The role of cigarette smoking and liver enzymes polymorphisms in anti-tuberculosis drug-induced hepatotoxicity in Brazilian patients

Zaverucha-do-Valle, Camila; Monteiro, Sergio Pereira; El-Jaick, Kênia Balbi; Rosadas, Leonardo Azevedo Silva; Costa, Maria Alice Nunes; Quintana, Marcel de Souza Borges; Castro, L. de

doi:10.1016/j.tube.2014.03.006

Cited by 31 publications

(35 citation statements)

References 24 publications

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“…Several elegant review articles [2][3][4]14] and research papers [19,20] on smoking-drug interactions have been published, but none of them mentioned the possible inclusion of relevant information in drug labelling. There is an urgent need to increase the awareness of this issue in the research community.…”

Section: Discussion and Perspectivesmentioning

confidence: 99%

Drugs and Diseases Interacting with Cigarette Smoking in US Prescription Drug Labelling

Shi

2015

Clin Pharmacokinet

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The US Food and Drug Administration (FDA) draft guidance for industry on drug interaction studies recommends, but does not mandate, that both cigarette smokers and non-smokers can be used to study drug metabolism in clinical trials, and that important results related to smoking should be included in drug labelling to guide medication usage. This study aimed to provide a comprehensive review of drugs or diseases interacting with smoking, as presented in all US drug labelling. The 62,857 drug labels deposited in the FDA Online Label Repository were searched using the keywords 'smoke', 'smoker(s)', 'smoking', 'tobacco' and 'cigarette(s)' on 19 June 2014. The resultant records were refined to include only human prescription drug labelling, for manual examination. For 188 single-active-ingredient drugs and 36 multiple-active-ingredient drugs, the labelling was found to contain smoking-related information. The pharmacokinetics of 29 and 21 single-active-ingredient drugs were affected and unaffected, respectively, by smoking. For the remaining drugs, the provided information related to smoking affecting efficacy, safety or diseases but not pharmacokinetics. Depending on the nature of specific drugs, the perturbation in pharmacokinetic parameters in smokers ranged from 13 to 500%, in comparison with non-smokers. Dosage modifications in smokers are necessary for four drugs and may be necessary for six drugs, but are unnecessary for seven drugs although the pharmacokinetic parameters of four of them are affected by smoking. Cigarette smoking is a risk factor for 16 types of diseases or adverse drug reactions. For one single-active-ingredient contraceptive drug and 10 multiple-active-ingredient contraceptive drugs, a black box warning (the FDA's strongest safety warning) is included in the labelling for increased risks of heart attacks and strokes in female smokers, and "women are strongly advised not to smoke" when using these drugs. This study presents the first comprehensive overview of cigarette smoking interacting with drugs and/or diseases, as presented in US drug labelling.

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Section: Discussion and Perspectivesmentioning

confidence: 99%

Drugs and Diseases Interacting with Cigarette Smoking in US Prescription Drug Labelling

Shi

2015

Clin Pharmacokinet

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“…In contrast, smoking has been reported to attenuate isoniazid-associated hepatotoxicity by increasing N-acetyltransferase 2 activity, with potential implications for efficacy of therapy [123]. Although the impact of smoking on the efficacy of combined HAART/TB therapy, as well as on the frequency of therapy-associated adverse effects, requires additional research, cessation of smoking simply on the basis of its negative effects on the individual types of therapy is clearly warranted.…”

Section: Tuberculosismentioning

confidence: 99%

Impact of HIV infection and smoking on lung immunity and related disorders

2015

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HIV-infected persons not only have higher rates of smoking than the general population, but are also unusually vulnerable to the associated adverse health effects, both infective and noninfective in origin. Indeed, in the setting of well-organised care and availability of highly active antiretroviral therapy, HIV-infected smokers lose more life-years to smoking than to HIV infection per se, presenting a major challenge to healthcare providers. Not surprisingly, the respiratory system is particularly susceptible to the damaging interactive chronic inflammatory and immunosuppressive effects of HIV and smoking, intensifying the risk of the development of opportunistic infections, as well as lung cancer and obstructive lung disorders. The impact of smoking on the immunopathogenesis and frequencies of these respiratory conditions in the setting of HIV infection, as well as on the efficacy of antiretroviral therapy, represent the primary focus of this review. @ERSpublications Smoking exacerbates the immunosuppressive/pro-inflammatory effects of HIV, increasing the risk of pulmonary disease

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“…Several surveys found an association between the c1/c1 (RsaI + ) variant and the development of ATDH [13,21], but other studies found no associations [19,41,42]. Notably, a significant association was observed between c2 allele carriers and the development of ATDH, which suggests that this allele is an independent risk factor for hepatotoxicity in our population (Table 3).…”

Section: Discussionmentioning

confidence: 69%

“…The CYP2E1 c1/c2 polymorphism and ATDH susceptibility were studied widely in several populations [19,21,23,[40][41][42]. Several surveys found an association between the c1/c1 (RsaI + ) variant and the development of ATDH [13,21], but other studies found no associations [19,41,42].…”

Section: Discussionmentioning

confidence: 99%

Effect of gene–gene and gene–environment interactions associated with antituberculosis drug-induced hepatotoxicity

Chamorro

Castagnino

Aidar

et al. 2017

Pharmacogenetics and Genomics

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a Objectives This study evaluated the association between environmental factors and genetic variations in enzymes that metabolize antituberculosis (anti-TB) drugs [arylamine N-acetyltransferase 2, cytochrome P450 2E1 (CYP2E1), glutathione S-transferase theta 1 (GSTT1), and glutathione S-transferase mu 1] with antituberculosis drug-induced hepatotoxicity (ATDH). We also investigated the potential gene-gene and gene-environment interactions as well as their association with ATDH development in a population of hospitalized TB patients from Buenos Aires.Patients and methods We investigated 364 TB patients who received anti-TB drugs. Physicians collected demographic and clinical data to identify environmental risk factors for ATDH development. Polymorphisms were detected using gene sequencing, PCR, and PCR-restriction fragment length polymorphisms. A binary logistic regression analysis was carried out to compare the results of TB patients with and without the development of hepatotoxicity. The multifactor dimensionality reduction method was used to examine genetic and environmental interactions in association with ATDH.Results This study suggests that the slow acetylator profile [odds ratio (OR): 3.02; 95% confidence interval (CI): 1.82-5.00; P < 0.001], genotypes carrying the c2 variant (OR: 2.16; 95% CI: 1.33-3.51; P = 0.002) or the A4 variant of CYP2E1 (OR: 2.13; 95% CI: 1.06-4.29; P = 0.050), and female sex (OR: 1.94; 95% CI: 1.20-3.14; P = 0.006) were independent predictor variables for ATDH. Patients carrying the slow acetylator profile and the c2 variant showed an increased risk (OR: 7.068; 95% CI: 3.34-14.95; P < 0.001).We also identified a synergic interaction (epistasis) between GSTT1 and CYP2E1 associated with an increased risk for ATDH. A meaningful gene-environment interaction was associated with an increased risk of ATDH [testing balance accuracy = 0.675 (P = 0.001) and cross-validation consistency = 10/10].Conclusion ATDH is a severe and prevalent adverse drug reaction and leads to drug discontinuation in 11% of TB patients. Our study created a prediction model that properly classified the 67.5% of TB patients in their risk of developing ATDH. The considerable number of TB patients in our country supports the use of pharmacogenetic testing and a comprehensive clinical history to identify patients with a high risk of suffering hepatotoxicity. Pharmacogenetics and Genomics 00:000-000

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The role of cigarette smoking and liver enzymes polymorphisms in anti-tuberculosis drug-induced hepatotoxicity in Brazilian patients

Cited by 31 publications

References 24 publications

Drugs and Diseases Interacting with Cigarette Smoking in US Prescription Drug Labelling

Drugs and Diseases Interacting with Cigarette Smoking in US Prescription Drug Labelling

Impact of HIV infection and smoking on lung immunity and related disorders

Effect of gene–gene and gene–environment interactions associated with antituberculosis drug-induced hepatotoxicity

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