Cannabis Drug Interactions

Potential increase in apixaban exposure, raising bleeding risk. Less well-characterized than warfarin interaction due to lack of INR monitoring.

Potential increase in bleeding risk due to elevated rivaroxaban levels.

Increased sedation, somnolence, and ataxia. This interaction was identified in Epidiolex clinical trials and is the most well-characterized CBD drug interaction. Paradoxically, the elevated norclobazam may contribute to enhanced seizure control.

Phenytoin toxicity: nystagmus, ataxia, diplopia, cognitive impairment, and at very high levels, cardiac arrhythmias.

Elevated liver enzymes observed in clinical trials. Also additive CNS depression (cognitive slowing, somnolence).

Reduced cannabinoid efficacy. Patients on carbamazepine may require higher CBD/THC doses to achieve therapeutic effect.

Potential for increased SSRI plasma levels and serotonergic effects. Theoretical serotonin syndrome risk at high doses (rare). May also enhance antidepressant effect through complementary mechanisms.

TCA toxicity: anticholinergic effects (dry mouth, urinary retention, constipation), sedation, QTc prolongation, and at toxic levels, cardiac arrhythmias.

Potential worsening of psychotic symptoms. Additive QTc prolongation risk.

Enhanced sedation, respiratory depression, cognitive impairment, and psychomotor impairment. Risk of falls, particularly in elderly patients.

Excessive sedation, next-day impairment, increased fall risk, complex sleep behaviors.

Additive respiratory depression (primary concern), sedation, and cognitive impairment. Potential for opioid-sparing effect at lower doses. Methadone QTc prolongation risk increased.

Elevated statin plasma levels, increasing risk of myopathy and rhabdomyolysis.

THC may transiently increase heart rate and blood pressure, opposing beta-blocker effects. Potential for increased beta-blocker side effects (bradycardia, hypotension) with CBD co-administration.

Potential digoxin toxicity (nausea, visual disturbances, arrhythmias). Narrow therapeutic index drug.

Increased cannabinoid exposure, potentially enhancing both therapeutic and adverse effects (sedation, psychoactivity with THC).

Substantially reduced cannabinoid efficacy. Patients may lose therapeutic benefit during rifampin treatment.

Potential increase in docetaxel exposure, increasing myelosuppression and neurotoxicity risk.

Substantially increased cannabinoid exposure. Enhanced therapeutic and adverse effects. Potential for increased PI toxicity with CBD co-administration.

Additive tachycardia and blood pressure elevation. May increase anxiety and psychosis risk. Unpredictable effects on ADHD symptoms.

Significantly enhanced impairment of driving ability, reaction time, and cognitive function. "Greening out" (acute cannabis toxicity) more likely with concurrent alcohol use.

Potential lithium toxicity: tremor, polyuria, cognitive impairment, and at high levels, seizures and cardiac arrhythmias.

Reduced theophylline efficacy (loss of bronchodilation). If cannabis smoking is stopped, theophylline levels may rise into toxic range.