ReviewThe American journal of pathology2026
Understanding How Alcohol Induces Human Acute Alcoholic Pancreatitis.
Review in The American journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Fear of disease progression and its associated factors in patients with acute pancreatitis: a cross-sectional study.BMC gastroenterology · 2026Article
- Approach to the Patient With Pancreatogenic Diabetes.The Journal of clinical endocrinology and metabolism · 2026Review
- Restoring redox homeostasis through S-adenosyl-L-methionine and B-vitamins co-supplementation alleviates ethanol induced hepato-pancreatic injury by regulating glutathione biosynthesis in C57BL/6J mice.Frontiers in pharmacology · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Why only a minority of heavy alcohol drinkers develop acute alcoholic pancreatitis has been a puzzle. In this review, the sparse data available from published studies were collected and, based on them, a hypothesis was formed. Long-term high alcohol consumption results in lowered cholecystokinin and cholinergic stimulus of the pancreas, and causes concentration and acidification of pancreatic fluid, predisposing to protein secretion. Early during the withdrawal period when returning to a normal or high-fat nonalcoholic diet, there is a relative hyperstimulation of the pancreas, a well-established mechanism that results in experimental acute pancreatitis. Lower, physiological stimulation is enough to start acute pancreatitis, when the secretions cause temporary obstruction in the duct system. The stimulation against temporary obstruction results in experimental acute pancreatitis. Finally, the magnitude of alcohol-induced deficits in acinar cell defense mechanisms determines the onset of pancreatitis.
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Registered trials
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