DIAGNOSTIC APPROACH TO PANCREATIC CANCER

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• 作者：Division of Gastroenterology ; University of Miami ; School of Medicine/Mount Sinai Medical Center ; Miami Beach ; Florida ; Jamie S. Barkin ; MD ; FACP ; MACG ; Jeffrey A. Goldstein ; MD
• 刊名：Gastroenterology Clinics of North America
• 出版年：1999
• 出版时间：1 September 1999
• 年：1999
• 卷：28
• 期：3
• 页码：709-722
• 全文大小：872 K

文摘

Adenocarcinoma of the pancreas ranks fourth as a cause of cancer death in the United States and is the second most common cause of cancer deaths of all gastrointestinal-related carcinomas. This malignancy arises from the pancreatic exocrine ductal system and is responsible for approximately 90 % of all pancreatic growths. Its prevalence has risen by 24 % over the past 35 years in the United States, but in the past 10 years, the mortality and the rate of increase in frequency have declined. The incidence of pancreatic cancer rises as one ages, with 80 % of cases discovered between the ages of 60 and 80 years. Men are two times more likely than women to develop pancreatic cancer. The incidence of pancreatic cancer as well as the mortality rate is greater in African-Americans and Japanese Americans compared with other ethnic groups, suggesting a possible genetic or environmental risk factor. Direct evidence linking specific dietary carcinogens to pancreatic cancer in humans is lacking. There is a correlation between per capita saturated and total saturated fat intake and an increased risk of pancreatic cancer, however.

Occupational exposure probably has a small role in the cause of pancreatic carcinoma. Such exposures include nonchlorinated solvents and the pesticide DDT and two of its derivatives. Chronic pancreatitis predisposes to the development of pancreatic carcinoma, although its risk is low except in patients with familial pancreatitis. Alcohol consumption remains the most common cause of chronic pancreatitis. Two Scandinavian and one U.S. study reported an increased risk of pancreatic cancer in heavy alcohol users. Other studies have not confirmed this association. The increased incidence of pancreatic carcinoma in alcoholics may be in the subset of patients who develop chronic pancreatitis.

The best-established risk factor for pancreatic cancer is cigarette smoking. There is a dose relationship to the number of cigarettes smoked and the occurrence of pancreatic carcinoma. Its mechanism may be the N-nitroso compounds that can induce pancreatic cancer in laboratory animals and are present in cigarette smoke. These compounds cause hyperplastic changes in the pancreatic ducts, which may be a precursor lesion to ductal adenocarcinoma. Up to 25 % of pancreatic carcinoma is believed to be attributable to cigarette smoking. This relationship to cigarette smoking probably accounts for the increasing frequency of cases in women. A 15-year period must elapse from the time the patient quits heavy cigarette smoking until the risk falls to a level compatible with those who have never smoked, and a 5-year period is needed for the fall in risk after decreased cigarette usage.

There is an inherited predisposition to developing pancreatic carcinoma in some families, as pancreatic carcinoma had occurred through three generations. In addition, pancreatic carcinoma occurs in those who have chronic familial relapsing pancreatitis. Chronic familial relapsing pancreatitis, so-called hereditary pancreatitis, is inherited as an autosomal dominant trait with apparent complete penetrance. Symptoms of abdominal pain are the most prominent clinical manifestations and frequently begin in childhood (mean age 10 years). The prevalence rate of cancer is 20 % (see the article on hereditary pancreatitis elsewhere in this issue). Pancreatic cancer also occurs as part of the tumor spectrum in hereditary, nonpolyposis colorectal cancer (Lynch II variant), Gardner's syndrome, and a subset of familial and atypical multiple mole melanoma (FAMMM) syndrome kindreds. There is an association between p16 ink4 gene (MTS 1 gene) mutation and pancreatic cancer and familial melanoma. This gene is thought to function as a tumor-suppressor gene, and mutation is believed to result in unregulated cellular expression and tumor formation. In addition, there is a familial association of pancreatic cancer and extrapancreatic cancer, such as the breast and ovary.