Antituberculous antibiotic
ATC code: J04AB02 (J04AB02)
Brand names
Rifadin, Rimactane, Rifamate
Inhibits bacterial DNA-dependent RNA polymerase, blocks RNA synthesis in mycobacteria and many other pathogens. Strongest known CYP3A4, CYP2C9, P-gp inducer – reduces concentrations of dozens of drugs from OCs to warfarin.
First line
Rifampicin is a mandatory component of the standard regimen for drug-susceptible tuberculosis. 2022 and /CDC/ATS 2016 recommend a 6-month regimen: 2-month intensive phase with isoniazid + rifampicin + pyrazinamide + ethambutol (HRZE), and 4-month continuation phase with isoniazid + rifampicin (HR). Rifampicin dose is 10 mg/kg/day (usually 600 mg). The alternative 4-month rifapentine-based regimen (HPMZ) is suitable for selected patients per WHO 2022.
Therapy is administered by tuberculosis specialists under DOT supervision. In HIV-coinfected patients, rifampicin is switched to rifabutin when a compatible ART regimen cannot be selected.
Sources
First line
Rifampicin 600 mg daily for 4 months (4R) is one of the preferred regimens for latent tuberculosis infection. CDC 2020 lists 4R alongside 3HP (isoniazid + rifapentine for 12 weeks) and 3HR (isoniazid + rifampicin for 3 months), favoring these over isoniazid monotherapy for 9 months in terms of tolerability and completion. Efficacy is 80-90% with proper course completion.
First line
Rifampicin 600 mg twice daily for 2 days is a first-line option for post-exposure meningococcal prophylaxis in close contacts. NG240 2024 ranks rifampicin alongside ceftriaxone IM as a single dose and ciprofloxacin 500 mg orally as a single dose. Prophylaxis is started within 24 hours of confirming the diagnosis in the index case.
Adjunct
Rifampicin 300-450 mg twice daily is added to base therapy (vancomycin, cefazolin, levofloxacin) in staphylococcal periprosthetic infections after surgical debridement. 2013 includes rifampicin in DAIR (debridement, antibiotics, implant retention) regimens and for patients with retained prostheses. Its advantage is activity against staphylococcal biofilms. Not used as monotherapy due to rapid selection of resistance.
The drug is promoted for these uses outside international guidelines. Each entry below is analyzed against AEMPS, FDA, EMA, Cochrane and major RCTs.
Not recommended
For acute uncomplicated viral upper respiratory infection, rifampicin is not prescribed. An antimycobacterial agent with a long list of significant drug interactions (CYP3A4/CYP2C9 induction) is used only under strict indications. Prescribing rifampicin for URI is an example of irrational therapy and increases the risk of selecting rifampicin-resistant M. tuberculosis strains in the population.
Rifampicin induces CYP3A4 and accelerates inactivation of 25(OH)D and 1,25(OH)2D, leading to vitamin D deficiency in 30-70% of patients on prolonged therapy. Check serum 25(OH)D before starting and every 3 months on long therapy. At levels below 30 ng/mL, prescribe cholecalciferol 2000-4000 IU/day.
Rifampicin accelerates vitamin K metabolism through hepatic enzyme induction. Newborns of mothers who received rifampicin in the third trimester have an increased risk of hemorrhagic disease of the newborn. Vitamin K1 10 mg intramuscularly is given to the mother 24 hours before delivery and to the newborn in the first hours of life.
Rifampicin in TB regimens is combined with isoniazid, which displaces pyridoxine. In patients at risk of neuropathy (diabetes, HIV, chronic kidney disease, alcohol use, pregnancy), pyridoxine 25-50 mg/day is added to prevent peripheral neuropathy.
21 pairs found. Sorted from critical to minor.
Mechanism
Rifampicin is a potent CYP3A4 inducer. Dronedarone plasma levels fall by 80% and antiarrhythmic effect is lost. Multaq Section 4.3 specifically lists rifampicin.
Symptoms
Recurrence of atrial fibrillation symptoms: palpitations, irregular pulse, fatigue, dyspnoea. Possible rhythm breakthroughs requiring admission.
Management
The combination is not prescribed. For tuberculosis in a patient with atrial fibrillation, switch the antiarrhythmic to amiodarone or perform catheter ablation during anti-TB therapy. Rifampicin is hard to substitute – it remains part of standard first-line regimens.
Mechanism
Rifampicin strongly induces CYP3A4 – the main N-deethylation pathway of amiodarone. Amiodarone and N-desethyl-amiodarone plasma levels fall by about 50%; antiarrhythmic effect weakens.
Symptoms
Atrial fibrillation symptoms return: palpitations, irregular pulse, fatigue, dyspnoea. Rhythm breakthroughs may require admission.
Management
During anti-TB therapy, replace amiodarone with a beta-blocker for rate control or plan catheter ablation. Induction persists for 2 weeks after rifampicin stops – restart amiodarone gradually.
Mechanism
Rifampicin strongly induces CYP3A4 – the main amlodipine metabolic route. Amlodipine plasma levels fall by 80%; the antihypertensive effect practically disappears.
Symptoms
Blood pressure returns to baseline or higher, headache. In angina, episodes reappear. Symptoms develop 1–2 weeks after starting rifampicin.
Management
During anti-TB therapy, replace amlodipine with an ACE-I (enalapril) or a diuretic (hydrochlorothiazide) – their metabolism is less affected by rifampicin. Induction persists for 2 weeks after rifampicin stops – reintroduce amlodipine gradually.
Mechanism
Rifampicin strongly induces CYP3A4 and P-glycoprotein – two apixaban clearance routes. Apixaban plasma levels fall by 50%; anticoagulant effect weakens.
Symptoms
The patient feels nothing. Thromboembolic risk rises: stroke in atrial fibrillation, deep vein thrombosis, pulmonary embolism.
Management
The combination is not prescribed. Alternative anticoagulants: warfarin with INR monitoring or low molecular weight heparin for short courses. Induction persists for 2 weeks after rifampicin stops.
Sources
Mechanism
Rifampicin strongly induces CYP3A4 and the OATP1B1 transporter – two atorvastatin clearance routes. Atorvastatin plasma levels fall by 80%; lipid-lowering effect weakens.
Symptoms
The patient feels nothing. Laboratory: cholesterol and total cholesterol rise. In high cardiovascular risk patients, myocardial infarction and stroke risk increase.
Management
During anti-TB therapy, switch to pravastatin (less induction-sensitive metabolism) or temporarily stop the statin for a short course. Induction persists for 2 weeks after rifampicin stops.
Mechanism
Rifampicin strongly induces CYP3A4 and P-glycoprotein. Cyclosporine plasma levels fall by 50–70%; immunosuppression is lost, raising transplant rejection risk.
Symptoms
Rejection symptoms depend on the organ: fever, graft tenderness, rising creatinine (kidney), jaundice (liver), dyspnoea (heart, lungs). Symptoms appear 1–3 weeks after starting rifampicin.
Management
Avoid the combination. Alternative anti-TB drug: rifabutin (weaker CYP3A4 induction) with cyclosporine dose titration. If rifampicin is unavoidable, raise cyclosporine 2- to 3-fold with trough (C0) twice weekly.
Sources
Mechanism
Rifampicin strongly induces P-glycoprotein, the main dabigatran clearance route. Dabigatran plasma levels fall by 66%; stroke prevention in atrial fibrillation or VTE treatment fails.
Symptoms
The patient feels nothing. Stroke risk in atrial fibrillation rises, as do deep vein thrombosis and pulmonary embolism risks.
Management
The combination is not prescribed. Alternative anticoagulants: warfarin with INR monitoring or low molecular weight heparin for short courses. Induction persists for 2 weeks after rifampicin stops.
Mechanism
Rifampicin is the most potent available CYP3A4 inducer. Diltiazem plasma levels fall 5- to 10-fold. The antianginal and antihypertensive effect practically disappears.
Symptoms
Return of hypertension, anginal episodes in ischaemic heart disease. Rate control in atrial fibrillation is lost.
Management
During anti-TB therapy, replace diltiazem with amlodipine (at higher than usual dose, since induction also affects it) or an ACE-I + beta-blocker. After rifampicin stops, induction persists for 2 weeks.
Mechanism
Rifampicin is the most potent CYP3A4 inducer in clinical practice. Ethinylestradiol plasma levels fall by 40–60% within the first week. Combined oral contraceptive efficacy drops to chance.
Symptoms
Breakthrough bleeding, missed periods, unplanned pregnancy. The patient feels no symptoms at the moment of dosing – the problem becomes apparent only later.
Management
Switch hormonal contraception to non-hormonal methods (copper IUD or barrier methods) for the duration of rifampicin and an additional 4 weeks after stopping. Alternatives: depot progesterone or a levonorgestrel IUD (minimal CYP3A4 effect).
Mechanism
Rifampicin strongly induces CYP3A4, which partly metabolises fluconazole. Fluconazole plasma levels fall by 25%; antifungal efficacy decreases.
Symptoms
Recurrence of mycosis symptoms: ongoing fever, skin or mucosal lesions; in immunocompromised patients, risk of systemic mycosis progression.
Management
When combined, increase fluconazole by 50–100% with efficacy monitoring. Alternative antifungal during anti-TB therapy: echinocandins (micafungin, caspofungin; no CYP3A4 dependence).
Mechanism
Rifampicin strongly induces CYP3A4 – the main haloperidol metabolic route. Haloperidol plasma levels fall by 70%; antipsychotic effect weakens.
Symptoms
Return of positive symptoms: hallucinations, delusions, agitation. In schizophrenia: risk of acute relapse.
Management
During anti-TB therapy, increase haloperidol 2- to 3-fold with clinical monitoring. Alternative antipsychotics without CYP3A4 dependence: olanzapine or aripiprazole.
Mechanism
Dual mechanism. Rifampicin strongly induces CYP3A4, which partly metabolises ketoconazole. Ketoconazole plasma levels fall by 50–80%; antifungal efficacy is lost.
Symptoms
Recurrence of mycosis symptoms: ongoing fever, skin or mucosal lesions; in immunocompromised patients, risk of systemic mycosis progression.
Management
The combination is not prescribed. Alternative antifungal during anti-TB therapy: echinocandins (micafungin, caspofungin; resistant to CYP3A4 induction) or terbinafine for dermatophytosis.
Mechanism
Rifampicin is the most potent CYP3A4 inducer available. Quetiapine plasma levels fall 5- to 8-fold – clinical inefficacy of the antipsychotic.
Symptoms
Return of positive symptoms: hallucinations, delusions, agitation. In bipolar disorder: manic episode risk.
Management
During anti-TB therapy, increase quetiapine 5-fold with clinical monitoring. Alternative antipsychotics without CYP3A4 dependence: olanzapine or aripiprazole. Alternative anti-TB drug: rifabutin (weaker CYP3A4 induction).
Mechanism
Rifampicin strongly induces CYP3A4 – the main ritonavir metabolic route. Ritonavir plasma levels fall by 35%, reducing its ability to boost other antiretrovirals. Antiretroviral efficacy is lost.
Symptoms
The patient feels nothing. Laboratory: rising HIV viral load. Risk of antiretroviral resistance.
Management
Avoid the combination. Alternative anti-TB drug in HIV patients: rifabutin (weaker CYP3A4 induction). Alternative ritonavir-free regimens: dolutegravir + tenofovir + emtricitabine (no booster needed).
Mechanism
Rifampicin strongly induces CYP3A4 and P-glycoprotein – two rivaroxaban clearance routes. Rivaroxaban plasma levels fall by 50%; anticoagulant effect weakens.
Symptoms
The patient feels nothing. Thromboembolic risk rises: stroke in atrial fibrillation, deep vein thrombosis, pulmonary embolism.
Management
The combination is not prescribed. Alternative anticoagulants: warfarin with INR monitoring (rifampicin also weakens warfarin, but titration is easier) or low molecular weight heparin for short courses. Induction persists for 2 weeks after rifampicin stops.
Mechanism
Rifampicin strongly induces CYP3A4 and the OATP1B1 transporter – the routes of simvastatin activation and hepatocyte uptake. Simvastatin plasma levels fall by 87%; lipid-lowering effect practically disappears.
Symptoms
The patient feels nothing. Laboratory: cholesterol and total cholesterol rise. In high cardiovascular risk patients, myocardial infarction and stroke risk increase.
Management
During anti-TB therapy, switch simvastatin to pravastatin (less induction-sensitive metabolism). Induction persists for 2 weeks after rifampicin stops – reintroduce simvastatin gradually.
Mechanism
Rifampicin is the strongest known CYP3A4, CYP2C9, and P-glycoprotein inducer. Tacrolimus is a CYP3A4 and P-gp substrate with a narrow therapeutic window (target trough 5–15 ng/mL). Tacrolimus exposure drops 3- to 7-fold; acute graft rejection risk is high.
Symptoms
Graft rejection on biochemistry and biopsy. There are no symptoms from reduced tacrolimus exposure itself – the loss of immunosuppression is silent.
Management
Avoid the combination. For tuberculosis in transplant recipients use rifampicin-free regimens (isoniazid + ethambutol + pyrazinamide) or rifabutin (much weaker CYP3A4 induction). If rifampicin is essential – empirically increase tacrolimus 2- to 5-fold with trough monitoring every 2–3 days for the first 2 weeks, then weekly.
Mechanism
Rifampicin strongly induces CYP1A2 – the main theophylline metabolic route. Theophylline plasma levels fall by 30–50%; bronchodilator effect weakens.
Symptoms
Recurrence of asthma or COPD symptoms: dyspnoea, wheezing, need for additional short-acting β2-agonist doses.
Management
During anti-TB therapy, increase theophylline 1.5- to 2-fold with level monitoring at 1 week. Alternative bronchodilators: long-acting inhaled β2-agonists (formoterol, salmeterol) with anticholinergics.
Mechanism
Rifampicin strongly induces CYP2C9, the main S-warfarin clearance route. Warfarin plasma levels fall by 50–70% over 2–3 weeks; anticoagulant effect weakens.
Symptoms
INR drops below target. Clinically: increased thromboembolic risk – deep vein thrombosis, pulmonary embolism, ischaemic stroke.
Management
For short rifampicin courses (up to 2 weeks), check INR every 3–5 days and titrate warfarin to effect. For prolonged anti-TB therapy, warfarin dose typically rises 2- to 3-fold. After stopping rifampicin, induction persists for another 2 weeks – return warfarin to baseline dose gradually.
Mechanism
Rifampicin induces CYP3A4, modestly lowering bisoprolol plasma levels (bisoprolol is metabolised 50% via CYP3A4 and 50% renally). The effect is weaker than for fully CYP-dependent beta-blockers.
Symptoms
Gradual blood pressure rise or return of anginal symptoms 2–3 weeks after starting rifampicin. In tachyarrhythmias: return of symptoms.
Management
During anti-TB therapy, increase bisoprolol by 50% with blood pressure and pulse monitoring. After rifampicin stops, taper back gradually (induction persists for 2 weeks).
Mechanism
Rifampicin induces enterocyte P-glycoprotein. Digoxin bioavailability falls by 30%, levels drop — risking loss of rate control in atrial fibrillation or worsening of chronic heart failure.
Symptoms
Return of underlying disease: tachycardia in atrial fibrillation, dyspnoea and oedema in chronic heart failure. After rifampicin stops, digoxin levels may rise sharply.
Management
On the combination, check digoxin levels at 2 and 4 weeks after rifampicin start and 2 weeks after rifampicin stops. Digoxin dose is usually raised by 25–50% during rifampicin and returned to baseline afterward. In atrial fibrillation, consider adding a beta-blocker (bisoprolol, metoprolol) for rate control.
Sources
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FDA category C. In humans, rifampicin is used for active TB during pregnancy because untreated TB poses a greater risk to mother and fetus. Newborns of mothers on rifampicin in the third trimester are at risk of postpartum hemorrhage due to vitamin K deficiency – vitamin K is given to both mother and infant. The decision is made jointly with the tuberculosis specialist and obstetrician-gynecologist.
Rifampicin passes into breast milk in small amounts. LactMed classifies it as compatible with breastfeeding during TB treatment. Monitor the infant for jaundice and reduced appetite.
Reference information, not a clinical decision. Discuss feeding pauses or changes with your physician or an IBCLC.
Rifampicin is evaluated for the following indications with varying evidence strength: Latent tuberculosis infection (evidence tier A), Meningococcal prophylaxis for close contacts (evidence tier A), Drug-susceptible tuberculosis (evidence tier A). See the full indication matrix with dosing and citations above on this page.
Common side effects of Rifampicin (≥ 1 in 100): Orange-red discoloration of urine, tears, sweat, sputum (harmless, resolves after discontinuation), Nausea, abdominal discomfort, Transient liver transaminase elevation, Reduced efficacy of hormonal contraceptives. See the Safety section for uncommon and serious reactions.
FDA category C. FDA category C. In humans, rifampicin is used for active TB during pregnancy because untreated TB poses a greater risk to mother and fetus. Newborns of mothers on rifampicin in the third trimester are at risk of postpartum hemorrhage due to vitamin K deficiency – vitamin K is given to both mother and infant. The decision is made jointly with the tuberculosis specialist and obstetrician-gynecologist.
Rifampicin passes into breast milk in small amounts. LactMed classifies it as compatible with breastfeeding during TB treatment. Monitor the infant for jaundice and reduced appetite.
Rifampicin is contraindicated in: Hypersensitivity to rifamycins in history; Active hepatitis or jaundice on prior rifamycin therapy; Concurrent use with drugs critically dependent on CYP3A4: HIV protease inhibitors, voraxapar, simeprevir, apixaban/rivaroxaban without dose adjustment, tacrolimus without monitoring; History of porphyria; Severe hepatic impairment. Full list in the Safety section.
discoloration of urine and other secretions is a normal pharmacologic effect, harmless, and resolves 1-2 days after discontinuation.
rifampicin reduces their efficacy below a reliable threshold. Barrier or non-hormonal methods are required during the course and for 4 weeks after.
the minimum effective rifampicin monotherapy course for LTBI is 4 months. Shorter courses increase the risk of reactivation and resistance.