2, 0703, V0261], hepatitis C [ICD-9: 07041, 07044, 07051, 07

2, 070.3, V02.61], hepatitis C [ICD-9: 070.41, 070.44, 070.51, 070.54, V02.62], unspecified chronic hepatitis [ICD-9: 070.9, 571.4, 571.8, 571.9], alcoholic liver disease [ICD-9: 571.0, 571.1, 571.2, 571.3], cirrhosis [ICD-9: 571.5, 571.6]) and biliary tract19 (cholangitis [ICD-9: 575.8, 576.1], cholecystitis [ICD-9: 575.0, 575.11, 575.12], cholelithiasis [ICD-9: 574], choledocholithiasis [ICD-9: 574.5], biliary cirrhosis [ICD-9: 571.6]) from inpatient claims (1997-2006) and related

ambulatory care claims of both diabetic and control subjects (1997-2006). We counted the above clinical risk factors occurring in individuals in both groups only when the dates of diagnosis for the selected illnesses (clinical risk factors)

were noted before or the day on which the study subjects’ endpoints or censoring took place. The following criteria were set as censoring dates for the study subjects. First, if a subject died in the hospital Selleck BMS 907351 from causes other than the study endpoints, the date of censoring was the date of death. Second, if a subject did not encounter in-hospital mortality, the date of censoring was either the date of their last withdrawal from NHI or the date of termination of the study (December 31, 2006). We performed two major statistical analyses in this study. First, the age-specific and sex-specific hazard rate was estimated using person-years Trichostatin A manufacturer as the denominator under the Poisson assumption. Second, to determine the independent effects of diabetes on the risks of malignant neoplasms of the liver and biliary tract, we used

Cox proportional hazard regression models with age, sex, geographic area, urbanization statuses, and related clinical risk factors adjusted simultaneously in the model. We adjusted geographic variables for possible geographic variations in the incidence of hepatocellular carcinoma.28 Furthermore, we explored the relative hazards of malignant neoplasm of the liver and biliary tract in relation to diabetes accompanied by the selected clinical risk factors individually with Cox proportional hazard regression models with age, sex, geographic area, and urbanization statuses adjusted in the model. All statistical analyses were performed with SAS version 9.1 (SAS Institute, Cary, NC). A P value <0.05 was considered see more statistically significant. The mean (± standard deviation) age of the diabetic group was 60.09 ± 12.73 years, whereas that of the control subjects was 60.00 ± 12.84 years. The percentages of people aged <45, 45-64, and >64 years were 11.3%, 48.3%, and 40.4% in both the control group and the diabetic population. The ratio of men to women was 51.9:48.1 in both groups. The details of geographic and clinical risk factors distribution are shown in Table 1. The median time of follow-up was similar at 6.9 years for both groups. The overall and age-specific and sex-specific hazard rate of malignant neoplasm of the liver are presented in Table 2.

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