isoniazid
Sources réglementaires consultées
Indications approuvées
- Tuberculose active sensible toujours en association et traitement préventif de l’infection tuberculeuse selon un schéma approuvé.
Contre-indications
Absolues
- Maladie hépatique aiguë ; lésion hépatique antérieure liée à l’isoniazide ; réaction indésirable sévère ou hypersensibilité antérieure à l’isoniazide.
Mises en garde cliniques
- Elle peut provoquer une hépatite sévère ou mortelle même plusieurs mois après le début. Évaluer le risque lié à l’âge, à l’alcool et à l’hépatopathie ; surveiller symptômes et bilan hépatique et arrêter selon les seuils de la notice. — DailyMed, set_id 93252cc8-c8d4-401b-bde5-ca8a3b57651e
- Mise en garde majeure · Elle peut provoquer neuropathie périphérique, convulsions et syndrome lupique ; administrer de la pyridoxine aux personnes à risque de neuropathie. — DailyMed, set_id 93252cc8-c8d4-401b-bde5-ca8a3b57651e
- Elle peut provoquer des réactions cutanées sévères, notamment SJS, TEN, DRESS et PEAG ; arrêter immédiatement en cas de suspicion. Un syndrome cérébelleux a été rapporté, surtout en cas de maladie rénale chronique. — DailyMed, set_id 93252cc8-c8d4-401b-bde5-ca8a3b57651e
Interactions médicamenteuses
- SévèreAlcool
Mécanisme: Il augmente le risque d’hépatotoxicité.
Recommandation: Éviter l’alcool et surveiller la fonction hépatique.
DailyMed, set_id 93252cc8-c8d4-401b-bde5-ca8a3b57651e
- SévèrePhénytoïne ou carbamazépine
Mécanisme: L’isoniazide peut augmenter leurs concentrations et leur toxicité.
Recommandation: Surveiller les concentrations et les symptômes neurologiques et adapter.
DailyMed, set_id 93252cc8-c8d4-401b-bde5-ca8a3b57651e
- ModéréeAliments riches en histamine ou tyramine
Mécanisme: Ils peuvent provoquer céphalées, palpitations ou bouffées vasomotrices.
Recommandation: Éviter les excès et consulter en cas de symptômes.
DailyMed, set_id 93252cc8-c8d4-401b-bde5-ca8a3b57651e
Effets indésirables
Communs (≥1%)
Élévation des transaminases, neuropathie périphérique, nausées et éruption
Rares mais graves
Hépatite fulminante, convulsions, agranulocytose, syndrome cérébelleux et réactions cutanées sévères
Grossesse et allaitement
Utiliser pour une tuberculose active pendant la grossesse lorsque le bénéfice justifie le risque. L’allaitement ne doit pas être déconseillé à cause de l’isoniazide, mais les concentrations dans le lait ne permettent ni de prévenir ni de traiter la tuberculose du nourrisson.
Bibliographie récente (PubMed)
Tuberculosis (TB) remains the foremost cause of death by an infectious disease globally. Multidrug-resistant or rifampicin-resistant TB (MDR/RR-TB; resistance to rifampicin and isoniazid, or rifampicin alone) is a burgeoning public health challenge in several parts of the world, and especially Eastern Europe, Russia, Asia and sub-Saharan Africa. Pre-extensively drug-resistant TB (pre-XDR-TB) refers to MDR/RR-TB that is also resistant to a fluoroquinolone, and extensively drug-resistant TB (XDR-TB) isolates are additionally resistant to other key drugs such as bedaquiline and/or linezolid. Collectively, these subgroups are referred to as drug-resistant TB (DR-TB). All forms of DR-TB can be as transmissible as rifampicin-susceptible TB; however, it is more difficult to diagnose, is associated with higher mortality and morbidity, and higher rates of post-TB lung damage. The various forms of DR-TB often consume >50% of national TB budgets despite comprising <5-10% of the total TB case-load. The past decade has seen a dramatic change in the DR-TB treatment landscape with the introduction of new diagnostics and therapeutic agents. However, there is limited guidance on understanding and managing various aspects of this complex entity, including the pathogenesis, transmission, diagnosis, management and prevention of MDR-TB and XDR-TB, especially at the primary care physician level.
One of predominant contributors to global mortality is tuberculosis (TB), an infection caused by Mycobacterium tuberculosis (MTB). Inappropriate and ineffectual treatment can lead to the development of drug-resistant TB. One of the most common forms of drug-resistant TB is multidrug-resistant tuberculosis (MDR-TB), caused by mutations in the rpoB and katG genes that lead to resistance to anti-TB drugs, rifampicin (RIF) and isoniazid (INH), respectively. Although culturing remains the gold standard, it is not rapid thereby delaying potential treatment and potentially increasing the incidence of MDR-TB. In contrast, molecular techniques provide a highly sensitive and specific alternative. This review discusses the classification of biomarkers used to detect MDR-TB, some of the commonly used anti-TB drugs, and DNA mutations in MTB that lead to anti-TB resistance. The objective of this review is to increase awareness of the need for rapid and precise detection of MDR-TB cases to decrease morbidity and mortality of this infectious disease worldwide.
Tuberculosis (TB) is a global health challenge and one of the leading causes of death worldwide. In the last decade, the TB treatment landscape has dramatically changed. After long years of stagnation, new compounds entered the market (bedaquiline, delamanid, and pretomanid) and phase III clinical trials have shown promising results towards shortening duration of treatment for both drug-susceptible (Study 31/A5349, TRUNCATE-TB, and SHINE) and drug-resistant TB (STREAM, NiX-TB, ZeNix, and TB-PRACTECAL). Dose optimization of rifamycins and repurposed drugs has also brought hopes of further development of safe and effective regimens. Consequently, international and WHO clinical guidelines have been updated multiple times in the last years to keep pace with these advances. This narrative review aims to summarize the state-of-the-art on treatment of drug-susceptible and drug-resistant TB, as well as recent trial results and an overview of ongoing clinical trials. A non-systematic literature review was conducted in PubMed and MEDLINE, focusing on the treatment of TB. Ongoing clinical trials were listed according to the authors' knowledge and completed consulting clinicaltrials.gov and other publicly available websites (www.resisttb.org/clinical-trials-progress-report, www.newtbdrugs.org/pipeline/trials). This review summarizes the recent, major changes in the landscape for drug-susceptible and drug-resistant treatment, with a specific focus on their potential impact on patient outcomes and programmatic TB management. Moreover, insights in host-directed therapies, and advances in pharmacokinetics and pharmacogenomics are discussed. A thorough outline of ongoing therapeutic clinical trials is presented, highlighting different approaches and goals in current TB clinical research. Future research should be directed to individualize regimens and protect these recent breakthroughs by preventing and identifying the selection of drug resistance and providing widespread, affordabl
Tuberculosis (TB) affects more than 10 million people each year. We have contested this burden with a paradoxically slow development of treatments, as compared to other infectious diseases. This review aims to update health care professionals on the last developments for the management of TB. The combination of drugs established more than 40years ago is still adequate to cure most people affected by TB. However, with the generalisation of regimens based on rifampicin and isoniazid for (only) 6months, resistance emerged. Resistant cases needed long treatments based on injectable drugs. Now, after an exciting decade of research, we can treat resistant TB with oral regimens based on bedaquiline, nitroimidazoles, and linezolid for (only) 6months, and we may soon break the 6-month barrier for treatment duration. However, these improvements are not enough to end TB without an engagement of people affected and their communities to achieve adherence to treatment, transmission control, and improve socioeconomic determinants of health.
Targeted next-generation sequencing (NGS) can rapidly and simultaneously detect mutations associated with resistance to tuberculosis drugs across multiple gene targets. The use of targeted NGS to diagnose drug-resistant tuberculosis, as described in publicly available data, has not been comprehensively reviewed. We aimed to identify targeted NGS assays that diagnose drug-resistant tuberculosis, determine how widely this technology has been used, and assess the diagnostic accuracy of these assays. In this systematic review and meta-analysis, we searched MEDLINE, Embase, Cochrane Library, Web of Science Core Collection, Global Index Medicus, Google Scholar, ClinicalTrials.gov, and the WHO International Clinical Trials Registry Platform for published and unpublished reports on targeted NGS for drug-resistant tuberculosis from Jan 1, 2005, to Oct 14, 2022, with updates to our search in Embase and Google Scholar until Feb 13, 2024. Studies eligible for the systematic review described targeted NGS approaches to predict drug resistance in Mycobacterium tuberculosis infections using primary samples, reference strain collections, or cultured isolates from individuals with presumed or confirmed tuberculosis. Our search had no limitations on study type or language, although only reports in English, German, and French were screened for eligibility. For the meta-analysis, we included test accuracy studies that used any reference standard, and we assessed risk of bias using the Quality Assessment of Diagnostic Accuracy Studies-2 tool. The primary outcomes for the meta-analysis were sensitivity and specificity of targeted NGS to diagnose drug-resistant tuberculosis compared to phenotypic and genotypic drug susceptibility testing. We used a Bayesian bivariate model to generate summary receiver operating characteristic plots and diagnostic accuracy measures, overall and stratified by drug and sample type. This study is registered with PROSPERO, CRD42022368707. We identified and scre