While alcohol and its by-products alone do not directly cause this disease, they can predispose the pancreas to damage from otherwise benign agents. As a result, one of the main strategies to prevent recurrent attacks involve providing alcohol cessation counseling and strategies to patients. Due to inability to explain the pathogenesis of alcoholic pancreatitis by theories as mentioned above the focus was directed to pancreatic acinar cells. It is now believed that acinar cells are capable of metabolizing alcohol and the toxic effect may predispose the gland to injury in the presence of an appropriate triggering factor. The characteristics of pancreatic stellate cells showing the involvement of acinar cells in pancreatic fibrosis may be another possible link . It is speculated that metabolites of ethanol like acetaldehyde and FAEEs have direct effects on acinar cells/or induce metabolic alterations within cells indirectly.

alcohol induced pancreatitis

Hypotension, hypoxemia, or oliguria that is unresponsive to intravenous hydration should prompt transfer to the intensive care unit. Pancreatitis is treated with bowel rest, fluid hydration, and pain control. Patients with mild pancreatitis may be treated as outpatients; however, most patients require hospitalization.

Alcohol and pancreatitis

Imaging tests, such as an ultrasound, a CT scan, or an MRI, to help physicians look at the pancreas and determine if there is any damage. Before sharing sensitive information, make sure you’re on a federal government site.

Reducing both alcohol and tobacco consumption was shown to reduce the risk of recurrent attacks, the progression to chronic pancreatitis, and the development of secondary pancreatic malignancy. Various scoring systems have been created to predict the severity of acute pancreatitis based on clinical, laboratory, and radiology findings; however, they have largely demonstrated low specificity and low positive predictive values. These include Ranson’s criteria, the APACHE II score, BISAP, and the CT severity index, among others. Further, the American Pancreatic Association and the American College of Gastroenterology differ in their criteria for prognosticating a severe disease course.


Ponnappa BC, Hoek JB, Waring AJ, Rubin E. Effect of ethanol on amylase secretion and cellular calcium homeostasis in pancreatic acini from normal and ethanol-fed rats. Apte MV, Pirola RC, Wilson JS. Molecular mechanisms of alcoholic pancreatitis. Teyssen S, Lenzing T, González-Calero G, Korn A, Riepl RL, Singer MV. Alcoholic beverages produced by alcoholic fermentation but not by distillation are powerful stimulants of gastric acid secretion in humans. Teyssen S, González-Calero G, Schimiczek M, Singer MV. Maleic acid and succinic acid in fermented alcoholic beverages are the stimulants of gastric acid secretion.

Chronic pancreatitis patients are also at increased risk of developing pancreatic cancer, pancreatic diabetes, bile duct obstruction, and splenic vein thrombosis. Alcohol also leads to premature activation of trypsinogen and other digestive and lysosomal enzymes within the acinar cells themselves; this causes the pancreatic tissue to auto-digest and leads to further inflammation. Tissue distribution of 3H-nicotine in rats demonstrated that nicotine is distributed and accumulated significantly in the pancreas and parts of the gastrointestinal tract. But nicotine metabolism in pancreas has not been reported yet. In liver, low doses of nicotine and ethanol induces CYP2E1 activity as reported by Howard et al. The study suggests that nicotine may increase CYP2E1-induced toxicity and contribute to cross-tolerance in smokers and people treated with nicotine.

Peterson WL, Barnett C, Walsh JH. Effect of intragastric infusions of ethanol and wine on serum gastrin concentration and gastric acid secretion. McArthur K, Hogan D, Isenberg JI. Relative stimulatory effects of commonly ingested beverages on gastric acid secretion in humans. Norton ID, Apte MV, Haber PS, McCaughan GW, Pirola RC, Wilson JS. Cytochrome P4502E1 is present in rat pancreas and is induced by chronic ethanol administration.


▪Pseudocysts cause localized collections of pancreatic fluid confined by a capsule of fibrous or granulation tissue. ▪Activated pancreatic enzymes are extravasated, causing pancreatic autodigestion and necrosis. Approximately 80% of chronic pancreatitis cases are due to alcohol.

alcohol induced pancreatitis

Kelly JP, Kaufman DW, Koff RS, Laszlo A, Wiholm BE, Shapiro S. Alcohol consumption and the risk of major upper gastrointestinal bleeding. Barona E, Pirola RC, Leiber CS. Small intestinal damage and changes in cell population produced by ethanol ingestion in the rat. Pestalozzi DM, Bühler R, von Wartburg JP, Hess M. Immunohistochemical localization of alcohol dehydrogenase in the human gastrointestinal tract. Reimbursement claims with a date of service on or after October 1, 2015 require the use of ICD-10-CM codes.

The Pharmacist’s Role

Endoscopic or surgical intervention may be necessary in select cases. Initial laboratory studies include complete blood count , a complete metabolic panel, including calcium and liver function tests, blood alcohol level, amylase, lipase, and lipid panel. A pregnancy test should be obtained in any female of reproductive age. About 10% of individuals with chronic alcohol use disorder will develop acute pancreatitis. Alcohol pancreatitis is a serious medical condition that requires immediate medical attention.

These tests, in addition with the patient’s presentation, are used to determine the diagnosis of either acute or chronic pancreatitis. Studies indicate males between the ages of 30 and 40 are the largest demographic group diagnosed with the disorder. Although, it is important to note, that anyone can develop chronic pancreatitis, especially if they misuse alcohol.

This is usually manifested due to individuals drinking consistently over a five-year period with around 4-5 drinks daily. Other conditions, such as lupus or high levels of triglycerides, may increase the risk eco sober house review for chronic pancreatitis. Kimura S, Okabayashi Y, Inushima K, Kochi T, Yutsudo Y, Kasuga M. Alcohol and aldehyde dehydrogenase polymorphisms in Japanese patients with alcohol-induced chronic pancreatitis.

Many clinicians prefer to evaluate the bile duct prior to surgery. Because most stones that cause biliary pancreatitis pass, it is not clear who should undergo evaluation. ERCP would be inappropriate in a patient with a moderate to low risk of choledocholithiasis, when the risk of PEP is greater than the benefit of ERCP (normal-sized bile duct and normal liver chemistry tests). However, if the bile duct is dilated and/or liver chemistry tests are elevated, further evaluation prior to surgery may be reasonable. Although EUS is an accurate method of detecting bile duct stones and has been recommended for evaluating the bile duct prior to cholecystectomy, it is rarely needed or used in this setting.

Monaghan KG, Jackson CE, KuKuruga DL, Feldman GL. Mutation analysis of the cystic fibrosis and cationic trypsinogen genes in patients with alcohol-related pancreatitis. Kuwata K, Hirota M, Sugita H, Kai M, Hayashi N, Nakamura M, Matsuura T, Adachi N, Nishimori I, Ogawa M. Genetic mutations in exons 3 and 4 of the pancreatic secretory trypsin inhibitor in patients https://rehabliving.net/ with pancreatitis. Strate T, Yekebas E, Knoefel WT, Bloechle C, Izbicki JR. Pathogenesis and the natural course of chronic pancreatitis. A code also note instructs that 2 codes may be required to fully describe a condition but the sequencing of the two codes is discretionary, depending on the severity of the conditions and the reason for the encounter.

Consistent with risk factors for gallstones, women develop gallstone pancreatitis more often than men. In China, herbal medicines, including licorice root, ginger root, ginseng, peony root, and cinnamon Chinese bark, are used for the treatment of pancreatitis. Treatment for both acute and chronic pancreatitis can help respectively reverse or manage the course of the disease. Specifically, damaged cells block enzyme secretion through the pancreatic ducts, resulting in a slower flow of enzymes like amylase. Alcohol-induced pancreatitis is the result of heavy drinking for several years. It can damage the pancreas in a way that may be untreatable toward a cure, but treatable toward management.

With regard to ADH-2 isoenzyme, results are not conclusive and further studies need to be done. Cytochrome P-450 is involved in metabolizing alcohol in endoplasmic reticulum. Several studies have been done to evaluate the association between polymorphism of enzyme Cyto-P4502E1 and alcoholic pancreatitis with no success.