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anti-TB Drugs (anti-tb + drug)
Selected AbstractsAdverse reactions of anti-tuberculosis drugs in hospitalized patients: incidence, severity and risk factors,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 10 2007Mohammad Reza Javadi Abstract Background Tuberculosis (TB) has been a common chronic infectious disease in human communities. Besides disease-related complications, there could be serious adverse reactions due to anti-tuberculosis (anti-TB) drug therapy. Objectives To assess the incidence and severity of adverse drug reactions (ADRs) induced by anti-TB drugs. To determine possible covariates associated with detected ADRs. Methods All patients with respiratory TB admitted to a teaching hospital who received anti-TB drugs during the research period entered the study and were monitored for ADRs. Socio-demographic and medical history of patients were used as independent covariates. The relationship between independent covariates with frequency and severity of ADRs was analysed using multivariate logistic regression. Preliminary analyses of the Mann,Whitney, Chi-square, Kruskal,Wallis and the Fisher's exact tests were applied to determine factors unlikely associated with the independent variables. Results Among 204 patients admitted, there were 92 patients (45.1%) with ADRs induced by anti-TB drugs. Patients with a previous history of anti-TB drugs usage (OR,=,5.81, 95% confidence interval [95%CI]: 1.31,25.2), patients with a history of drug allergy (OR,=,6.68, CI: 1.28,36.2), those from Afghani ethnic (OR,=,4.91, 95%CI: 1.28,18.30) as well as smoker patients with concurrent diseases (OR,=,19.67, CI: 1.24,341.51) had a higher rate of ADR incidence. Being female (OR,=,1.63, 95%CI: 1.96,36.40) and having previous history of ADR (OR,=,17.46, 95%CI: 1.96,20.42) were identified as risk factors. Conclusion Anti-TB drugs could cause severe and frequent adverse effects. Females, those with a previous history of ADRs to anti-TB drugs and Afghani patients, should be considered as high-risk groups. Copyright © 2007 John Wiley & Sons, Ltd. [source] Drug-resistant tuberculosis: Past, present, futureRESPIROLOGY, Issue 3 2010Chen-Yuan CHIANG ABSTRACT In a population of Mycobacterium tuberculosis, random chromosomal mutation that results in genetic resistance to anti-tuberculosis (TB) drugs occurs at a relatively low frequency. Anti-TB drugs impose selection pressure so that mycobacterial mutants gradually outnumber susceptible bacilli and emerge as the dominant strains. Resistance to two or more anti-TB drugs represents cumulative results of sequential mutation. The fourth report on global anti-TB drug resistance provides the latest data on the extent of such problem in the world. The median prevalence of multi-drug-resistant TB (MDR-TB) in new TB cases was 1.6%, and in previously treated TB cases 11.7%. Of the half a million MDR-TB cases estimated to have emerged in 2006, 50% were in China and India. The optimal duration of any given combination of anti-TB drugs for treatment of MDR- and extensively drug-resistant TB (XDR-TB) has not been defined in controlled clinical trials. Standardized treatment may be feasible for MDR-TB patients not previously treated with second-line drugs, but a different strategy needs to be applied in the treatment of MDR-TB patients who have received second-line drugs before. Unfortunately, the reliability of drug susceptibility testing of most second-line anti-TB drugs is still questionable. Drug-resistant TB is not necessarily less virulent. Findings from modelling exercise warned that if MDR-TB case detection and treatment rates increase to the World Health Organization target of 70%, without simultaneously increasing MDR-TB cure rates, XDR-TB prevalence could increase exponentially. Prevention of development of drug resistance must be accorded the top priority in the era of MDR-/XDR-TB. [source] Antituberculosis drug-related liver dysfunction in chronic hepatitis B infectionHEPATOLOGY, Issue 1 2000Wai-Man Wong Liver toxicity is a common side effect of antituberculosis (anti-TB) drugs. We studied the differences in liver dysfunction observed during anti-TB treatment between hepatitis B virus carriers (HBV) and noncarriers. Three hundred twenty-four patients on anti-TB drugs were recruited and followed up for 1 year. Forty-three patients with HBV and 276 non-HBV patients were included for analysis. Liver function tests and viral markers were monitored monthly. Liver biopsy was requested whenever the alanine transaminase (ALT) was persistently abnormal. Eighty-six HBV carriers who were not given anti-TB drugs were chosen as a second control and evaluated prospectively. The incidence of liver dysfunction was significantly higher in HBV carriers given anti-TB drugs (34.9%) when compared to noncarriers (9.4%, P < .001) and with HBV carriers not given anti-TB drugs (8.1%, P < .001). For patients given anti-TB drugs, HBV carriers who developed liver dysfunction were younger (P = .011) and had more severe liver injury compared with noncarriers (P = .008). By multiple logistic regression analysis, age (P = .002) and hepatitis B infection (P < .001) were the only 2 significant risk factors for hepatotoxicity related to anti-TB therapy. [source] Potentiation of isoniazid-induced liver toxicity by rifampicin in a combinational therapy of antitubercular drugs (rifampicin, isoniazid and pyrazinamide) in Wistar rats: A toxicity profile studyHEPATOLOGY RESEARCH, Issue 10 2007Sheikh Abdullah Tasduq Aim:, Biochemical characterization of long-term toxic manifestations of anti-tubercular (anti-TB) drugs , rifampicin (RIF), isoniazid (INH) and pyrazinamide (PZA) , individually and in two combinations: (i) RIF + INH, and (ii) RIF + INH + PZA in Wistar rats. Methods:, Animals received anti-TB drugs , alone or in combination , once daily p.o. for up to 90 days (doses, in mg/kg: RIF, 250; INH, 50; PZA, 100). Assays for alanine aminotransferase (ALT), alkaline phosphatase (ALP), bilirubin (serum) and lipid peroxidation (LPO), glutathione (GSH), glutathione peroxidase (GPx), catalase, Na+K+-ATPase and CYP 2E1 (liver) were performed to assess liver toxicity. Clinical biochemistry was done by commercial kits. Determinations were made at 0, 15, 30 and 90 days of treatment schedule. Results:, Anti-TB drugs-treated animals showed abnormal rises or falls (>1.5,2 fold) in the serum/liver parameters. Mild hyperlipidemia, hypercholesterolemia and hyperuricemia were the other pathologies. Of all the treated groups, INHalone or in combination with other drugs produced a progressive enhancement of toxicity over 15,90 days. The in vivo results were further supported by in vitro results (MTT assay, GSH and LPO) in primary cultures of rat hepatocyte. Results indicated that anti-TB drugs in combination: (i) caused membrane damage resulting in leakage of ALT, ALP and bilirubin; (ii) caused imbalance in endogenous enzymatic oxidant,antioxidant defense via increased lipid peroxidation and in glutathione homeostasis; and (iii) enhanced the CYP 2E1-mediated bioactivation mechanism. Conclusion:, Toxicity manifestations seemed to be heptocytic injury targeted at hepatocytes, bile ducts or sinusoidal cells related to hepatitis and primary biliary cholestasis. [source] Adverse reactions of anti-tuberculosis drugs in hospitalized patients: incidence, severity and risk factors,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 10 2007Mohammad Reza Javadi Abstract Background Tuberculosis (TB) has been a common chronic infectious disease in human communities. Besides disease-related complications, there could be serious adverse reactions due to anti-tuberculosis (anti-TB) drug therapy. Objectives To assess the incidence and severity of adverse drug reactions (ADRs) induced by anti-TB drugs. To determine possible covariates associated with detected ADRs. Methods All patients with respiratory TB admitted to a teaching hospital who received anti-TB drugs during the research period entered the study and were monitored for ADRs. Socio-demographic and medical history of patients were used as independent covariates. The relationship between independent covariates with frequency and severity of ADRs was analysed using multivariate logistic regression. Preliminary analyses of the Mann,Whitney, Chi-square, Kruskal,Wallis and the Fisher's exact tests were applied to determine factors unlikely associated with the independent variables. Results Among 204 patients admitted, there were 92 patients (45.1%) with ADRs induced by anti-TB drugs. Patients with a previous history of anti-TB drugs usage (OR,=,5.81, 95% confidence interval [95%CI]: 1.31,25.2), patients with a history of drug allergy (OR,=,6.68, CI: 1.28,36.2), those from Afghani ethnic (OR,=,4.91, 95%CI: 1.28,18.30) as well as smoker patients with concurrent diseases (OR,=,19.67, CI: 1.24,341.51) had a higher rate of ADR incidence. Being female (OR,=,1.63, 95%CI: 1.96,36.40) and having previous history of ADR (OR,=,17.46, 95%CI: 1.96,20.42) were identified as risk factors. Conclusion Anti-TB drugs could cause severe and frequent adverse effects. Females, those with a previous history of ADRs to anti-TB drugs and Afghani patients, should be considered as high-risk groups. Copyright © 2007 John Wiley & Sons, Ltd. [source] Drug-resistant tuberculosis: Past, present, futureRESPIROLOGY, Issue 3 2010Chen-Yuan CHIANG ABSTRACT In a population of Mycobacterium tuberculosis, random chromosomal mutation that results in genetic resistance to anti-tuberculosis (TB) drugs occurs at a relatively low frequency. Anti-TB drugs impose selection pressure so that mycobacterial mutants gradually outnumber susceptible bacilli and emerge as the dominant strains. Resistance to two or more anti-TB drugs represents cumulative results of sequential mutation. The fourth report on global anti-TB drug resistance provides the latest data on the extent of such problem in the world. The median prevalence of multi-drug-resistant TB (MDR-TB) in new TB cases was 1.6%, and in previously treated TB cases 11.7%. Of the half a million MDR-TB cases estimated to have emerged in 2006, 50% were in China and India. The optimal duration of any given combination of anti-TB drugs for treatment of MDR- and extensively drug-resistant TB (XDR-TB) has not been defined in controlled clinical trials. Standardized treatment may be feasible for MDR-TB patients not previously treated with second-line drugs, but a different strategy needs to be applied in the treatment of MDR-TB patients who have received second-line drugs before. Unfortunately, the reliability of drug susceptibility testing of most second-line anti-TB drugs is still questionable. Drug-resistant TB is not necessarily less virulent. Findings from modelling exercise warned that if MDR-TB case detection and treatment rates increase to the World Health Organization target of 70%, without simultaneously increasing MDR-TB cure rates, XDR-TB prevalence could increase exponentially. Prevention of development of drug resistance must be accorded the top priority in the era of MDR-/XDR-TB. [source] Anti-TB drug resistance levels and patterns among Mycobacterium tuberculosis isolated from newly diagnosed cases of pulmonary tuberculosis in Dar es Salaam, TanzaniaAPMIS, Issue 4 2009MECKY MATEE Anti-tuberculosis drug resistance levels and patterns of Mycobacterium tuberculosis (Mtb) isolated from newly diagnosed tuberculosis (TB) patients in Temeke district in Dar es Salaam, Tanzania were investigated. A total of 226 Mtb isolates from 564 TB suspects with no previous history of anti-TB treatment were tested for drug resistance against rifampicin, isoniazid, streptomycin and ethambutol on Lowenstein Jensen (LJ) medium using the proportion method. Of the 226 isolates, 22 (9.7%) were resistant to any one of the four anti-TB drugs; nine (3.99%) isolates were isoniazid mono-drug resistant and eight (3.54%) isolates were streptomycin mono-drug resistant. Multi-drug resistance, defined as resistance to both rifampicin and isoniazid, was observed in three (1.3%) isolates and two were also resistant to streptomycin and ethambutol. One (0.44%) isolate had poly resistance to isoniazid and streptomycin. The level of anti-TB drug resistant Mtb in Temeke, an HIV endemic area, remained constant between 1995 and 2007. The level of resistance to any one of the four anti-TB drugs was between 9.0% and 10%, resistance to individual drugs <4% and multi-drug resistance <2%. [source] |