Clinics and research in hepatology and gastroenterology · 2026
A rare case of stimulant-associated isolated gastric ischemia Presenting with pneumatosis and necrosis, initially mimicking acute pancreatitis.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Mehta Radhika, Lobon Krissie, Jayaram Nikhil Bush
Аннотация
BACKGROUND: Stimulant-associated gastrointestinal ischemia is rare, and isolated gastric involvement without small bowel injury has not been previously described in association with amphetamine-class drugs. Markedly elevated lipase can further obscure the diagnosis by raising clinical suspicion for acute pancreatitis.
CASE PRESENTATION: A 59-year-old male with polysubstance use disorder was found unresponsive and later reported acute epigastric pain. CT demonstrated diffuse gastric pneumatosis and intrahepatic portal venous gas. Markedly elevated lipase (5190 U/L) without radiographic pancreatitis initially prompted consideration of acute pancreatitis; however, CT imaging findings redirected the diagnostic workup. Urine toxicology was positive for amphetamines. CT angiography confirmed gastric mucosal necrosis without vascular occlusion. Endoscopy demonstrated confluent gastric mucosal necrosis with sparing of the antrum and normal duodenum. The patient recovered with supportive care. Serial lipase levels trended down from 5190 U/L at presentation to 2840 U/L on day 2 and 1120 U/L on day 3, paralleling clinical improvement and consistent with a non-pancreatic source.
DISCUSSION: This case expands the spectrum of stimulant-related GI ischemia to include isolated gastric involvement. While an elevated lipase raised initial concern for pancreatitis, it was CT imaging rather than the lipase alone that correctly guided the diagnostic pathway. GI ischemia is an important but underrecognised cause of non-pancreatic hyperlipasaemia.
CONCLUSION: Clinicians should be aware that GI ischemia can cause marked hyperlipasaemia. CT imaging findings rather than lipase levels alone should guide clinical decision-making in patients with stimulant use and acute abdominal pain.
CASE PRESENTATION: A 59-year-old male with polysubstance use disorder was found unresponsive and later reported acute epigastric pain. CT demonstrated diffuse gastric pneumatosis and intrahepatic portal venous gas. Markedly elevated lipase (5190 U/L) without radiographic pancreatitis initially prompted consideration of acute pancreatitis; however, CT imaging findings redirected the diagnostic workup. Urine toxicology was positive for amphetamines. CT angiography confirmed gastric mucosal necrosis without vascular occlusion. Endoscopy demonstrated confluent gastric mucosal necrosis with sparing of the antrum and normal duodenum. The patient recovered with supportive care. Serial lipase levels trended down from 5190 U/L at presentation to 2840 U/L on day 2 and 1120 U/L on day 3, paralleling clinical improvement and consistent with a non-pancreatic source.
DISCUSSION: This case expands the spectrum of stimulant-related GI ischemia to include isolated gastric involvement. While an elevated lipase raised initial concern for pancreatitis, it was CT imaging rather than the lipase alone that correctly guided the diagnostic pathway. GI ischemia is an important but underrecognised cause of non-pancreatic hyperlipasaemia.
CONCLUSION: Clinicians should be aware that GI ischemia can cause marked hyperlipasaemia. CT imaging findings rather than lipase levels alone should guide clinical decision-making in patients with stimulant use and acute abdominal pain.