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The pancreas
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
accounts for 25% of cases. Gallstone pancreatitis is thought to be triggered by the passage of gallstones down the common bile duct. If the biliary and pancreatic ducts join to share a common channel before ending at the ampulla, then obstruction of this passage may lead to reflux of bile or activated pancreatic enzymes into the pancreatic duct. Patients who have small gallstones and a wide cystic duct may be at a higher risk of passing stones. The proposed mechanisms for alcoholic pancreatitis include the effects of diet, malnutrition, direct toxicity of alcohol, concomitant tobacco smoking, hypersecretion, duct obstruction or reflux, and hyperlipidaemia. The remaining cases may be due to rare causes or be idiopathic.
Alcoholic Pancreatitis
Published in Victor R. Preedy, Ronald R. Watson, Alcohol and the Gastrointestinal Tract, 2017
Alcoholic pancreatitis is usually classified as an example of chronic pancreatitis which may present acutely. Although the patient may initially appear to have discrete episodes of pancreatitis (often precipitated by an alcoholic binge) with complete recovery between attacks, there is evidence that patients with alcoholic pancreatitis may have irreversible pathological changes and radiological evidence of chronic pancreatitis present at the time of the first attack.7,8 Furthermore, pancreatic fibrosis has been described at post-mortem examination in alcoholics without a history of clinical pancreatitis.9 Therefore, patients presenting with an acute episode of pancreatic inflammation related to alcohol abuse should be considered as having acute exacerbations of chronic pancreatitis. Recently, however, this view has been challenged. There is increasing evidence that chronic pancreatitis may result from recurrent clinical and subclinical necroinflammatory episodes. A large prospective Swiss study10 concluded that chronic changes of alcoholic pancreatitis were likely to occur in patients with recurrent episodes of acute inflammation, and suggested that these acute episodes lead to chronic changes. This notion is supported by an autopsy study of 247 cases of fatal alcoholic pancreatitis in which 53% of specimens had no evidence of chronic changes.11 Further support comes from animal studies where repeated acute experimental pancreatitis led to changes similar to those seen in chronic pancreatitis (atrophy, fibrosis, and fatty infiltration).12 Given the above evidence, it is possible that a rigid distinction between acute and chronic pancreatitis may have hampered our understanding of the pathogenesis of alcoholic pancreatitis.
Lifetime alcohol intake and pattern of alcohol consumption in patients with alcohol-induced pancreatitis in comparison with patients with alcohol use disorder
Published in Scandinavian Journal of Gastroenterology, 2018
Sigurdur Jon Juliusson, Jon Kristinn Nielsen, Valgerdur Runarsdottir, Ingunn Hansdottir, Ragna Sigurdardottir, Einar S. Björnsson
Patients in the alcoholic pancreatitis group consisted mainly of consecutive patients from 2010–2013 who were at least once hospitalized for alcoholic-induced pancreatitis. Some patients were also identified in a computerized diagnoses database at the National University Hospital in Reykjavik, Iceland, identifying alcohol-induced pancreatitis patients by ICD-10 codes. Their medical records were subsequently reviewed to confirm the diagnosis.
Post-pancreatitis diabetes mellitus: insight on optimal management with nutrition and lifestyle approaches
Published in Annals of Medicine, 2022
Amandeep Singh, Manik Aggarwal, Rajat Garg, Tyler Stevens, Prabhleen Chahal
Alcohol Abstinence: Alcohol can impair hepatic glucose production and can lead to hypoglycaemia, especially in diabetics on insulin therapy. Alcohol abstinence in patients with alcoholic pancreatitis can prevent EPI and reduce pain. Alcohol also tends to be associated with smoking and use of other recreational drug use which could either be a direct or indirect risk factor for pancreatitis and worsen its complications, along with pain, poor dietary habits, and medication non-compliance [38]. Beside routine counselling for alcohol cessation, patients at high risk of relapse to alcohol should be encouraged to join alcoholic anonymous (AA) groups [39]. Abstinence after an episode of acute alcoholic pancreatitis protects against recurrent attacks and pancreatic dysfunction is also rare among abstinent patients [40]. Patients at risk for hospital admission due to alcohol misuse may benefit from targeted interventions to increase rates of outpatient follow-up after hospital discharge [41].Nutrition: Pancreatitis is a state of stress and catabolism and the energy expenditure could be up to 1.2–1.5 times than baseline. Any lag in this can lead to a state of malnutrition and decreased immunity leading to a poor intestinal mucosal barrier, increase in intestinal bacterial translocation, poor inflammatory response, and worse prognosis [42]. Patients with both acute and chronic pancreatitis are at risk of malnutrition. In a meta-analysis of 22 studies including 2,024 patients with AP, oral intake intolerance was noted in 16.3% [42]. Assessing for sarcopenia is another way of estimating malnutrition by assessing muscle strength, quality/quantity, and physical performance. Sarcopenia prevalence in CP ranges from 17%–64% and negatively affects the quality of life (QOL), increases hospitalizations and mortality. Sarcopenia and albumin levels have also been linked with EPI in patients with CP [43,44]. Another confounding factor is chronic nausea and pain in patients with pancreatitis which could lead to poor oral intake. Therefore, in patients with pancreatitis, it is important to assess and manage malnutrition aggressively. In this review, we will focus on dietary therapies for PPDM.