PANCREATITIS AND PANCREATIC-CANCER - A POPULATION-BASED STUDY
PANCREATITIS AND PANCREATIC-CANCER - A POPULATION-BASED STUDY
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DOI：
10.1093/jnci/86.8.625
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发表时间：
1994-04-20
期刊：
影响因子：
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通讯作者：
FRAUMENI, JF
中科院分区：
文献类型：
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作者：
EKBOM, A;MCLAUGHLIN, JK;FRAUMENI, JF
背景：对于产生多种消化酶的胰腺外分泌部分癌症的病因知之甚少。吸烟、某些饮食因素和糖尿病被认为是危险因素，尽管在大多数情况下风险估计并不高。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。目的：我们的目的是评估不同临床类型的胰腺炎与胰腺癌之间的关系。方法：本研究的数据由瑞典国家卫生和福利委员会从 1965 年至 1983 年从瑞典所有住院医疗机构收集。住院患者登记册中记录了各个医院入院和出院的数据。所有在住院登记中记录有急性、慢性或未明确胰腺炎记录的患者均被考虑纳入该研究。通过与瑞典癌症登记处和死因登记处的记录联系，对 7956 名至少有一次出院诊断为胰腺炎的患者进行了人群队列监测（长达 19 年的随访），以了解胰腺癌的发生情况。结果：乌普萨拉卫生保健区在随访期间总共诊断出 46 例胰腺癌，而预期诊断为 21 例（标准化发病率 [SIR] 为 2.2；95% 置信区间 [CI] 1.6-2.9）。女性和男性的超额风险相似——在出院后的第一个随访期（2-4 年）最为明显，并在 10 多年的随访后接近一致。与仅有 1 次出院诊断为急性或未明确胰腺炎 (SIR = 1.6; 95% CI 0.9-2.7) 或未明确胰腺炎 (SIR = 4.8; 95% CI 1.9-9.9) 的患者相比，慢性胰腺炎患者和出院超过 1 次诊断为急性或未明确胰腺炎的患者风险较高 (分别为 SIR = 3.8; 95% CI 1.4-8.2 和 SIR = 4.8; 95% CI 1.9-9.9)。 2.1；95% CI 1.2-3.2) 胰腺炎。结论：我们发现胰腺炎患者，尤其是慢性或复发性胰腺炎患者中胰腺癌发病率适度偏高，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。首次出院后 10 年或更长时间内，胰腺炎风险并未增加，这与直接因果关系相悖。由于胰腺炎和胰腺癌的诊断间隔相对较短，因此某些形式的胰腺炎可能是胰腺癌的先兆，或者也可能涉及两种疾病的共同危险因素（例如吸烟）。
Background: 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. Purpose: Our purpose was to evaluate the relationship between various clinical types of pancreatitis and pancreatic cancer. Methods: 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. Results: A total of 46 pancreatic cancers were diagnosed during followup 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. Conclusions: 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 straightforward 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.