Delayed Treatment of Misdiagnosed Mushroom Poisoning: Do Organic Anion Transporting Polypeptide Substrates Matter?

Abstract

A middle-aged male was admitted to the clinic 4 d after ingestion of wild mushrooms. His medical history included type 2 diabetes, hypertension, and coronary bypass. Initially misdiagnosed with infectious enterocolitis, the patient was treated as an outpatient with intravenous fluids while continuing his chronic medications (i.e., statins, beta-blockers, and aspirin). On Day 3, blood tests confirmed hepatorenal syndrome, and the patient was transferred to the clinic. On admission, he was alert with a blood pressure of 100/60 mmHg, heart rate of 100 beats/min, sinus rhythm, right upper quadrant pain, and jaundice. Lab results showed thrombocytopenia, severe hepatorenal dysfunction, prolonged prothrombin time (29.3 s), and a Model for End-Stage Liver Disease score of 30. For 3 d, the patient was simultaneously exposed to amatoxin and chronic cardiovascular medications, both substrates for the same transporters. Treatment was adjusted to intravenous acetylcysteine (double regimen), oral silymarin (600 mg/d), and supportive therapy. The patient recovered within 10 d, with transaminases normalizing after 3 mo. Understanding transporter-related drug interactions and patient-specific metabolic differences may improve future management strategies and patient survival. Further research is needed on alternative inhibitors of amatoxin uptake and competitive organic anion-transporting polypeptide substrates to expand treatment options.