Analysis of pure pancreatic juice in patients with chronic alcoholism

Abstract

To elucidate early biochemical changes of pancreatic juice and their reversibility in chronic alcoholics, pure pancreatic juice was collected from 23 chronic alcoholics by endoscopic retrograde catheterization of the papilla. Samples were collected at 1 minute intervals for 20 minutes after intravenous injection of secretin (Eisai, 1 U/kg) and for 10 minutes after CCK-PZ injection (Boots, 1 U/kg). Volume, bicarbonate concentration, protein concentration and three hydrolases were determined. Following results were obtained. (1) Five patients showed hypersecretory state. Four of the five patients showed hyperconcentration of protein. (2) Seventeen patients showed hyposecretory state. Lipase secretion was most frequently affected (94%). Maximal bicarbonate concentration was the next to be affected (82%). Amylase and chymotrypsinogen secretion were less frequently affected (65%). Flow rate was least frequently affected (24%). (3) It was suggested that exocrine dysfunction in chronic alcoholics is reversible in an early stage and that sequence of events with advancement of the stage is hypersecretion, hyperconcentration of protein, normalization of water secretion with a decrease in lipase secretion and maximal bicarbonate concentration, a decrease in amylase and chymotrypsinogen output, and finally a decrease in flow rate.

Exocrine Pancreatic Secretion in Normal Controls and Chronic Calcifying Pancreatitis Patients from Burundi: Possible Dietary Influences

“…In European or American alcoholics apparently free of pancreatic lesions, protein concentration and output are increased if the patient is studied in the days following alcohol excess [11. 12], but only concentration is signifi cantly higher than in normal controls if pancreatic juice is collected 1-2 weeks after cessation of alcohol consump tion [9][10][11] while later this difference vanishes [15], Hyperconcentration of protein in the early stage of the disease was expected in view of the biochemical changes of pancreatic juice observed in chronic alcoholic patients and in the experimental data [27], This is now confirmed by the present finding: in cases of early CP. we demonstrate an increase in the total concentration of protein in pancreatic juice, when compared ot local controls; the lipase concen tration, even though the secretory level of lipase was low in that population, was also higher than in controls.…”

“…This has also been shown in Japan [10]. In apparently normal alcoholic Europeans, one study found a significant decrease in bicarbonate concentration and output with volume being unchanged [9], In the late calcified stage, bicarbonate secretion was even lower than in the non-calcified stage and did not respond to secretin, but it increased slightly after cerulein which suggests that this cerulein-induced bicarbonate se cretion may be derived from the acini.…”

“…6] and Africa [7,8], Biochemical modifications of pancreatic juice due to chronic alcoholism have already been studied with consis tent results in countries in which protein and lipid malnu trition do not usually occur: protein concentration and sometimes output are increased [9][10][11][12][13]. In contrast, bicar bonate concentration and sometimes output are de creased [ 10,12], the volume being unchanged.…”

“…6] and Africa [7,8], Biochemical modifications of pancreatic juice due to chronic alcoholism have already been studied with consis tent results in countries in which protein and lipid malnu trition do not usually occur: protein concentration and sometimes output are increased [9][10][11][12][13]. In contrast, bicar bonate concentration and sometimes output are de creased [ 10,12], the volume being unchanged. There is an increase in the ratio anionic/cationic trypsinogen [14], The concentration and output of citrate, a secretory cal cium chelator, are decreased [15], Calcium and serum protein secretion are increased [15][16][17], This is probably not directly related to alcohol consumption but is second ary to lesions of the ductal epithelium after the onset of CP [18], In a few tropical regions only, such as Kerala (South India) [19], Zaire [20] and Nigeria [21], alcohol consump tion is not the usual cause of CP.…”

Cholinergic Hypothesis of Alcoholic Pancreatitis

“…[37][38][39]. The effect of pancreozymin on acinar cells is potentiated by raised intrapancreatic cholinergic tone [40], The latter phenomenon, as well as the diminished release of anti-pan creozymin factors caused by chronic alcohol consumption [41], may mediate the increased response to pancreozymin.…”