Case Report: Raw grass carp gallbladder ingestion and acute liver injury
Abstract
Raw grass carp gallbladder ingestion for folk medicinal purposes may cause severe acute liver injury driven by the hepatotoxin 5α-cyprinol sulfate, yet high-dose human poisoning cases remain infrequently documented. We report a 60-year-old male (60 kg body weight) who developed severe intoxication 22 h after consuming six raw gallbladders from grass carps of approximately 1.5 kg each. Nausea, vomiting, abdominal pain and watery diarrhoea occurred within 2 hours of ingestion. Laboratory testing on admission demonstrated extreme hepatocellular injury (ALT 6285 U/L, AST 9321 U/L). Conventional hepatoprotective agents plus pre-hospital haemoperfusion yielded limited biochemical improvement. While admitted to the intensive care unit, the patient received one session of double plasma molecular adsorption system, three sessions of plasma exchange and four sessions of continuous renal replacement therapy (CRRT, CVVHDF modality) alongside comprehensive supportive care. Liver function normalized within 14 hospital days; no acute kidney injury was observed. Complete symptomatic recovery was documented at the 4-week follow-up visit, though longer-term outcomes remain unknown given the limited follow-up duration. Toxin-mediated hepatocyte damage is partially supported by pre-clinical cyprinol-sulfate experimental work; many downstream oxidative, mitochondrial, endoplasmic-reticulum and inflammatory molecular pathways remain hypothetical and are largely extrapolated from unrelated liver-injury models, without direct validation in human carp-gallbladder-poisoning tissue specimens. Biochemical improvement was temporally associated with multimodal extracorporeal purification, but causal therapeutic benefit can’t be proven from this uncontrolled single case; spontaneous hepatic regeneration may also contribute to recovery. This case highlights substantial hazards associated with folk-health beliefs promoting raw fish-gallbladder consumption, emphasising the need for early clinical recognition of fish-gallbladder poisoning.
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BibTeX
@article{xiang2026case,
title = {{Case Report: Raw grass carp gallbladder ingestion and acute liver injury}},
author = {Shizhao Xiang and Zixiang Zheng and Yuying Chen and Yu Du},
journal = {Frontiers in Pharmacology},
year = {2026},
month = nov,
doi = {10.3389/fphar.2026.1925389},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1925389},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Case Report: Raw grass carp gallbladder ingestion and acute liver injury
AU - Shizhao Xiang
AU - Zixiang Zheng
AU - Yuying Chen
AU - Yu Du
PY - 2026
DA - 2026/11/02
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1925389
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1925389
AB - Raw grass carp gallbladder ingestion for folk medicinal purposes may cause severe acute liver injury driven by the hepatotoxin 5α-cyprinol sulfate, yet high-dose human poisoning cases remain infrequently documented. We report a 60-year-old male (60 kg body weight) who developed severe intoxication 22 h after consuming six raw gallbladders from grass carps of approximately 1.5 kg each. Nausea, vomiting, abdominal pain and watery diarrhoea occurred within 2 hours of ingestion. Laboratory testing on admission demonstrated extreme hepatocellular injury (ALT 6285 U/L, AST 9321 U/L). Conventional hepatoprotective agents plus pre-hospital haemoperfusion yielded limited biochemical improvement. While admitted to the intensive care unit, the patient received one session of double plasma molecular adsorption system, three sessions of plasma exchange and four sessions of continuous renal replacement therapy (CRRT, CVVHDF modality) alongside comprehensive supportive care. Liver function normalized within 14 hospital days; no acute kidney injury was observed. Complete symptomatic recovery was documented at the 4-week follow-up visit, though longer-term outcomes remain unknown given the limited follow-up duration. Toxin-mediated hepatocyte damage is partially supported by pre-clinical cyprinol-sulfate experimental work; many downstream oxidative, mitochondrial, endoplasmic-reticulum and inflammatory molecular pathways remain hypothetical and are largely extrapolated from unrelated liver-injury models, without direct validation in human carp-gallbladder-poisoning tissue specimens. Biochemical improvement was temporally associated with multimodal extracorporeal purification, but causal therapeutic benefit can’t be proven from this uncontrolled single case; spontaneous hepatic regeneration may also contribute to recovery. This case highlights substantial hazards associated with folk-health beliefs promoting raw fish-gallbladder consumption, emphasising the need for early clinical recognition of fish-gallbladder poisoning.
SN - 1663-9812
ER -