1,721,175 research outputs found
A review of epidemiological studies on cancer in relation to the use of anti-ulcer drugs
No full textH2-receptor antagonists have been widely used since the late 1970s for the treatment of gastrointestinal ulcers and other benign conditions of the stomach, oesophagus and duodenum. Several case reports suggested that long-term therapy with H2-receptor antagonists, mainly cimetidine and ranitidine, might increase the risk of gastric cancer. After early case reports, at least six analytical epidemiological studies (two cohort and four case-control) were published, including a total of about 1000 cases of gastric cancer. The relative risks (RR) were systematically and substantially elevated in the first year since starting H2-receptor antagonist use, and levelled off in the following years. Some excess risk was still apparent during the first 5 years of drug use, probably due to incorrect diagnosis and treatment of pre-existing neoplastic gastric lesions, but the estimated RR was not above unity for ≥10 years since starting drug treatment in the two studies including information on long-term use. The findings of analytical epidemiological studies are thus consistent with the absence of a causal association between H2-receptor antagonist use and gastric cancer risk. Data on oesophageal and colorectal cancer do not support a relevant relation between cimetidine use and the risk of these neoplasms. With reference to total cancer mortality, in a Danish cohort study, for males the RR was 1.9 in the first year, and 1.4 in the first 5 years; corresponding values for females were 1.7 and 1.5. In a British cohort study, the RR was 3.4 in the first year, and 1.3 in the years 2-10. The excess risk in the first year was essentially due to gastric cancer. Post-marketing surveillance data for omeprazole and other proton pump inhibitors are much scantier than for H2-receptor antagonists, particularly on long-term use
Epidemiology of renal-cell carcinoma
No full textRenal-cell cancer is responsible for about 2% of all cancer deaths in developed countries and represents 80-85% of all tumors of the kidney. Its etiology is still largely undefined. Recently the results of a large international population-based case-control study (International Renal-Cell Cancer Study), conducted between 1989 and 1991 in Australia, Denmark, Germany, Sweden and USA, including 1732 cases and 2309 controls, showed an increased risk of renal-cell cancer in relation to tobacco smoking, elevated body mass index, a few medical conditions, the use of beta-blockers, a family history of the disease, high intake of dairy products and low intake of fruit and vegetables and, in women, multiparity. Most other studies agree about a causal role of cigarette smoking in the etiology of renal-cell cancer, although its association is less strong than for several other tobacco-related neoplasms, with a relative risk of about 2 for current smokers. Other established risk factors are elevated body mass index (mainly in women) and a family history of the disease. Occupational exposure to chemicals appears to have little significance, although associations with specific products, such as asbestos fibres, have been reported. Some relationship has been observed between renal-cell cancer and hypertension, use of anti-hypertensives and kidney diseases, although this issue remains open to discussion. Data are inconsistent on the role of nutrition, mainly for fats and proteins, while vegetable and fruit consumption seems to convey some protection on renal-cell cancer risk. The risk of renal-cell cancer was not materially elevated in relation to coffee, tea and alcohol intake and, in women, oral contraceptive use, hormone replacement therapy, and menstrual factors
Beta-Carotene and risk of coronary heart disease : A review of observational and intervention studies
No full textThe production of free radicals may favour the processes of atherosclerosis, and antioxidant vitamins (including Î2-carotene), which partly prevent such processes, might favorably influence cardiovascular disease (CVD); thus, their supplementation might be a useful tool in the prevention of coronary heart disease (CHD). The relationship between Î2- carotene and CHD has been investigated in several observational studies, including ecological, cohort and case-control studies. Six cohort studies reported relative risks (RR) of CHD between 0.27 and 0.78 for high Î2- carotene levels (plasma/serum levels and dietary intake), but four more recent ones reported RR around unity (range 0.84 to 1.19). The evidence from case-control studies supports a role of Î2-carotene in the prevention of CHD (odds ratios, OR, between 0.37 and 0.71), with a possible stronger protection for current smokers. The four published randomized clinical trials of Î2- carotene supplementation found RR close to unity (range 0.96 to 1.26) for the relation between Î2-carotene and CHD. The apparent discrepancy between observational and intervention studies may depend on several factors. The benefit reported in some observational studies may be related to consumption of foods rich in Î2-carotene rather than Î2-carotene itself, as foods rich in Î2-carotene are usually rich also in other antioxidant vitamins and micronutrients, or to time-related factors, i.e., longer supplementation in intervention studies. Thus, a reasonable recommendation for the prevention of CHD for the general population is to consume a balanced diet with emphasis on antioxidant rich fruit and vegetables and whole grains
Epidemiological evidence on hair dyes and the risk of cancer in humans
No full textEpidemiological data on occupational exposure and personal use of hair dyes was reviewed with specific focus on bladder cancer and lymphoid neoplasms. At least seven cohort and 11 case-control studies included data on occupational exposure to hair dyes by hairdressers, barbers and beauticians, and their subsequent bladder cancer risk. The relative risk (RR) estimate was 1.4 (183 observed vs 129 expected) for cohort studies, and in several case-control studies the RRs were somewhat above unity. These results are compatible with some moderate association between past professional exposure to hair dyes and subsequent bladder cancer risk, but also with errors and biases in observational epidemiological studies, particularly since allowance for smoking was lacking or inadequate in most studies. An open question is whether current occupational exposure to modern hair dyes is still related to some excess bladder cancer risk. Five case-control studies included information on personal use of hair dyes and bladder cancer risk. There was no evidence of any association. Nine cohort and eight case-control studies considering occupational exposure to hair dyes and lymphoid neoplasms were reviewed. In the cohort studies, a total of 100 lymphoid neoplasms was observed compared with 84.4 expected (RR 1.2). The RR estimates were 1.5 for non-Hodgkin's lymphomas (NHL, 17 observed vs 11.2 expected) and 1.1 for multiple myeloma (MM, 19 observed cases vs 16.8 expected). Interpretation of case-control studies of occupational exposure is seriously hampered by the small number of exposed cases. Five case-control studies considered personal use of hair dyes and the risk of lymphoid neoplasms. Of these, three reported some association, particularly with NHL and MM. However, the RR estimates were only moderately above unity, and inadequate allowance was made for potential confounding factors, including social class and greying hair, which could be correlates of both hair dye use and lymphoid neoplasms. Further, there is little information on the biodistribution and bioavailability of potential carcinogens in hair dyes, particularly their concentrations in lymphoid tissue. These findings, therefore, require further research, particularly since they may be influenced by selective publication of positive findings (publication bias). None of the other neoplasms extensively studied, including breast, skin and lung was related to hair dye use
Coffee, decaffeinated coffee, tea and cancer of the colon and rectum : a review of epidemiological studies, 1990-2003
No full textThe literature from 1990 to 2003 on the relation between coffee, decaffeinated coffee, tea and colorectal cancer risk has been reviewed. For the relation with coffee, three cohort (517 total cases) and nine case-control studies (7555 cases) analysed colon cancer; three cohort (307 cases) and four case-control studies (2704 cases) rectal cancer; six case-control studies (854 cases) colorectal cancer. For colon cancer most case-control studies found risk estimates below unity; the results are less clear for cohort studies. No relation emerged for rectal cancer. A meta-analysis, including five cohort and twelve case-control studies, reported a pooled relative risk of 0.76 (significant). Any methodological artefact is unlikely to account for the consistent inverse association in different countries and settings. Plausible biological explanations include coffee-related reductions of cholesterol, bile acids and neutral sterol secretion in the colon; antimutagenic properties of selected coffee components; increased colonic motility. Decaffeinated coffee was not related to either colon or rectal cancer in three case-control studies. No overall association between tea and either colon or rectal cancer risk emerged in seven cohort (1756 total cases of colon, 759 of rectal and 60 of colorectal cancer) and 12 case-control studies (8058 cases of colon, 4865 of rectal, 604 of colorectal cancer)
Fruit and vegetables, and human cancer
No full textA large body of evidence indicates that high intakes of fruit and vegetables are associated with a reduced risk of cancer at several sites. The association is generally most marked for epithelial cancers, apparently stronger for those of the digestive and respiratory tracts, and somewhat weaker for hormone-related cancers. The relationship between frequency of consumption of vegetables and fruit and cancer risk was analysed using data from a series of case-control studies conducted in northern Italy since 1983. The relative risks (RRs) for most common neoplasms ranged from 0.2 to 0.5 for the highest compared with the lowest tertile of vegetable intake. Protective effects were highest for epithelial neoplasms, but were also observed for hormone-related neoplasms. Fruit was related to reduced RRs for cancers of the oral cavity and pharynx, oesophagus, stomach, larynx, as well as of the urinary tract. There was a specific and consistent pattern of protection by tomatoes, a typical Mediterranean food, with RRs between 0.4 and 0.7, most notably for gastrointestinal neoplasms. No significant association was observed between fruit and vegetable consumption and non-epithelial lymphoid neoplasms. For digestive tract cancer, population attributable risks for low intake of fresh vegetables and fruit ranged from 15 to 40% of all cases in this Mediterranean population. Combined with tobacco and alcohol, the population attributable risks exceeded 85% for men and 55% for women for upper digestive and respiratory tract neoplasms. Thus, from a public health viewpoint, epidemiological evidence indicates that a substantial reduction in epithelial cancer risk can be obtained by increasing fruit and vegetable consumption
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