Diet and Drinking Habits in Relation to the Development of Alcoholic Pancreatitis
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Gut: first published as 10.1136/gut.26.9.882 on 1 September 1985. Downloaded from Gut, 1985, 26, 882-887 Diet and drinking habits in relation to the development of alcoholic pancreatitis J S WILSON, L BERNSTEIN, C MCDONALD, A TAIT, D MCNEIL, AND R C PIROLA From the Department of Gastroenterology, Division ofMedicine, Prince Henry Hospital, Sydney, NSW, Australia, and the Department ofStatistics, Macquarie University, North Ryde, NSW, Australia SUMMARY To determine whether increased intakes of fat and protein or particular drinking habits are associated with the development of alcoholic pancreatitis, a dietary study has been conducted. Patients with clinically evident alcoholic pancreatitis were compared with individuals with clinically evident alcoholic cirrhosis with respect to dietary and drinking habits before the onset of clinical illness. There was no significant difference between the two groups regarding intake of nutrients, drinking habits or type of alcoholic beverage consumed. Although alcoholism is common in western society increasing the dietary protein content has been re- (affecting 3-5% of men and 0-1% of women)1 only a ported to increase pancreatic protease content'1'4 small minority of alcoholic individuals develop and possibly also lipase activity.10 Although the clinical pancreatitis. Dietary factors and drinking mechanism of such dietary adaptation is unknown, habits have been considered as possible determi- its occurrence may predispose the pancreas to nants of individual susceptibility to alcoholic pan- autodigestion. (b) High fat diets appear to increase creatitis. The study described in this paper was the severity of experimental pancreatitis in dogs'5 http://gut.bmj.com/ undertaken to determine whether patients with this and there is a report of pancreatitis developing disease differed from suitable controls with regard spontaneously in dogs consuming large amounts of to: (a) their consumption of fat and protein, (b) the fat.'6 In addition, Maki et al17 have reported that type of alcoholic beverage consumed and the increases in dietary protein enhance the develop- pattern of its consumption prior to the onset of ment of experimental pancreatitis in rats. (c) Several clinical disease. dietary surveys of patients with alcoholic pancreati- tis have been carried out. Sarles' group 89 have on September 28, 2021 by guest. Protected copyright. DIET AND PANCREATITIS reported that patients with this condition consume Malnutrition has traditionally been considered to be more fat and more protein than the normal popula- an important association of alcoholic pancreatitis. tion. The use of normal controls in these studies was Malnutrition (in the absence of alcoholism) is unfortunate as they differed from the index group in associated with pancreatitis in parts of Africa, India, more than one variable - they did not have and South-East Asia.2 In addition, Mezey et a13 pancreatitis and they were not alcoholic. In addi- have reported that pancreatic hyposecretion in tion, it was not made clear whether the patients alcoholics is caused by malnutrition and is reversed were interviewed about their dietary habits before by feeding adequate diets. or after the onset of clinical disease. Pitchumoni et On the other hand, there is experimental and al. 20 reported that patients with alcoholic pancreati- clinical evidence to suggest that 'hypernutrition' tis consumed more fat than patients with alcoholic may be a predisposing factor in this disease: (a) cirrhosis. Both study groups were alcoholic and both Several investigators have been able to increase groups had consumed enough alcohol to result in lipase content of the pancreas of experimental organ damage. The difference in fat intakes re- animals by feeding high fat diets.49 Similarly, ported, however, may have been related to the 13 year average age difference between the two groups. Address for correspondence: Dr R C Pirola, 1st Floor Clinical Sciences Bldg. DRINKING HABITS AND ALCOHOLIC PANCREATITIS Prince Henry Hospital, Anzac Parade, Little Bay, NSW 2036, Australia. A survey of the literature reveals considerable Received for publication 30 October 1984 geographic variation in patterns of alcohol consump- 882 Gut: first published as 10.1136/gut.26.9.882 on 1 September 1985. Downloaded from Diet and drinking habits in relatioh to the development of alcoholic pancreatitis 883 tion in association with alcoholic pancreatitis. In normal 300 U/1) or features of moderate or ad- France2' 22 and Sweden23 patients are reported as vanced chronic pancreatitis on a retrograde pan- consistent heavy drinkers with little variation in creatogram (according to the criteria of Kasugai et alcohol intake between one day and the next. In the a135), (iii) negative radiographic studies of the gall United States,24 South Africa,25 26 Scotland,27 and bladder, normal serum calcium (in remission), Australia,28 29 however, bout drinking is said to be fasting serum triglycerides less than twice the upper more prominent in these patients. limit of normal and no relevant drug history. The relationship of drinking bouts to attacks of pancreatitis is controversial. Phillips, 24 Marks and (b) Alcoholic liver disease Bank,25 Boyer and Mackay,28 and Imrie27 have Patients presenting with clinical evidence of alcoho- reported that attacks of pancreatitis often coincide lic liver disease all admitted to drinking 80 g or more with periodic drinking bouts. On the other hand, of alcohol per day and had alcoholic cirrhosis Saint,3 " Mayday and Pheils,3' and Kager et a123 diagnosed by liver biopsy or (when deranged coagu- could find no association between attacks of pan- lation precluded a liver biopsy) by the presence of creatitis and the imbibition of larger than usual typical stigmata of chronic liver disease with ascites quantities of alcohol. and/or oesophageal varices and with a normal serum The type of beverage consumed appears to be iron or serum ferritin. unimportant in relation to the development of alcoholic pancreatitis. Wine, spirits, beer, and cider (c) Gall stone pancreatitis have all been incriminated in reports from various All patients in this category possessed the following countries.21-23 25 32-34 features: (i) typical attacks of acute abdominal pain With the exception of the reports of Sarles21 and and tenderness, (ii) a serum amylase greater than of Kager et a123 there are no published data to 1100 U/I (upper limit of normal: 300 U/1), (iii) support the above claims. The drinking habits and evidence of gall stones on biliary radiology or at the preferred alcoholic beverage of patients with laparotomy, (iv) normal serum triglycerides, (v) alcoholic pancreatitis need to be documented and normal serum calcium (in remission), (vi) no re- compared with those of a suitable control group levant drug or alcohol history. before such factors can be accepted or dismissed as contributing to the development of the disease. (d) Gall stones in the common bile duct without pancreatitis http://gut.bmj.com/ Methods All patients in this category had: (i) gall stones in the common bile duct found at the time of biliary STUDY GROUPS surgery or with endoscopic retrograde cholangiogra- The dietary fat and protein intakes and the drinking phy, (ii) no clinical evidence of pancreatitis, (iii) a habits of patients with clinically evident alcoholic normal serum amylase. pancreatitis were compared with those of patients with clinically evident alcoholic liver disease. This DIETARY INTERVIEWS on September 28, 2021 by guest. Protected copyright. particular control group was chosen because these All patients were interviewed by a research dietitian individuals had consumed enough alcohol to result who was unaware of their diagnosis. All interviews in damage of an organ other than the pancreas. took place within two years of the onset of clinical If dietary factors contribute to the development of disease. Information was recorded about the pa- alcoholic pancreatitis, they may also play a role in tients' dietary and drinking habits during the six other forms of pancreatic injury. Therefore, a study month period before the onset of symptoms. In was also made of the dietary intakes of patients with other words, an attempt was made to study patterns gall stone pancreatitis. In this instance, the control of fat, protein and alcohol intake in the premorbid group comprised individuals with one or more gall state. Where possible, information about the pa- stones in their common bile ducts but without tients' dietary habits was also obtained from rela- pancreatitis. tives. CRITERIA FOR ENTRY DATA ANALYSIS (a) Alcoholic pancreatitis Comparisons of dietary data between index patients Patients presenting with clinical evidence of alcoho- and their controls were made with multiple regres- lic pancreatitis admitted to drinking 80 g or more of sion analysis using the following multiple regression alcohol per day and manifested: (i) typical attacks of model: acute abdominal pain and tenderness, (ii) either a serum amylase greater than 1100 U/I (upper limit of y = Bo + Blxl + B2x2 + B3z Gut: first published as 10.1136/gut.26.9.882 on 1 September 1985. Downloaded from 884 Wilson, Bernstein, McDonald, Tait, McNeil, Pirola where Table 1 Study groups y is the response variable (lipid intake, protein caloric intake, etc) MalelFemale intake, Number Age ratio B(1 is a constant B1, B2, B3 are regression coefficients Alcoholic pancreatitis 20 40+9 3-8 xi, x2, z are explanatory variables with Alcoholic cirrhosis 33 51 + 11 2-2 x = age Gall stone pancreatitis 15 59±19 0-5 Gall stones in x2 = sex (in the case of males the variable x2 is common bile duct 31 61 ± 18 (-4 assigned the value 1 and in the case of females it is assigned the value 0) * Mean+standard deviation. z = group (for the index group z= 1; for the control group z=0). This model allows the response variable to be 300U/l). Of the remaining two, one had pancreatic related to the group while adjusting for sex and age, calcification shown radiologically and the other had assuming the latter effect is linear.