1,721,046 research outputs found

    A CASE-CONTROL STUDY OF DIABETES-MELLITUS AND CANCER RISK

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    The relationship between diabetes mellitus and cancer risk was investigated using data from an integrated series of case-control studies conducted in Northern Italy between 1983 and 1992. Cases were 9,991 patients with incident, histologically confirmed neoplasms below age 75, including 181 cancers of the oral cavity and pharynx, 316 of the oesophagus, 723 of the stomach, 828 of the colon, 498 of the rectum, 320 of the liver, 58 of the gall bladder, 362 of the pancreas, 242 of the larynx, 3,415 of the breast, 726 of the endometrium, 971 of the ovary, 125 of the prostate, 431 of the bladder, 187 of the kidney, 208 of the thyroid, 80 Hodgkin's lymphomas, 200 non-Hodgkin's lymphomas and 120 multiple myelomas. Controls were 7,834 subjects in hospital For acute, non-neoplastic, non-metabolic, non-hormone-related disorders. A history of diabetes was reported by 5.1% of male and 5.4% of female controls. Significantly elevated relative risks (RRs) among subjects with diabetes were observed for cancers of the liver [RR = 2.8, 95% confidence interval (CI) 2.0-3.9], pancreas (RR=2.1, 95% CI 1.5-2.9) and endometrium (RR=3.4, 95% CI 2.7-4.3). After allowance for obesity and education as well as age and sex, the RRs were 3.0 for liver, 2.3 for pancreas, and 2.8 for endometrium. Diabetic subjects had no elevated risk for any of the other cancer sites considered. For liver and endometrial cancer the RRs remained elevated up to 10 years after diagnosis of diabetes (RR 2.6 and 2.0 respectively), while the RR for pancreatic cancer declined from 3.2 in the first 5 years after diagnosis of diabetes to 2.3 from 5 to 9 years and to 1.3 (95% CI 0.7-2.3) 10 or more years since diagnosis. This suggests that the relationship between diabetes mellitus and liver and endometrial cancer is probably real, while that with pancreatic cancer is compatible with diabetes being an early symptom of the disease, or at least of preneoplastic lesions

    MODERATE BEER CONSUMPTION AND THE RISK OF COLORECTAL-CANCER

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    The relationship between beer consumption and the risk of colon and rectal cancer was considered in a case-control study conducted in northern Italy. The study was based on 828 histologically confirmed incident cases of colon cancer, 498 of rectal cancer, and 2,024 controls in hospital for a wide spectrum of acute, nonneoplastic, nonalcohol-related diseases. Beer drinking was reported by 6% of colon cancer cases, 7% of rectal cancer cases, and 10% of controls: regular beer drinkers (greater-than-or-equal-to 1 drinks/day) made up 2.6% of colon cancer cases, 3.2% of rectal cancer cases, and 4.1% of controls. Thus the multivariate relative risks (RR) for irregular drinkers were 0.6 [95% confidence interval (CI) 0.4-1.0] for colon and 0.7 (95% CI 0.4-1.2) for rectum. Corresponding values for regular drinkers were 0. 7 (95% CI 0.4-1.2) for colon and 0. 9 (95% CI 0.5-1.5) for rectal cancer. Despite the low frequency of beer drinking in this study, and hence its limited statistical power, the originality of the population in terms of colorectal cancer incidence, patterns of risk factor exposure, and the large dataset pro vide interesting and useful confirmation that moderate beer drinking is not associated with elevated colon or rectal cancer risk

    GENITAL AND URINARY-TRACT DISEASES AND BLADDER-CANCER

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    The relationship between selected urinary tract and genital diseases and the risk of bladder cancer was analyzed using data from a case-control study of 364 cases of bladder cancer and 447 controls hospitalized for acute, nonneoplastic, nongenital tract conditions, unrelated to known or suspected risk factors for bladder cancer. Cystitis was reported by 20% of the cases and 8% of the controls, corresponding to a multivariate relative risk (RR) of 3.8 (95% confidence interval, 2.4 to 5.9). No association was observed with urinary tract stones (RR = 1.2). With reference to genital diseases, the RR was elevated for gonorrhea (RR = 2.8, 95% confidence interval, 1.0 to 4.5) and condylomata acuminata (RR = 5.9, 95% confidence interval 1.0 to 3.6) but not for syphilis. The risk increased with the number of episodes of cystitis (RR = 5.0 for greater-than-or-equal-to 4 episodes, chi-2 for trend = 33.04, P < 0.001), was higher during the last 15 years after the first episode (RR = 5.1 versus 2.3 for over 15 years), and was not heterogeneous across strata of age and sex. The interaction between urinary tract infections and tobacco appeared multiplicative, with RR = 2.4 for ever smoking, 3.2 for cystitis alone, and 10.3 for both exposures. The present study, besides providing further quantitative evidence of a relationship between urinary tract infections (and, possibly, some genital infections, too) and bladder cancer, indicates that the role of infections is probably in one of the latter (promoting) stages of the process of carcinogenesis and suggests a multiplicative interaction with smoking. In terms of prevention and public health, therefore, it it is thus important to avoid at least one exposure for subjects with a history of urinary tract infections who smoke tobacco

    ACUTE MYOCARDIAL-INFARCTION - ASSOCIATION WITH TIME SINCE STOPPING SMOKING IN ITALY

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    Study objective - The study aimed to investigate the relationship between years since stopping smoking and the risk of acute myocardial infarction. Design - This was a hospital based, multicentre, case-control study conducted in Italy between September 1988 and June 1989 within the framework of the GISSI-2 clinical trial. Setting - Over 80 coronary care units in various Italian regions participated. Subjects - A total of 916 incident cases of acute myocardial infarction, below age 75 years, and with no history of ischaemic heart disease, and 1106 control subjects admitted to the same hospitals for acute, non-neoplastic, cardiovascular or cerebrovascular conditions that were not known or suspected to be related to cigarette smoking took part in the study. Main outcome measures and results - Measures were relative risk (RR) estimates of acute myocardial infarction according to the time since stopping smoking and adjusted for identified potential confounding factors. Compared with never smokers, the multivarlate RRs were 1.6 (95% confidence interval (CI) 0.8,3.2) for subjects who had given up smoking for one year; 1.4 (95% CI0.9,2.1) for those who had stopped for two to five years; 1.2 (95% CI0.7,2.1) for six to 10 years; and 1.1 (95% CI0.8,1.8) for those who had not smoked for over 10 years. The estimated RR for current smokers was 2.9 (95% CI 2.2,3.9). The risks of quitters were higher for heavier smokers and those below age 50 years, while no difference emerged in relation to the duration of smoking, sex, and other risk factors for myocardial infarction. Conclusions - These results indicate that there is already a substantial drop in the risk of acute myocardial infarction one year after stopping. The risk in ex-smokers, however, seemed higher (although not significantly) than that of those who had never smoked, even more than 10 years after quitting. This could support the existence of at least two mechanisms linking cigarette smoking with acute myocardial infarction - one involving thrombogenesis or spasms that occurs over the short term, and another involving atherosclerosis that is a long term effect
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