Although the association between alcohol and pancreatitis has been recognized for centuries, the precise magnitude of the impact of alcohol remains poorly quantified. Epidemiologic research on this condition has been seriously handicapped by several factors. Classifications are based on morphology rather than on etiology; the diagnostic differences between acute and chronic pancreatitis are imprecise and confusing; and coding by the International Classification of Diseases (ICD) has been inadequate. The current ICD (ICD-10), used in the United States since 1999, identifies alcohol-induced chronic pancreatitis as a separate code for the first time, an enhancement that will greatly improve the quality of data collected in current and future studies. Unfortunately, no code yet exists for acute alcoholic pancreatitis. Of the approximately 2.4 million deaths in the United States in 1999, pancreatitis was listed as the underlying cause for 3289 deaths, making it the 235th leading cause of death. Acute pancreatitis accounted for 84% of these deaths, and chronic pancreatitis the remaining 16%. Alcohol is a primary cause of both acute and chronic pancreatitis in most developed countries. About one-third of acute pancreatitis in the United States is alcohol-induced. In the United States and other developed countries, 60%–90% of chronic pancreatitis is alcohol induced. Both forms are more common in men. The development of chronic pancreatitis is proportional to the dose and duration of alcohol consumption (minimum, 6–12 years of approximately 80g of alcohol per day). Autopsy studies reveal subclinical chronic pancreatitis in another 10% of alcohol abusers. Yet, since <10% of chronic alcoholics develop chronic pancreatitis, clearly other predisposing factors besides alcohol are involved. Genetic variability and environmental exposures, such as diet, are prime candidates for further investigation. To date, there have been few large epidemiological studies of alcoholic pancreatitis in the United States or other developed countries. Additional studies are needed to improve the quality of existing baseline epidemiologic data and allow better assessment of risk. Improved diagnostic precision, more complete and specific coding, and greater understanding of covariables and mechanisms would also advance the field.
From the Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland.
Received for publication June 3, 2003; accepted June 23, 2003.
Reprints: Megan D. Adamson, MD, Division of Biometry and Epidemiology, NIAAA, NIH, 6000 Executive Blvd., Wilco Building, Suite 514, Bethesda, MD 20892-7003 (e-mail: firstname.lastname@example.org).