+ regulatory T cell (T_reg)

Warfarin-induced skin necrosis in HIV-1-infected patients with tuberculosis and venous thrombosis.

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BACKGROUND At the turn of the century, only 300 cases of warfarin-induced skin necrosis (WISN) had been reported. WISN is a rare but potentially fatal complication of warfarin therapy. There are no published reports of WISN occurring in patients with HIV-1 infection or tuberculosis (TB). METHODS We

Mitochondria are targets for the antituberculosis drug rifampicin in cultured epithelial cells.

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Rifampicin is a widely used drug for antituberculosis therapy. Its target is the bacterial RNA polymerase. After entry into the human or mammalian organism, rifampicin is accumulated in cells of epithelial origin (kidneys, liver, lungs) where it induces apoptosis, necrosis, and fibrosis. The purpose

The impact of immune disturbances on the failure of antituberculosis treatment.

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OBJECTIVE Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis complex, with an evolution and treatment outcome determined by the interaction between the mycobacterial and human genotypes. Various deficiencies of innate immune response starting from the first encounter of M.

Interleukin-4 and interleukin-10 polymorphisms and antituberculosis drug-induced hepatotoxicity in Chinese population.

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OBJECTIVE Evidence demonstrates that the delicate balance between pro- and anti-inflammatory cytokines determines the further progress to severe injury or recovery. Therefore, understanding which cytokines are associated with the development of drug-induced hepatotoxicity (DIH) might guide the

Dynamics of plasma cytokine levels in patients with advanced HIV infection and active tuberculosis: implications for early recognition of patients with poor response to anti-tuberculosis treatment.

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OBJECTIVE To examine whether the serial measurement of plasma cytokine levels can assist in the early recognition of AIDS/tuberculosis patients with poor response to anti-tuberculosis treatment. METHODS Longitudinal, prospective cohort study. METHODS A university hospital, the largest centre for

[Serum levels of solubule tumor necrosis factor (TNF) receptors in patients with pulmonary tuberculosis].

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Tumor necrosis factor alpha (TNF-alpha) is released from cells of monocyte/macrophage lincage and mediates the development of a variety of clinical and pathomorphological features in various infectious diseases, autoimmune diseases and cancer. In the case of tuberculosis, it is suggested that the

[Evaluating clinical significance of tumor necrosis factor-alpha and hydroxyproline in blood of patients with active pulmonary tuberculosis].

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OBJECTIVE To evaluate the clinical significance of tumor necrosis factor-alpha (TNF-alpha) and hydroxyproline (HYP) in blood of patients with active pulmonary tuberculosis (APT). METHODS Contents of TNF-alpha and HYP in blood of 28 patients with APT and 17 normal subjects were determined with

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