Dynamic myocardial injury and variable hallucination latency in Psilocybe keralensis poisoning: a molecularly confirmed case series from China
Zhifan He, Rui Tang, Min Feng, Xiaohui Li, Changhong Zhang, Jing Li
Clinical Toxicology September 15, 2025 DOI: 10.1080/15563650.2025.2552438 via OpenAlex
Summary
AI-generated from the abstractFour patients in Chengdu, China, were poisoned after eating 16–90 g of wild mushrooms misidentified as edible but later confirmed as Psilocybe keralensis. Symptoms began within 5–20 minutes, with hallucinations starting between 10 and 180 minutes. All developed hypertension, one with a rapid rise to 182/110 mmHg and evidence of myocardial injury (peak cardiac troponin T 188.70 pg/mL) and transient skeletal muscle involvement. Supportive treatment led to full recovery. The authors note that altered myocardial biomarkers signal potential cardiovascular risks and recommend cardiac monitoring for high-risk patients in future psilocybin research, and that wild mushroom foraging should be avoided.
Study at a glance
| Characteristics | Case series Case report Peer reviewed |
|---|---|
| Sample size | 4 |
| Population | Patients who ingested Psilocybe keralensis mushrooms in Chengdu, China |
| Interventions | supportive treatment (gastric lavage intravenous ranitidine fluid therapy) |
| Dose | 16–90 g of wild mushrooms |
| Citations | 1 |
| Key finding | Psilocybe keralensis poisoning caused hypertension and myocardial injury in all four patients, with one showing elevated cardiac troponin T. |
Abstract
Introduction Psychoactive Psilocybe spp. mushrooms pose significant public health risks. We report a cluster of Psilocybe keralensis poisonings in Chengdu, China, highlighting its unique clinical features and cardiovascular complications.Case Series Four patients ingested 16–90 g of wild mushrooms (misidentified as an edible species, but later molecularly confirmed as Psilocybe keralensis). Prodromal symptoms (e.g., dizziness) emerged within 5–20 min, but the onset of hallucinations varied widely (10–180 min). All patients developed hypertension (systolic blood pressure >150 mmHg), with one patient exhibiting rapid blood pressure elevation to 182/110 mmHg at 4 h post-ingestion, which was accompanied by evidence of myocardial injury (peak cardiac troponin T concentration 188.70 pg/mL [reference range <14 pg/mL]) and transient mild skeletal muscle involvement (peaked myoglobin concentration 127.3 ng/mL, which normalized by day 2). Supportive treatment (gastric lavage, intravenous ranitidine, and fluid therapy) led to full recovery without sequelae.Discussion We observed altered myocardial biomarkers following Psilocybe keralensis poisoning, which signals potential cardiovascular risks.Conclusion Future clinical research on psilocybin should prioritize cardiovascular comorbidity screening and implement cardiac monitoring for high-risk patients. We believe that public health education should emphasize that both traditional morphological identification methods and folk-based toxicity testing lack scientific basis; it must advocate avoidance of wild mushroom foraging, which is the most reliable prevention strategy.