General information
Inflammation of the pancreas that damages and malfunctions the retroperitoneal organ is known as pancreatitis. The two most common types are Acute and Chronic Pancreatitis (CP). CP is thought to be the result of recurrent acute pancreatitis attacks. There is no direct link between alcohol and pancreatic cancer, but alcohol and its by-products can put the organ at risk for damage from other, more benign agents. Consequently, providing patients with alcohol (and smoking) cessation counseling and strategies is crucial for preventing recurrent attacks. Chronic alcohol consumption is the second most common cause of acute pancreatitis (AP) after gallstones, accounting for 17 percent to 25 percent of acute pancreatitis cases worldwide (Singhvi & Yadav, 2018). It usually appears in patients who have been drinking heavily for over five years (about four to five drinks a day) and only hardly ever occurs due to a single binge.
How often do heavy drinkers develop chronic pancreatitis?
Chronic alcohol use is the most frequent cause of chronic pancreatitis, accounting for 40% to 70% of all cases. It also raises the chance of getting pancreatic cancer in the person who consumes it (Adejumo et al., 2019). The recurrence of acute pancreatitis is linked to the development of chronic pancreatitis, and it is more prevalent in alcoholics who use alcohol often. In addition, most studies indicate that an AP episode begins with some degree of chronic pancreatic damage. Although studies have established a connection between heavy drinking and the condition, the exact mechanism by which alcohol triggers pancreatic inflammation is unknown. Alcohol-induced acute pancreatitis is the second most frequent cause of gallstones, accounting for 17 percent to 25 percent of all cases worldwide.
People who regularly consume four to five drinks a day for five years are more likely to develop this symptom. Acute pancreatitis seldom occurs as a consequence of a single night of heavy drinking. Chronic alcohol use is a common cause of chronic pancreatitis, accounting for 40 to 70 percent of all cases. Acute pancreatitis sufferers who are also heavy drinkers may develop chronic pancreatitis as a result of repeated attacks. Pancreatitis due to alcohol is also seen in those who drink heavily regularly and for an extended period. Chronic epigastric discomfort that radiates to the mid-back or flanks is one of the symptoms of nausea and vomiting.
What are the proposed mechanisms of alcohol-induced chronic pancreatitis?
One of the most severe side effects of alcoholism is alcoholic pancreatitis. Alcoholic pancreatitis risk rises linearly with alcohol use, indicating that alcohol is harmful to the pancreas in a dose-dependent manner. Though the illness strikes just a tiny percentage of drinkers, something other than alcohol may be needed to start clinically apparent pancreatic damage. The pancreas now processes alcohol in two ways: oxidatively and non-oxidatively via non-oxidative metabolites. Alcohol and its metabolites alter the acinar cells in a way that increases the risk of autodigestive damage by promoting the early activation of digestive enzymes inside the cells. Alcohol and its metabolites, cytokines, and growth factors produced during alcohol-induced pancreatic necroinflammation activate pancreatic stellate cells (PSCs) (Juliusson et al., 2018). Alcoholic chronic pancreatitis caused fibrosis, and activated PSCs are the primary cells responsible for this.
Why may a proton pump inhibitor be helpful for this patient?
Doctors may help many acid-related diseases with the use of PPIs, and one study found that the PPI pantoprazole reduced tissue infiltration of inflammatory cells and necrosis of acinar tissue in rats with severe acute pancreatitis. Small, low-fat meals and adequate hydration have been shown in studies to reduce the likelihood of painful flare-ups. Even if alcohol isn’t the cause of your pancreatitis, you should nonetheless abstain from it. Medications that reduce stomach acidity may also be beneficial (Weiss et al., 2019). Ranitidine, for example, or omeprazole, a proton pump inhibitor, may be used as an H2 receptor blocker. The inactivation of supplementary pancreatic enzymes by stomach acid is reduced when patients take these medications.
References
Adejumo, A. C., Akanbi, O., Adejumo, K. L., & Bukong, T. N. (2019). Reduced risk of alcohol‐induced pancreatitis with cannabis use. Alcoholism: Clinical and Experimental Research, 43(2), 277-286.
Juliusson, S. J., Nielsen, J. K., Runarsdottir, V., Hansdottir, I., Sigurdardottir, R., & Björnsson, E. S. (2018). Lifetime alcohol intake and pattern of alcohol consumption in patients with alcohol-induced pancreatitis compared with patients with alcohol use disorder.Scandinavian journal of gastroenterology, 53(6), 748-754.
Singhvi, A., & Yadav, D. (2018). Myths and realities about alcohol and smoking in chronic pancreatitis.Current opinion in gastroenterology, 34(5), 355.
Weiss, F. U., Laemmerhirt, F., & Lerch, M. M. (2019). Etiology and risk factors of acute and chronic pancreatitis. Visceral Medicine, 35(2), 73-81. Web.