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Delayed Treatment of Misdiagnosed Mushroom Poisoning: Do Organic Anion Transporting Polypeptide Substrates Matter?
Zanina Pereska1, Dushan Petkovski2, Valentina Arsova3
1Medical Faculty, University Clinic of Toxicology, Ss. Cyril and Methodius University, Skopje, North Macedonia.
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.
Insights
Wild mushroom poisoning caused severe liver and kidney damage. Early treatment with acetylcysteine and silymarin, alongside managing drug interactions, led to patient recovery.
Area of Science:
- Toxicology
- Pharmacology
- Hepatology
Background:
- Presents a case of a middle-aged male with pre-existing type 2 diabetes, hypertension, and coronary bypass who ingested wild mushrooms.
- Initial misdiagnosis as infectious enterocolitis led to delayed appropriate treatment.
- The patient developed hepatorenal syndrome, necessitating transfer to a specialized clinic.
Purpose of the Study:
- To describe a case of amatoxin poisoning complicated by drug-transporter interactions.
- To highlight the importance of considering drug interactions in patients with mushroom poisoning.
- To evaluate the efficacy of acetylcysteine and silymarin in treating severe amatoxin toxicity.
Main Methods:
- The patient received intravenous acetylcysteine (double regimen), oral silymarin (600 mg/d), and supportive care.
- Treatment was initiated after diagnosis of hepatorenal syndrome and severe liver dysfunction (MELD score 30).
- Simultaneous exposure to amatoxin and chronic cardiovascular medications (statins, beta-blockers, aspirin) was noted.
Main Results:
- The patient recovered within 10 days, with normalization of transaminases after 3 months.
- Demonstrated successful management of severe hepatorenal dysfunction secondary to mushroom poisoning.
- Underscored the potential for drug-transporter interactions between toxins and chronic medications.
Conclusions:
- Intravenous acetylcysteine and oral silymarin, combined with supportive therapy, can be effective in managing severe amatoxin poisoning.
- Understanding transporter-related drug interactions is crucial for optimizing treatment and improving survival in such cases.
- Further research into alternative inhibitors of amatoxin uptake and OATP substrates is warranted.
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