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Contains fulltext : 69857.pdf (Publisher’s version ) (Closed access) The cornerstone of tuberculosis management is a 6-month course of isoniazid, rifampicin, pyrazinamide and ethambutol. Compliance is crucial for curing tuberculosis. Adverse effects often negatively affect the compliance, because they frequently require a change of treatment, which may have negative consequences for treatment outcome. In this paper we review the incidence, pathology and clinical features of antituberculosis drug-induced hepatotoxicity, discuss the metabolism and mechanisms of toxicity of isoniazid, rifampicin and pyrazinamide, and describe risk factors and management of antituberculosis drug-induced hepatotoxicity. The reported incidence of antituberculosis drug-induced hepatotoxicity, the most serious and potentially fatal adverse reaction, varies between 2% and 28%. Risk factors are advanced age, female sex, slow acetylator status, malnutrition, HIV and pre-existent liver disease. Still, it is difficult to predict what patient will develop hepatotoxicity during tuberculosis treatment. The exact mechanism of antituberculosis drug-induced hepatotoxicity is unknown, but toxic metabolites are suggested to play a crucial role in the development, at least in the case of isoniazid. Priorities for future studies include basic studies to elucidate the mechanism of antituberculosis drug-induced hepatotoxicity, genetic risk factor studies and the development of shorter and safer tuberculosis drug regimens.

Contains fulltext : 52929.pdf (Publisher’s version ) (Open Access) BACKGROUND: A 54-year-old man with a 22-year history of rheumatoid arthritis and an 8-year history of chronic obstructive pulmonary disease presented with dyspnea on exertion, nonproductive cough and fatigue of 1 month's duration. His medication at presentation consisted of etanercept, azathioprine, naproxen and inhaled fluticasone and salbutamol. INVESTIGATIONS: At presentation, the patient underwent physical examination, chest X-ray and high-resolution CT, blood tests, and bronchoalveolar lavage fluid analysis including auramine stains and gene sequence analysis of cultured Mycobacterium szulgai. The patient underwent minithoracotomy after 6 months, and bronchoalveolar lavage fluid analysis, culture and chest X-ray after 18 months. Further chest imaging and culture of sputum samples were performed another year later. DIAGNOSIS: Pulmonary M. szulgai infection. MANAGEMENT: Triple drug therapy with rifampicin, ethambutol hydrochloride and clarithromycin. Anti-tumor necrosis factor treatment was continued.

Mycobacterium heckeshornense is a rare isolate in clinical specimens. We performed simultaneous 16S rRNA sequence analysis of a mycobacterium culture and a histopathology specimen to determine the relevance of M. heckeshornense infection in an immunocompetent patient initially presenting with pneumothorax.

A growing number of tuberculosis patients worldwide is also co-infected with HIV. This number is rising particularly rapidly in countries of sub-Saharan Africa but also in Southeast Asia (WHO/CDS/TB/2001). HIV-infected individuals have an increased risk of primary tuberculosis, a reactivation of tuberculosis, or a re-infection with tuberculosis (Small et al., 1993). The course of an HIV infection is negatively affected by co-infection with Mycobacterium tuberculosis (Whalen et al., 1995) and vice versa. Treatment with anti-tuberculous agents and potent antiretroviral medication has positively changed the morbidity and mortality rates of this “cursed duet”. However, these drug regimes are complicated and expensive and often associated with numerous side effects. One class of side effects seen in HIV-positive patients, for example, is the paradoxical reaction caused by the restoration of the immune response by potent antiretroviral therapy coupled with anti-tuberculous agents for active tuberculosis.

Contains fulltext : 52926.pdf (Publisher’s version ) (Open Access)

A symptomatic patient had repeatedly positive cultures of Mycobacterium avium subsp. hominissuis after exposure to a hot tub contaminated with M. avium subsp. hominissuis. The pulmonary and tub water isolates were indistinguishable by IS1245 RFLP as well as rep-PCR typing. Discontinued use of the hot tub resulted in culture conversion.