Yes, simultaneous damage to both the pancreas and liver are associated in subjects who drink excessive amounts of alcohol!

It has generally been accepted that although excessive alcohol intake might lead to liver damage or pancreatic damage, both conditions are rarely associated, and the pathogenesis of the tissue injury is not related. Indeed, many have believed that subjects with alcohol-induced liver damage are somehow not apt to develop pancreatic damage and vice versa. The study by Pace et al 1 in this issue of Clinical Gastroenterology and Hepatology refutes that remarkably well. These authors evaluated the prevalence of simultaneous liver cirrhosis and chronic pancreatitis in subjects who were heavy imbibers. Postmortem autopsy data were evaluated from 620 individuals with a history of excessive alcohol use and 100 nonalcoholic control subjects. The individuals were classified into groups on the basis of macroscopic observations of the pancreas (no injury, acute pancreatitis, fibrosis, and chronic pancreatitis) and liver (no injury, moderate steatosis, severe steatosis, and cirrhosis). The same classification system was used for histologic data that were used to confirm and correlate macroscopic findings. Of 183 subjects with liver cirrhosis, 33 (18%) had chronic pancreatitis, and 93 (51%) had pancreatic fibrosis. Of the 230 subjects with severe steatosis, 37 (16%) had chronic pancreatitis, and 97 (42%) were found to have pancreatic fibrosis. Thirtythree (39%) subjects with chronic pancreatitis also had liver cirrhosis, and 37 (44%) had severe steatosis. Thirty-eight percent of the subjects with pancreatic fibrosis were found to have liver cirrhosis, and in another 40%, severe steatosis occurred. Thirtyfive subjects demonstrated neither liver nor pancreatic damage. In the control group neither chronic pancreatitis nor cirrhosis was detected. Thus, Andrea and associates demonstrated the simultaneous occurrence of liver and pancreatic damage in these individuals who were heavy drinkers. Recent studies indicated that both chronic pancreatitis and cirrhosis have precursor lesions. Chronic pancreatitis develops through fibrosis of the pancreas. 2,3 The precursor form of liver cirrhosis appears to be hepatic steatosis. 4,5 Thus, hepatic and stellate cells are important in the development of fibrosis in both the liver and the pancreas, implying similar molecular mechanisms for the fibrotic changes in both organs. 3,6 The authors were unable to accurately evaluate the effect of nicotine use as a risk factor for liver and/or pancreatic damage because smoking data were only available for 49% of the subjects. Why is it that the consensus opinion was that these lesions in the pancreas and liver did not occur simultaneously? First, the studies in the literature that defended the nonoccurrence of these lesions were usually performed in small numbers of patients. 7 In addition, none of these studies looked systematically into morphologic changes such as pancreatic fibrosis. 8,9 Indeed, the importance of fibrosis as a crucial initial event in chronic pancreatitis has only been emphasized relatively recently. Andrea and associates readily recognized the limitations of their study such as having no quantitative data on exactly how much alcohol was taken by these “heavy drinkers” and the duration of drinking; the semiquantitative analysis of the tissue damage; the inability to evaluate nicotine use as a risk factor for either liver or pancreatic damage; and the lack of data on other potential risk factors such as diabetes, body mass index, and nutrition status. These criticisms notwithstanding, the data obtained in this large number of subjects should convincingly demonstrate, contrary to common belief, that there is a close association between pancreatic and liver injury in patients with heavy alcohol intake. The authors also make a good case for a correlation of organ damage between the pancreas and the liver.