rifampicin
Fuentes regulatorias consultadas
Indicaciones aprobadas
- Tuberculosis activa sensible, siempre en combinación; otras infecciones por microorganismos sensibles según ficha.
Contraindicaciones
Absolutas
- Hipersensibilidad a rifampicina o a sus excipientes; ictericia; uso concomitante de saquinavir/ritonavir u otras combinaciones expresamente contraindicadas por inducción intensa.
Advertencias clínicas
- Puede causar hepatotoxicidad grave; controla síntomas y pruebas hepáticas y suspende si aparece lesión. — CIMA/AEMPS, ficha técnica 49034
- Las pautas intermitentes pueden causar trombocitopenia, hemólisis, shock o insuficiencia renal inmunológica; retira y no reexpongas tras una reacción grave. — CIMA/AEMPS, ficha técnica 49034
- Colorea de naranja rojizo orina, lágrimas y otros fluidos; puede teñir lentes de contacto. — CIMA/AEMPS, ficha técnica 49034
Interacciones medicamentosas
- SeveraAnticonceptivos hormonales
Mecanismo: La inducción enzimática reduce su eficacia.
Recomendación: Usa anticoncepción no hormonal adicional durante el tratamiento y el periodo indicado después.
CIMA/AEMPS, ficha técnica 49034
- SeveraWarfarina, antirretrovirales, azoles, anticonvulsivos o inmunosupresores
Mecanismo: La inducción potente de CYP/P-gp reduce concentraciones y efecto de numerosos sustratos.
Recomendación: Revisa cada combinación, controla INR/concentraciones o respuesta y ajusta.
CIMA/AEMPS, ficha técnica 49034
Eventos adversos
Comunes (≥1%)
Náuseas, dolor abdominal, erupción y coloración naranja de fluidos
Raros pero graves
Hepatitis, trombocitopenia, hemólisis, shock e insuficiencia renal
Embarazo y lactancia
Usa en embarazo cuando esté indicado para tuberculosis; cerca del parto puede aumentar hemorragia materna/neonatal y puede requerir vitamina K. Valora lactancia según beneficio y riesgo.
Bibliografía reciente (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.
Tuberculous meningitis is a devastating brain infection that is caused by Mycobacterium tuberculosis and is notoriously difficult to diagnose and treat. New technologies characterising the transcriptome, proteome, and metabolome have identified new molecules and pathways associated with tuberculous meningitis severity and poor outcomes that could offer novel diagnostic and therapeutic targets. The next-generation GeneXpert MTB/RIF Ultra assay, when used on CSF, offers diagnostic sensitivity for tuberculous meningitis of approximately 70%, although it is not widely available and a negative result cannot rule out tuberculous meningitis. Small trials indicate that clinical outcomes might be improved with increased doses of rifampicin, the addition of linezolid or fluoroquinolones to standard antituberculosis therapy, or treatment with adjunctive aspirin combined with corticosteroids. Large phase 3 clinical trials are underway worldwide to address these and other questions concerning the optimal management of tuberculous meningitis; these studies also form a platform for studying pathogenesis and identifying novel diagnostic and treatment strategies, by allowing the implementation of new genomic, transcriptomic, proteomic, and metabolomic technologies in nested substudies.
This paper discusses the mechanisms of S. aureus drug resistance including: (1) introduction. (2) resistance to beta-lactam antibiotics, with particular emphasis on the mec genes found in the Staphylococcaceae family, the structure and occurrence of SCCmec cassettes, as well as differences in the presence of some virulence genes and its expression in major epidemiological types and clones of HA-MRSA, CA-MRSA, and LA-MRSA strains. Other mechanisms of resistance to beta-lactam antibiotics will also be discussed, such as mutations in the gdpP gene, BORSA or MODSA phenotypes, as well as resistance to ceftobiprole and ceftaroline. (3) Resistance to glycopeptides (VRSA, VISA, hVISA strains, vancomycin tolerance). (4) Resistance to oxazolidinones (mutational and enzymatic resistance to linezolid). (5) Resistance to MLS-B (macrolides, lincosamides, ketolides, and streptogramin B). (6) Aminoglycosides and spectinomicin, including resistance genes, their regulation and localization (plasmids, transposons, class I integrons, SCCmec), and types and spectrum of enzymes that inactivate aminoglycosides. (7). Fluoroquinolones (8) Tetracyclines, including the mechanisms of active protection of the drug target site and active efflux of the drug from the bacterial cell. (9) Mupirocin. (10) Fusidic acid. (11) Daptomycin. (12) Resistance to other antibiotics and chemioterapeutics (e.g., streptogramins A, quinupristin/dalfopristin, chloramphenicol, rifampicin, fosfomycin, trimethoprim) (13) Molecular epidemiology of MRSA.
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. Limited information indicates that there are low levels of rifampin in breastmilk that would not be expected to cause any adverse effects in breastfed infants. The amount of rifampin in milk is insufficient to treat tuberculosis in the breastfed infant. The Centers for Disease Control and Prevention and other professional organizations state that breastfeeding should not be discouraged in women taking rifampin.[1-3] Breastmilk may be stained a yellow, orange, red or brown color.