Ekbom A, McLaughlin J K, Karlsson B M, Nyrén O, Gridley G, Adami H O, Fraumeni J F
Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden.
J Natl Cancer Inst. 1994 Apr 20;86(8):625-7. doi: 10.1093/jnci/86.8.625.
Little is known about the etiology of cancer of the exocrine portion of the pancreas, which produces a variety of digestive enzymes. Smoking, certain dietary factors, and diabetes mellitus are considered to be risk factors, although the risk estimates are modest in most instances. A recent cohort study of patients with chronic pancreatitis indicated a ninefold to 16-fold increased risk for pancreatic cancer.
Our purpose was to evaluate the relationship between various clinical types of pancreatitis and pancreatic cancer.
Data for this study were collected from all inpatient medical institutions in Sweden from 1965 until 1983 by the Swedish National Board of Health and Welfare. Data were recorded on individual hospital admissions and discharges in the Inpatient Register. All patients with records in the Inpatient Register coded for acute, chronic, or unspecified pancreatitis were considered for inclusion in the study. A population-based cohort of 7956 patients with at least one discharge diagnosis of pancreatitis was monitored (up to 19 years of follow-up) for the occurrence of pancreatic cancer by record linkages to the Swedish Cancer Registry and Registry of Causes of Death.
A total of 46 pancreatic cancers were diagnosed during follow-up compared with 21 expected (standardized incidence ratio [SIR] of 2.2; 95% confidence interval [CI] 1.6-2.9) for the Uppsala Health Care Region. The excess risk for women and men was similar--most pronounced during the first period of follow-up (2-4 years) after discharge and close to unity after more than 10 years of follow-up. Patients with chronic pancreatitis and patients with more than one discharge diagnosis of either acute or unspecified pancreatitis were at higher risk (SIR = 3.8; 95% CI 1.4-8.2 and SIR = 4.8; 95% CI 1.9-9.9, respectively) compared with those with only one discharge of acute (SIR = 1.6; 95% CI 0.9-2.7) or unspecified (SIR = 2.1; 95% CI 1.2-3.2) pancreatitis.
Our finding of a moderate excess of pancreatic cancer among patients with pancreatitis, especially the chronic or recurrent forms, supports some earlier clinical and case-control studies, but it is not consistent with the ninefold to 16-fold risk reported in a recent cohort study. The absence of an increased risk 10 years or more after first discharge for pancreatitis argues against a straight-forward causal relationship. Because of the relatively short interval between diagnosis of pancreatitis and pancreatic cancer, it is possible that some forms of pancreatitis are a precursor to pancreatic cancer or that shared risk factors for both diseases (e.g., cigarette smoking) may also be involved.
胰腺外分泌部可产生多种消化酶，人们对该部位癌症的病因了解甚少。吸烟、某些饮食因素以及糖尿病被认为是风险因素，不过在大多数情况下风险评估值并不高。最近一项针对慢性胰腺炎患者的队列研究表明，患胰腺癌的风险增加了9至16倍。
我们的目的是评估各种临床类型的胰腺炎与胰腺癌之间的关系。
本研究的数据由瑞典国家卫生与福利委员会从1965年至1983年期间瑞典所有住院医疗机构收集。数据记录在住院登记册中的个人入院和出院信息里。住院登记册中记录为急性、慢性或未明确类型胰腺炎的所有患者都被纳入本研究。通过与瑞典癌症登记处和死亡原因登记处进行记录关联，对一个基于人群的7956例至少有一次出院诊断为胰腺炎的队列进行监测（随访长达19年），以观察胰腺癌的发生情况。
在随访期间共诊断出46例胰腺癌，而乌普萨拉医疗保健地区预期为21例（标准化发病比[SIR]为2.2；95%置信区间[CI]为1.6 - 2.9）。女性和男性的额外风险相似——在出院后的第一个随访期（2 - 4年）最为明显，随访超过10年后接近1。与仅有一次急性（SIR = 1.6；95% CI 0.9 - 2.7）或未明确类型（SIR = 2.1；95% CI 1.2 - 3.2）胰腺炎出院记录的患者相比，慢性胰腺炎患者以及有不止一次急性或未明确类型胰腺炎出院诊断的患者风险更高（SIR分别为3.8；95% CI 1.4 - 8.2和SIR = 4.8；95% CI 1.9 - 9.9）。
我们发现胰腺炎患者中胰腺癌有适度增加，尤其是慢性或复发性胰腺炎患者，这支持了一些早期的临床和病例对照研究，但与最近一项队列研究报告的9至16倍风险不一致。首次出院10年或更长时间后风险未增加，这反驳了一种直接的因果关系。由于胰腺炎诊断与胰腺癌之间的间隔相对较短，有可能某些形式的胰腺炎是胰腺癌的先兆，或者两种疾病的共同风险因素（如吸烟）也可能起作用。
