血清KL-6水平在胰腺癌诊断与鉴别诊断中的价值

目的 检测胰腺癌患者血清KL-6水平,探讨其临床诊断价值.方法 收集随访资料完整的53例胰腺癌(PC)、68例慢性胰腺炎(CP)、51例高危人群(high risk person,HR)的血清样本,以50例健康体检者作为对照.用ELISA方法检测血清CA50、MUCA、KL-6水平,放免法测定血清CA19-9水平.分析它们诊断胰腺癌的敏感性、特异性及与临床病理参数、患者预后的关系.结果 PC组、CP组、HR组及对照组的血清KL-6水平分别为(753±548)、(135 ±93)、(105±55)及(99±50)U/ml,PC组显著高于其他3组(P<0.01).以>232 U/ml为界,KL-6诊断胰腺癌的敏感性为96%,特异性为94%;以>244 U/ml为界,鉴别诊断PC与CP的敏感性为97%,特异性为91%.KL-6诊断胰腺癌的临床价值高于CA19-9、CA50及MUC4.胰腺癌患者血清KL-6水平与肿瘤的临床病理参数均无相关性.血清KL-6≤300 U/ml患者的平均生存期为(9.3±1.2)个月,较KL-6>300 U/ml患者平均生存期(4.6±0.7)个月显著延长(P=0.006).结论 KL-6可作为诊断胰腺癌的血清学指标,且对胰腺癌和慢性胰腺炎的鉴别诊断有一定意义.     

胰腺癌内镜超声引导下细针穿刺活检物中肿瘤标志物检测价值研究

目的 探讨检测内镜超声引导下细针穿刺(EUS-FNA)活检物中CEA、CA19-9常用肿瘤标志物对胰腺癌诊断的价值.方法 2004年6月至2006年1月间的65例胰腺癌患者和25例慢性胰腺炎患者行EUS-FNA,采用电化学发光法对EUS-FNA活检物的离心上清进行CEA、CA19-9检测,并与该患者外周静脉血清中的CEA、CA19-9进行对比和分析.随后对临床可疑胰腺癌而EUS-FNA病理学检测阴性的12例的病例进行随访,观察该方法诊断胰腺癌的敏感性.结果 (1)胰腺癌患者中EUS-FNA标本中CEA和CA19-9均高于血清(P＜0.01).慢性胰腺炎患者EUS-FNA标本与血清中的CEA(P=0.122)和CA19-9(P=0.035)都没有明显差别.(2)对于EUS-FNA标本,胰腺癌中的CEA、CA19-9高于慢性胰腺炎(P＜0.01).对于血清标本,慢性胰腺炎与胰腺癌中的CEA没有明显差别(P=0.079),胰腺癌中的CA19-9高于慢性胰腺炎患者(P＜0.01).(3)12例可疑胰腺癌随访后确诊10例为胰腺癌,2例为慢性胰腺炎.对于胰腺癌的诊断,血清CEA的敏感性为30%,血清CA19-9为70%;EUS-FNA活检物中CEA和CA19-9的预测敏感性均为90%.结论 胰腺癌EUS-FNA活检物中的CEA、CA19-9对提高胰腺癌诊断的敏感性具有较高的临床实用价值,为提高胰腺癌的诊断率提供了一种新的方法.     

慢性胰腺炎局灶性肿块术前病变性质预测因子

目的 建立慢性胰腺炎(CP)局灶性肿块病变性质预测模型,分析其主要预测因子.方法 收集上海市7家三级甲等医院1998年7月至2007年4月收治的CP局灶性肿块病变性质不明患者121例,经病理(97例)或随访(24例)判断肿块性质,分为胰腺癌组和CP组.通过查阅病历等方式记录患者性别、年龄、既往疾病史、初诊时的主要临床表现、实验室检查和影像学检查结果,采用病例对照研究设计,应用χ~2 检验、t检验等方法进行单因素分析.选择单因素分析中P≤0.25的因素进行多因素分析,建立病变性质Logistic回归预测模型,计算各因素的OR值及95%可信限.结果 121例患者最终确诊为胰腺癌21例,CP 100例.腹部压痛、直接胆红素、CA19-9和CEA是肿块病变性质的独立预测因子,它们的OR值分别为5.691、1.011、1.003、1.019;95%可信限分别为1.468,22.070、1.001,1.021、1.001,1.005和0.988,1.051;P值分别为0.012、0.030、0.003和0.23.结论 本研究的Logistic回归模型可以较为准确地预测CP局灶性肿块的病变性质,可能有一定的临床应用价值.     

CA19-9和IL-33对胰腺癌的临床诊断价值分析

目的评估白细胞介素-33(interleukin-33,IL-33)和糖类抗原19-9(carbohydrate antigen 19-9,CA19-9)对胰腺癌的临床诊断价值。方法选取50例胰腺癌患者、70例胰腺炎患者、50名健康人群作为研究对象,比较3组患者外周血内IL-33和CA19-9水平,评价IL-33和CA19-9单独应用及联合应用对胰腺癌的诊断灵敏度、特异度和准确率,并比较不同病理分期胰腺癌患者外周血内IL-33和CA19-9的水平差异。结果 CA19-9水平超过临界值37 U/ml时对胰腺癌的诊断准确率为96.70%,当超过100 U/ml时诊断准确率有所上升,但超过1 000 U/ml时其诊断精确度却不再上升;当IL-33水平超过临界值50 pg/ml时对胰腺癌的诊断具有较高准确率,且在超过100 pg/ml时有所增长,但超过300 pg/ml时其诊断正确率不再明显上升。CA19-9单独应用诊断胰腺癌的灵敏度、特异性及准确率均高于IL-33,两者联合应用可提高诊断诊断灵敏度和准确性,但特异性略有下降。不同病理分期胰腺癌外周血内的IL-33和CA19-9水平差异均有统计学意义,随着病理程度的严重,IL-33和CA19-9的水平呈上升趋势(P0.05)。结论IL-33和CA19-9对胰腺癌的确诊和病理分期评估均有重要价值,且能弥补影像学诊断胰腺癌的不足,值得临床推广。     

CT和血清CA19-9联合检测在胰腺癌诊断中的价值

目的探讨CT和血清CA19-9联合检测对胰腺癌诊断的价值。方法回顾性分析胰腺病变93例,所有患者术前均行螺旋CT增强扫描及血清CA19-9检测,并对CT、CA19-9以及二者联合检测与病理诊断进行比较。结果 93例胰腺病变患者中,被病理证实为胰腺癌患者63例。经CT诊断为胰腺癌的68例患者中,55例被病理证实为胰腺癌。CT对胰腺癌诊断的敏感性、特异性和符合率分别为87.3%、56.7%和77.4%。胰腺癌患者的血清CA19-9中位值显著高于非胰腺癌患者(426.7 vs 23.7,P<0.001)。60例CA19-9≥37 U/ml的患者中,48例被病理证实为胰腺癌。CA19-9对胰腺癌诊断的敏感性、特异性和符合率分别为76.2%、60.0%和71.0%。CT联合CA19-9检测对胰腺癌诊断的敏感性、特异性和符合率分别为68.3%、90.0%和75.3%。CT、CA19-9以及二者联合检测与病理诊断均有较好的一致性(均P<0.001),但联合检测的一致性更高。以ROC曲线和Youden指数指示的CA19-9判定胰腺癌的最佳阈值(235.1 U/ml)作为诊断分界点时,CA19-9对胰腺癌诊断的敏感性、特异性和符合率分别为65.1%、90%和73.1%,显著提高了诊断的特异性。以235.1 U/ml为诊断分界点,CA19-9与CT联合检测对胰腺癌诊断的敏感性、特异性和符合率分别为60.3%、96.7%和72.1%,进一步提高了诊断的特异性。结论对于无法获取病理组织的患者,CT联合CA19-9检测是临床诊断胰腺癌较好的方法之一。     

联合检测血清TK1、CA19-9对胰腺癌和胰腺炎鉴别诊断的价值

目的 探讨联合检测血清胸苷激酶1（TK1）、糖类抗原19-9（CA19-9）对胰腺癌和胰腺炎鉴别诊断的价值.方法 选择胰腺癌患者37例（胰腺癌组）、胰腺炎患者40例（胰腺炎组）及健康体检者50例（对照组）,采用化学增强发光印迹法检测其血清TK1,直接化学发光法检测血清CA19-9.结果 胰腺癌组、胰腺炎组血清CA19-9水平明显高于对照组（P均＜0.05）,但胰腺癌组与胰腺炎组比较差异无统计学意义.胰腺癌组血清TK1水平明显高于胰腺炎组、对照组（P均＜0.05）,而胰腺炎组与对照组比较差异无统计学意义.两者联合检测能明显提高诊断胰腺癌的敏感性（92.7％）.结论 联合检测血清CA19-9、TK1有助于胰腺炎和胰腺癌的鉴别诊断.     

肿瘤标志物CA242与CA19-9对胰腺癌的诊断价值

目的:比较血清肿瘤标志物CA242与CA19-9对胰腺癌的诊断价值。方法:1996年4月至1997年6月,北京医院对门诊及住院197例患者进行了血清CA19-9的检测,148例进行了CA242的检测,其中25例为临床明确诊断为胰腺癌,12例为急性胰腺炎,18例为良性阻塞性黄疸。结果显示:胰腺癌患者血清CA19-9和CA242较对照明显增高,其中25例胰腺癌患者有21例CA19-9阳性,检测的灵敏度为84％,特异性为74.4％,有17例CA242阳性,检测的灵敏度为68％,特异性为87.8％。CA242与CA19-9比较,灵敏度无显著差异(0.10相似文献   

胰腺癌患者血清CEMIP、CA19-9和CA242水平变化及其临床意义*

目的 研究胰腺癌患者血清CEMIP、CA19-9和CA242水平变化及其临床意义。方法 2013年4月～2016年8月我院诊治的92例胰腺癌患者、105例胰腺良性疾病患者和选择的83例健康人，采用ELISA法检测血清细胞迁移诱导透明质酸结合蛋白（CEMIP）水平，采用放射免疫法检测血清CA19-9和CA242水平。应用受试者工作特征曲线（ROC）下面积（AUC）评价各指标的诊断效能。采用Kaplan-Meier和Cox风险比例模型行生存分析。采用Logistic回归分析影响术后生存的因素。结果 胰腺癌患者血清CEMIP、CA19-9和CA242水平分别为0.7（0.4，1.0） ng/mL、180.1（89.1，230.3） U/mL和61.7（20.7，93.5）U/mL，均显著高于胰腺良性疾病患者和健康人，差异有统计学意义（P均<0.05）；应用血清CEMIP、CA19-9和CA242联合诊断胰腺癌的AUC为0.966，其诊断效能显著高于任一指标单独诊断；应用血清CEMIP、CA19-9和CA242水平预测胰腺癌患者根治术后1年生存的效能均较高；经Kaplan-Meier和Cox多因素分析，结果表明肿瘤分化程度、血管侵犯、术后化疗、血清CEMIP≥0.7 ng/mL、CA19-9≥90.3 U/mL和CA242≥32.8 U/mL均是影响胰腺癌患者根治术后生存的独立危险因素。结论 检测胰腺癌患者血清CEMIP、CA19-9和CA242水平可有助于对疾病的诊断和预后评估。     

胆胰疾病CA19-9升高相关因素及其临床价值研究

目的研究影响胆胰疾病CA19-9水平的因素,评价CA19-9升高在鉴别诊断消化道良恶性疾病中的临床价值。方法回顾性分析2003—2009年北京大学人民医院201例胆胰疾病(73例胰腺癌、45例胆管癌、83例胆总管结石),分析胆总管结石患者的CA19-9水平和胆汁淤积以及胆管炎症相关指标的相关性。分析胰腺癌、胆管癌患者CA19-9水平和肿瘤分期及分化程度的相关性。绘制胰腺癌、胆管癌CA19-9的ROC曲线。结果CA19-9升高组胆总管结石患者胆汁淤积以及胆管炎症相关指标均较CA19-9正常组高(P值均0.05),患者的CA19-9水平与上述指标呈正相关(P值均0.05)。胰腺癌患者的CA19-9水平与年龄和肿瘤分期呈正相关(P值均0.05)。CA19-9诊断胰腺癌的灵敏度(临界值为37kU/L)86.30%,特异度42.16%,据ROC曲线当临界值为42kU/L时灵敏度为86.30%,特异度为53.06%。CA19-9临界值为37kU/L诊断胆管癌的灵敏度95.56%,特异度42.16%,根据ROC曲线当临界值为63.14kU/L时,灵敏度95.56%,特异度60.24%。结论胆总管结石患者的CA19-9非特异性升高水平与胆汁淤积以及胆管炎症相关指标呈正相关。胰腺癌患者的CA19-9水平和肿瘤分期呈正相关。以CA19-9临界值为37kU/L诊断胰腺癌和胆管癌灵敏度较高,但是鉴别良恶性疾病的特异性不理想,提高临界值可以提高特异度。     

CEA、CA19-9、CA50水平与胰腺癌分期和肿瘤大小的关系

目的 探讨血清肿瘤标志物CEA、CA19-9、CA50水平与胰腺癌分期和肿瘤大小的关系.方法 分别测定35例胰腺癌和36例慢性胰腺炎患者血清CEA、CA19-9与CA50水平.外科手术和(或)病理学判定TNM分期和肿瘤大小,分析两者之间的关系.结果 血清CEA、CA19-9、CA50对胰腺癌诊断的敏感性分别为42%、82%、74%.特异性分别为75%、83%、77%.Ⅲ + Ⅳ期的CA19-9和CA50水平明显高于Ⅰ + Ⅱ期患者(P ＜ 0.05),CEA超过正常值者仅见于Ⅲ期以上胰腺癌患者.TS3 + TS4组的CEA、CA19-9、CA50水平比TS1 + TS2组明显增高(P ＜ 0.05).结论 胰腺癌血清CEA、CA19-9、CA50水平与胰腺癌分期和肿瘤大小有一定相关性,对手术前判断胰腺癌的可切除性有一定的参考价值.     

Alcohol and Smoking as Risk Factors in Chronic Pancreatitis and Pancreatic Cancer

The aim of this study was to compare alcohol andsmoking as risk factors in the development of chronicpancreatitis and pancreatic cancer. We considered onlymale subjects: (1) 630 patients with chronic pancreatitis who developed 12 pancreatic and 47extrapancreatic cancers; (2) 69 patients withhistologically well documented pancreatic cancer and noclinical history of chronic pancreatitis; and (3) 700 random controls taken from the Verona pollinglist and submitted to a complete medical check-up.Chronic pancreatitis subjects drink more than controlsubjects and more than subjects with pancreatic cancer without chronic pancreatitis (P < 0.001).The percentage of smokers in the group with chronicpancreatitis is significantly higher than that in thecontrol group [odds ratio (OR) 17.3; 95% CI 12.6-23.8; P < 0.001] and in the group with pancreaticcarcinomas but with no history of chronic pancreatitis(OR 5.3; 95% CI 3.0-9.4; P < 0.001). In conclusion,our study shows that: (1) the risk of chronic pancreatitis correlates both with alcoholintake and with cigarette smoking with a trendindicating that the risk increases with increasedalcohol intake and cigarette consumption; (2) alcoholand smoking are statistically independent risk factors forchronic pancreatitis; and (3) the risk of pancreaticcancer correlates positively with cigarette smoking butnot with drinking.     

The epidemiology and impact of pancreatic diseases in the United States

In the United States, acute pancreatitis, chronic pancreatitis, and pancreatic cancer are the most common pancreatic disorders requiring diagnosis and treatment. Pancreatic cancer is responsible for nearly 30,000 annual deaths and is the second most common cause of death from any type of gastrointestinal disease. Gallstone disease, which is strongly associated with obesity, and excessive consumption of alcohol are the major risk factors for benign pancreatic disease, whereas smoking is the most important factor known to cause pancreatic cancer. Therefore, to reduce the overall burden of pancreatic disease, we should focus on the control of three lifestyle factors: smoking, drinking, and obesity.     

Pancreatic carcinoma developing in chronic pancreatitis: a report of four cases

Although chronic pancreatitis microscopically surrounding pancreatic carcinoma is common, cancer developing in chronic pancreatitis has rarely been shown. We present four such cases seen between 1983 and 1988. All were male, mean age 56.7 years, and all had had previous surgery for complications of chronic pancreatitis (two a pancreatectomy, two a bypass). Chronic pancreatitis was caused by alcohol in three cases, and calcification was present in three. The delay between chronic pancreatitis and pancreatic carcinoma was 2 to 10 years, and in all, pancreatic carcinoma was at an advanced state, with post-surgical survival of 1.5 to 6 months. CA 19.9 level was very high in the three cases in which it was measured. That pancreatic carcinoma is more frequent in populations with chronic pancreatitis, occurring later in life than pancreatic carcinoma that has no coexisting chronic pancreatitis (sixth decade vs. fifth), often with intermediate histology, argues for chronic pancreatitis degenerating into pancreatic carcinoma rather than for a common toxic etiology. Pancreatic carcinoma occurs particularly in calcified chronic pancreatitis, and diagnosis is frequently quite late, due to the non-specificity of symptoms vs. chronic pancreatitis. Delay of appearance is variable, and previous surgery and histological examination excludes obvious coexisting pancreatic carcinoma. Aggressive surgery appears justified if needed for chronic pancreatitis, and chronic pancreatitis should be carefully followed, probably by serial CA 19.9 determinations and guided percutaneous fine needle biopsies when elevated, or when new symptoms are present in chronic pancreatitis.     

Incidence of and risk factors for pancreatic cancer in chronic pancreatitis: A cohort of 1656 patients

BackgroundRisk of pancreatic cancer may increase in chronic pancreatitis patients.AimsThis study aimed to identify the incidence of and risk factors for pancreatic cancer in chronic pancreatitis patients.MethodsChronic pancreatitis patients admitted to our center from January 2000 to December 2013 were enrolled. Cumulative rates of pancreatic cancer and survival rates were calculated. The standardized incidence ratio was calculated based on the pancreatic cancer incidence in general population of China. Risk factors for pancreatic cancer were identified.ResultsIn a total of 1656 patients, the median follow-up duration was 8.0 years. Pancreatic cancer was detected in 21 patients (1.3%). The expected number of cases of pancreatic cancer was 1.039, yielding a standardized incidence ratio of 20.22. The standardized incidence ratios for patients with a >60 pack-year smoking history were much higher (145.82). Two risk factors for pancreatic cancer were identified: age at the onset of chronic pancreatitis (hazard ratio, 1.05) and a >60 pack-year smoking history (hazard ratio, 11.83).ConclusionThe risk of pancreatic cancer is markedly increased in chronic pancreatitis patients compared with the general population, especially in patients with an older age at onset and a >60 pack-year smoking history. The high-risk populations were suggested to be followed up closely.     

Risk factors for pancreatic cancer: case-control study

OBJECTIVES: Although cigarette smoking is the most well-established environmental risk factor for pancreatic cancer, the interaction between smoking and other risk factors has not been assessed. We evaluated the independent effects of multiple risk factors for pancreatic cancer and determined whether the magnitude of cigarette smoking was modified by other risk factors in men and women. METHODS: We conducted a hospital-based case-control study involving 808 patients with pathologically diagnosed pancreatic cancer and 808 healthy frequency-matched controls. Information on risk factors was collected by personal interview, and unconditional logistic regression was used to determine adjusted odds ratios (AORs) by the maximum-likelihood method. RESULTS: Cigarette smoking, family history of pancreatic cancer, heavy alcohol consumption (>60 mL ethanol/day), diabetes mellitus, and history of pancreatitis were significant risk factors for pancreatic cancer. We found synergistic interactions between cigarette smoking and family history of pancreatic cancer (AOR 12.8, 95% confidence interval [CI] 1.6-108.9) and diabetes mellitus (AOR 9.3, 95% CI 2.0-44.1) in women, according to an additive model. Approximately 23%, 9%, 3%, and 5% of pancreatic cancer cases in this study were related to cigarette smoking, diabetes mellitus, heavy alcohol consumption, and family history of pancreatic cancer, respectively. CONCLUSIONS: The significant synergy between these risk factors suggests a common pathway for carcinogenesis of the pancreas. Determining the underlying mechanisms for such synergies may lead to the development of pancreatic cancer prevention strategies for high-risk individuals.     

Comparison of tumor marker CA 242 with CA 19-9 and carcinoembryonic antigen (CEA) in pancreatic cancer

BACKGROUND/AIMS: Although there are a variety of tumor markers used for diagnosis of pancreatic carcinoma, the sensitivity and specificity of those markers have not yet reached an ideal level. The aim of this study was to compare the diagnostic value of CA 242 with CA 19-9 and CEA in the patients with pancreatic cancer. METHODOLOGY: Serum CA 242, CA 19-9 and CEA levels were determined in 135 subjects in the following groups: Pancreatic cancer (n = 40), cholangiocellular carcinoma (n = 15), hepatocellular carcinoma (n = 10), cirrhosis (n = 7), chronic active hepatitis (n = 7), choledochal stone (n = 12), chronic pancreatitis (n = 9), acute pancreatitis (n = 6), and healthy controls (n = 29). RESULTS: An elevated serum CA 242 concentration (> 20 U/mL) was found in 30 out of 40 (70%) (mean; 2163 +/- 838 U/mL) patients with pancreas cancer, in 11 out of 15 patients with cholangiocellular carcinoma (93.3%) (mean 916 +/- 529 U/mL), in none of patients with hepatocellular carcinoma and healthy controls. Slightly elevated CA 242 concentration was found in 6 out of 41 patients with benign hepatobiliary and pancreatic disease (range 0.4-97.8 U/mL) (1 acute pancreatitis, 2 chronic pancreatitis, 1 cirrhosis, 2 choledochal stone). Mean serum CA 242, CA 19-9 and CEA levels of the pancreas cancer group were significantly higher than those of the other groups except the cholangiocellular carcinoma group. There was no significant difference between the stage of pancreas cancer regarding mean serum CA 242, CA 19-9 and CEA level. There was positive correlation between serum CA 242 and CA 19-9 level. In the pancreas cancer, the sensitivity of CA 242, CA 19-9 and CEA was 75%, 80%, 40%, respectively and the specificity of those markers was 85.5%, 67.5% and 73%, respectively. CONCLUSIONS: In conclusion, the advantage of CA 242 compared to CA 19-9 is that its specificity is higher than that of CA 19-9 in the diagnosis of pancreas cancer.     

慢性胰腺炎胰腺钙化与烟酒关系初探

目的 探讨国内慢性胰腺炎(CP)患者烟酒摄入量与发生胰腺钙化间的关系.方法 按入院时有无胰腺钙化分为两组进行比较分析,再将无胰腺钙化者出院后有无新发胰腺钙化分为新发组和持续无钙化组.Logistic回归或Cox比例风险模型进行逐步回归分析胰腺钙化的风险因素.结果 1997年1月到2007年7月共收治并成功随访449例CP患者,248例有胰腺钙化;201例无胰腺钙化,其中13例出院后新发生胰腺钙化.入院时胰腺钙化者的发病年龄小、病史长、糖尿病和腹泻发生率高.首发年龄≤40岁、酒精摄入量>20 g/d、糖尿病和腹泻为胰腺钙化风险因素;过量饮酒为无胰腺钙化CP 患者新发生钙化的唯一风险因素(OR 3.2).结论 饮酒增加CP患者胰腺钙化风险,建议戒酒;吸烟的作用需进一步研究.     

Pancreatitis as a risk for pancreatic cancer

Chronic pancreatitis clearly predisposes to pancreatic cancer, with early onset-long duration chronic pancreatitis from cystic fibrosis, TP, and HP conferring the highest risk. Chronic pancreatitis is not a critical step, however, but rather one of several conditions that accelerate the accumulation of critical genetic mutations and chromosomal losses necessary for carcinogenesis. Indeed, other germline mutations, environmental factors such as tobacco smoking and alcohol consumption, or dietary factors may also accelerate the pathway to carcinogenesis, and may be synergistic with the conditions created by chronic pancreatitis. Because patients with chronic pancreatitis are at high risk of pancreatic cancer, the physician is faced with decisions on how to manage this risk. Discontinuing smoking and alcohol consumption, and perhaps dietary modification are obvious recommendations for risk reduction. If, however, the patient is older and already in a very high-risk category (e.g., long-standing HP), then screening for cancers must be considered. Inclusion in multicenter trials is recommended, and information on ongoing studies can be obtained through the office of Dr. Whitcomb, or as posted on www.pancreas.org.     

不同时期胰腺癌易感因素分析与比较

目的　分析胰腺癌患者易感因素 ,以期能确认胰腺癌危险因素。方法　采用回顾性分析的方法 ,分析 1985年 10月～ 1991年 11月 (78例 )及 1995年 10月～ 2 0 0 1年 8月 (194例 )胰腺癌病例。结果　胰腺癌的发病率有逐年增高趋势 ;患者发病年龄以中老年为主 ,男性多见 ,且发病人数呈上升趋势 ;胰腺癌的易感因素依次为吸烟 (33.1% )、饮酒 (2 1.7% )、糖尿病 (11.8% )及慢性胰腺炎 (4.8% )等。1995～ 2 0 0 1年间患者有吸烟 (36 .6 % )、饮酒 (2 4 .7% )、糖尿病 (14 .9% )等病史者较 1985～ 1991年间有增加趋势 ,其中仅糖尿病 (3.8% )增加比率差异有显著性 ;随着吸烟量及年限增加 ,胰腺癌发病率有增加趋势 ;糖尿病胰腺癌组和非糖尿病胰腺癌组相比 ,肿瘤大小、部位、肿瘤切除率差异无显著性 ,但糖尿病组以高中分化腺癌为主 ,非糖尿病组低分化腺癌患者较多 ,两组之间相比差异有显著性 (P <0 .0 5 )。结论　吸烟、吸烟量与时间的长短与胰腺癌发生直接相关 ,合并糖尿病的胰腺癌者高分化腺癌比例明显高于未合并糖尿病者。胰腺癌的易感因素近期较以往亦增加。     

Associations of alcohol drinking and nutrient intake with chronic pancreatitis: findings from a case-control study in Japan

OBJECTIVE: The aim of this study was to examine the association of alcohol drinking and nutrient intake with chronic pancreatitis in a hospital-based case-control study. METHODS: From July, 1997, to December, 1998, 91 male patients, who were newly diagnosed as having chronic pancreatitis, were recruited as cases, and 175 controls were individually matched to each case for gender, age (+/-5 yr), hospital, and time of the first visit to a hospital (+/-1 yr). Information on demographic characteristics, smoking and drinking, and dietary habits were collected by a self-administered questionnaire. The strength of associations was examined by odds ratios (ORs) and 95% CIs calculated from conditional logistic regression models. RESULTS: Our study showed that the more the daily amount of alcohol drinking, the larger the OR. Men who consumed > or =100 g ethanol/day were at an approximately 11-fold increased risk as compared with nondrinkers. Long-term alcohol consumption (>35 yr) was associated with the increased risk (OR = 4.0). Risk of chronic pancreatitis remarkably increased with increasing cumulative alcohol consumption (trend p = 0.0001). Intakes of saturated fatty acid and vitamin E were negatively associated with the risk (trend p = 0.05 for saturated fatty acid and 0.03 for vitamin E). CONCLUSION: Our study clearly demonstrated that prolonged heavy alcohol consumption was an important and independent risk factor, and suggested a role of lower nutrient intakes in the development of chronic pancreatitis.