The profile of patients with chronic pancreatitis has changed dramatically, with a precipitous drop in the proportion of cases related to alcohol and an upsurge in those with other etiologies, Dr. Gregory A. Coté and his colleagues reported online in Clinical Gastroenterology and Hepatology.
"The era of dismissing all cases of chronic pancreatitis as alcohol induced has undoubtedly come to a close," said Dr. Coté of Indiana University, Indianapolis, and his associates.
Historically, heavy alcohol use has been implicated as the cause of chronic pancreatitis in 60%-90% of cases diagnosed in Western countries, but recent reports from Europe and Japan have suggested that a wider spectrum of etiologies is emerging. Dr. Coté and his colleagues in the North American Pancreatitis Study 2 used information in the NAPS2 database to characterize the current epidemiology of the disease in the United States (Clin. Gastroenterol. Hepatol. 2011 March [doi:10.1016/j.cgh.2010.10.015]).
The database includes prospectively enrolled patients treated at 19 academic and community practice referral centers with expertise in pancreatic disorders. This analysis, which the researchers described as "the largest epidemiologic study of chronic pancreatitis from the United States," included 539 patients (mean age, 49 years), of whom 53% were men and 85% were white; the study also included 695 controls.
Referring physicians cited one or more possible etiologies for each patient’s chronic pancreatitis from the following list: alcohol related; idiopathic (no known cause); or unrelated to alcohol, a category that included hereditary diseases, cystic fibrosis, pancreas divisum, autoimmune disorders, hyperlipidemia, hypercalcemia, trauma, or other known causes.
The referring physicians identified alcohol as the sole cause in 35% of cases and as a contributing factor in another 9%. This represents a marked decrease from the 60%-90% of cases attributed to alcohol historically, the investigators noted.
The majority of subjects in whom alcohol was not a contributing factor were equally distributed among the other etiologic categories.
Another "remarkable finding" was that more than one-fourth of all patients had no identifiable cause for their chronic pancreatitis. Data on trends in alcohol consumption are mixed "and do not explain the impressive shift in the etiologic profile," Dr. Coté and his associates said. They posited several reasons that might explain these findings.
First, there may have been referral bias in that patients who are actively drinking might be less likely to seek a referral to expert centers, and physicians caring for such patients might be less likely to make a referral because they already know the cause and the treatment for the disorder. Patients typically are referred if the cause of their disease is unclear or if treatment is not available in their communities, the researchers said.
Second, genetic research in recent years has improved the ability to detect genetic factors that may contribute to chronic pancreatitis. "For example, mutations in PRSS1, CFTR, SPINK1, and chymotrypsin C genes [now] can be detected in a significant subset of patients previously considered to have idiopathic disease," they said.
Third, advances in imaging technology may have led to the discovery of more anatomical abnormalities, such as strictures, pseudocysts, or pancreas divisum, that cause the pancreatitis. "Obstructive causes were considered as the [sole] working diagnosis in over 10% of all the subjects in our study," the investigators noted.
"Perhaps the most intriguing" finding in this study was an association with cigarette smoking. "After controlling for age, sex, BMI, and alcohol intake, ever smoking (odds ratio, 1.65), current smoking (OR, 1.80), and smoking 1 or more packs per day (OR, 1.87) were independently associated with idiopathic chronic pancreatitis," they said.
The discovery of this link "stresses the need to incorporate smoking cessation into the treatment algorithm for patients with chronic pancreatitis," they added. Patients with idiopathic disease were also significantly more likely than controls to have a history of chronic kidney disease or failure (5% vs. 1%, respectively).
This study was funded by the National Institutes of Health, the National Pancreas Foundation, Robert and Vicki Hall, and Andrew and Michelle Aloe. No financial conflicts of interest were reported.