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Antituberculosis Treatment (antituberculosi + treatment)
Selected AbstractsPleural fluid interferon-, and adenosine deaminase levels in tuberculosis pleural effusion: a cost-effectiveness analysisJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 2 2005S.K. Sharma Abstract Pleural fluid levels of interferon-, (IFN-,) and adenosine deaminase (ADA) have been found to be high in patients with tuberculosis (TB). The present study was carried out to compare the diagnostic utility of these two markers and to carry out a cost-effectiveness analysis of performing IFN-, estimation in comparison to ADA. A total of 52 patients with pleural effusion, 35 of which were found to have TB etiology, were prospectively included for estimation of ADA and IFN-, levels. The difference in the cost of performing the two diagnostic tests was compared with the cost of the treatment for a patient with TB. Pleural fluid IFN-, (median [range]: 2,100 [70,14,000] vs. 3 [0,160]; P<0.001) as well as ADA levels (mean [SD]: 93.1 [62.3] vs 15.4 [8.7]; P<0.001) were significantly higher in patients with TB effusion. Even though IFN-, estimation was more sensitive (97.1 vs. 91.4%), the extra cost of IFN-, estimation for detecting one patient with TB was found to be equivalent to the cost of a complete course of antituberculosis treatment for six patients. In developing countries, where TB is rampant and cost is a major concern, pleural fluid IFN-, estimation does not seem to be a cost-effective investigation method for differentiating TB from non-TB pleural effusion. J. Clin. Lab. Anal. 19:40,46, 2005. © 2005 Wiley-Liss, Inc. [source] Solitary pulmonary nodule in the liver transplant candidate: Importance of diagnosis and treatmentLIVER TRANSPLANTATION, Issue 6 2010Allan M. Concejero Our objectives were to define the incidence and etiology of solitary pulmonary nodules (SPNs) in patients undergoing living donor liver transplantation (LDLT), describe a diagnostic approach to the management of SPNs in LDLT, and define the impact of SPNs on the overall survival of adult LDLT recipients. Nine patients (9/152, 5.9%) were diagnosed with an SPN on the basis of chest radiography findings during the pretransplant survey. All were male. The mean age was 52 years. All the patients had hepatitis B virus,related cirrhosis with hepatocellular carcinoma. All were asymptomatic for the lung lesion. All underwent contrast-enhanced chest computed tomography (CT) to verify the presence and possible etiology of the SPNs. In 3 cases, CT was used to definitely determine that there was no pulmonary nodule; in 2, CT led to a definite diagnosis of pulmonary tuberculosis. In 4, CT led to a definite identification of an SPN but not to an etiological diagnosis. Two patients underwent outright thoracoscopy and biopsy of their SPNs. Biopsy showed cryptococcosis in both patients. One received a therapeutic trial of an antituberculosis treatment, and repeat CT after 1 month showed a regression in the size of the SPN. A diagnosis of tuberculosis was made. One patient had an inconclusive whole body positron emission tomography scan and subsequently underwent thoracoscopy where biopsy showed tuberculosis. A concomitant malignancy, either primary lung cancer or metastasis from the liver tumor, was not identified. All patients were surviving with their original grafts and were lung infection,free. The overall mean posttransplant follow-up was 54 months (range = 33-96 months). Liver Transpl 16:760-766, 2010. © 2010 AASLD. [source] Antimicrobial treatment of presumed ocular tuberculosisACTA OPHTHALMOLOGICA, Issue 2007S KOUPRIANOFF Purpose: Uveitis secondary to a tuberculosis is rarely reported, even in a tertiary a care center. The prevalence of tuberculosis is low in Western Europe and its microbiological identification is difficult. However, anti tuberculosis treatment may be useful when the diagnosis of tuberculosis is presumed. Methods: The clinical records of patients with suspected tuberculosis uveitis referred to the Ophthalmology Department of the Grenoble University, between January 2005 and January 2007 were retrospectively analyzed. Patients were included in this series if they received a specific antituberculosis treatment. Results: This series included 10 patients (3M/7F, mean age 54.1). The clinical features of ocular inflammation were: bilateral panuveitis, episcleritis, bilateral posterior uveitis, and pars planitis. Tuberculin skin test, chest computerized tomography, BK sputum, and internal medicine consultation were performed for all patients. The diagnosis of presumed tuberculosis was based upon: history, thoracic imaging, and tuberculin skin test. None had extra-ocular symptoms. Sputum cultures were negative, 2 adenopathy biopsies confirmed the diagnosis. Nine patients received specific antituberculosis therapy, without systemic steroid therapy. All of them improved; no relapse occurred after 1 to 2 years after the end of therapy. In one case, tuberculosis specific therapy allowed to taper the systemic steroid therapy. Conclusions: The diagnosis of uveitis associated with tuberculosis is difficult since it depends on a spectrum of indirect signs. Bacteriological identification is rarely obtained. In presumed ocular tuberculosis, antituberculosis therapy may be useful to control intraocular inflammation, with or without steroid therapy. [source] Isoniazid-resistance conferring mutations in Mycobacterium tuberculosis KatG: Catalase, peroxidase, and INH-NADH adduct formation activitiesPROTEIN SCIENCE, Issue 3 2010Christine E. Cade Abstract Mycobacterium tuberculosis catalase-peroxidase (KatG) is a bifunctional hemoprotein that has been shown to activate isoniazid (INH), a pro-drug that is integral to frontline antituberculosis treatments. The activated species, presumed to be an isonicotinoyl radical, couples to NAD+/NADH forming an isoniazid-NADH adduct that ultimately confers anti-tubercular activity. To better understand the mechanisms of isoniazid activation as well as the origins of KatG-derived INH-resistance, we have compared the catalytic properties (including the ability to form the INH-NADH adduct) of the wild-type enzyme to 23 KatG mutants which have been associated with isoniazid resistance in clinical M. tuberculosis isolates. Neither catalase nor peroxidase activities, the two inherent enzymatic functions of KatG, were found to correlate with isoniazid resistance. Furthermore, catalase function was lost in mutants which lacked the Met-Tyr-Trp crosslink, the biogenic cofactor in KatG which has been previously shown to be integral to this activity. The presence or absence of the crosslink itself, however, was also found to not correlate with INH resistance. The KatG resistance-conferring mutants were then assayed for their ability to generate the INH-NADH adduct in the presence of peroxide (t -BuOOH and H2O2), superoxide, and no exogenous oxidant (air-only background control). The results demonstrate that residue location plays a critical role in determining INH-resistance mechanisms associated with INH activation; however, different mutations at the same location can produce vastly different reactivities that are oxidant-specific. Furthermore, the data can be interpreted to suggest the presence of a second mechanism of INH-resistance that is not correlated with the formation of the INH-NADH adduct. [source] |