INCREASED SERUM PANCREATITIS ASSOCIATED PROTEIN (PAP) CONCENTRATION AFTER LONG-TERM ALCOHOL-CONSUMPTION - FURTHER EVIDENCE FOR REGULAR SUBCLINICAL PANCREATIC DAMAGE AFTER HEAVY DRINKING

Citation
I. Nordback et al., INCREASED SERUM PANCREATITIS ASSOCIATED PROTEIN (PAP) CONCENTRATION AFTER LONG-TERM ALCOHOL-CONSUMPTION - FURTHER EVIDENCE FOR REGULAR SUBCLINICAL PANCREATIC DAMAGE AFTER HEAVY DRINKING, Gut, 36(1), 1995, pp. 117-120
Citations number
19
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
GutACNP
ISSN journal
00175749
Volume
36
Issue
1
Year of publication
1995
Pages
117 - 120
Database
ISI
SICI code
0017-5749(1995)36:1<117:ISPAP(>2.0.ZU;2-1
Abstract
It has been shown recently that longterm but not short term heavy drin king of alcohol frequently results in increased serum activities of pa ncreatic enzymes suggesting subclinical pancreatic injury. Serum pancr eatitis associated protein (PAP) is a novel protein, whose synthesis i n the acinar cells and release into serum is specifically induced by a cute pancreatic damage. This study was performed to further characteri se the alcohol induced subclinical pancreatic injury by using serum PA P measurements. Three groups were studied: (1) control group (n = 25), (2) short term drinking group (n = 20), who consumed 2.0 g of ethanol per kg body weight during four hours, and (3) longterm drinking group (n = 32), who were admitted to withdrawal clinic after a median 30 mo nths heavy drinking period. Serum PAP concentration was low in the con trol group (8 (5 to 12) mu g/l, geometric mean (95% confidence interva ls)). In the short term drinking group serum-PAP was in the range of t he control group values during 56 hours after drinking. Longterm drink ing induced at least a 10-fold increase in serum PAP, the highest conc entrations being seen on day 2 after drinking had ended (106 (61 to 18 4) mu g/l). The patients did not develop abdominal symptoms, increased blood white cell count, or increased serum C reactive protein concent ration. These results further support the suggestion that heavy longte rm drinking often induces subclinical pancreatic damage, but not clini cal pancreatitis.