The majority of patients with alcoholic chronic pancreatitis are diagnosed between 35 and 40 years of age.15 Alcoholic chronic pancreatitis usually presents with an early phase of recurrent attacks of acute pancreatitis, followed by the late phase of the disease characterized by the development of chronic pain, pancreatic calcifications, and exocrine and later endocrine insufficiency. The pancreas demonstrates a large functional capacity so that exocrine and endocrine insufficiency develops with a considerable delay during the course of alcoholic chronic pancreatitis.
The interval between the start of continuous alcohol abuse and the clinical manifestation of alcohol-induced chronic pancreatitis usually requires between 13 to 21 years.2,5 Then, the interval between onset of the disease and the occurrence of exocrine insufficiency and calcifications averages 4.8 +/- 5.5 years in alcoholic chronic pancreatitis.16 Another study reported a median time of 13.1 years to pancreatic exocrine insufficiency after onset of the disease, whereas endocrine insufficiency was diagnosed after a median time of 19.8 years.6 Data regarding the progression of pancreatic insufficiency are conflicting. Several investigations did not show a progressive deterioration of exocrine pancreatic insufficiency or revealed even slight improvements in pancreatic insufficiency over time.6,17,18 In contrast, other reports show progressive deterioration of pancreatic function during a median follow-up of 10.4 years in patients with alcoholic chronic pancreatitis.19 The reasons for these differences are not clarified, but may result from differences in study designs or sensitivities of the pancreatic function tests used in the different investigations.18 Although the progression toward pancreatic insufficiency is not completely halted by cessation of alcohol abuse, abstinence may diminish the progression to exocrine and endocrine insufficiency.20 Moreover, a decrease in pain or a decrease in the frequency of episodes of acute pancreatitis has been shown in patients who stop consuming alcohol.21
The relationship between acute and chronic alcoholic pancreatitis remains controversial (see Chapter 16).22 Studies in patients with an initial episode of acute pancreatitis revealed that these patients already presented histological signs of chronic pancreatitis.6,9,23 However, several long-term clinical studies,14,16,19 pathologic studies,24 studies in patients with hereditary pancreatitis,2526 and recent experimental studies27 provide strong evidence that recurrent attacks of acute pancreatitis can result in chronic pancreatitis. Indeed, the concept that acute pancreatitis represents the first recognition of chronic pancreatitis appears to be valid in about half of the 247 alcoholic patients who died of acute pancreatitis, but not in the other half of patients who demonstrated no signs of chronic pancreatic damage.10
The mortality rate in patients with alcoholic chronic pancreatitis is approximately one-third higher than that in an age and sex matched general population.18 About 50% of patients with the disease die within 20 years after onset of the disease with a median age of 54 years.16 However, mortality is not related to chronic pancreatitis and its complications in 80% of the patients.6,16,28 The most common causes of death remain malignancies and cardiovascular diseases that are rather associated with smoking and ongoing alcohol abuse than with chronic pancreatitis.29
Table 15.1 Major Findings in Studies with Humans and Ethanol-Fed Animals on Pancreatic Exocrine Secretion
Acute Ethanol Administration
Oral and intragastric ethanol administration increases pancreatic bicarbonate and protein secretion.
Intravenous ethanol administration reduces basal and hormonally stimulated pancreatic bicarbonate and protein secretion.
Nonalcoholic constituents of beer may increase pancreatic secretion.
Chronic Ethanol Administration
In human alcoholics, the basal pancreatic enzyme secretion is increased.
In human alcoholics, the viscosity of the pancreatic juice is enhanced.
In human alcoholics, the pancreatic juice contains a higher concentration of proteins.
In human alcoholics, the pancreatic bicarbonate secretion is decreased.
In human alcoholics, an enhanced ratio of trypsinogen levels to pancreatic secretory trypsin inhibitor levels is present in the pancreatic juice.
In ethanol-fed animals, a diet rich in fat and protein increases the concentrations of enzymes in the pancreatic juice.
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