OBJECTIVE: Several studies have suggested that patients with acromegaly have an increased risk of benign and malignant neoplasms, especially of the colon. To further investigate this relationship we evaluated cancer risk in population-based cohorts of acromegaly patients in Sweden and Denmark. METHODS: Nationwide registry-based cohorts of patients hospitalized for acromegaly (Denmark 1977-1993; Sweden 1965-1993) were linked to tumor registry data for up to 15-28 years of follow-up, respectively. Standardized incidence ratios (SIR) and 95% confidence intervals (CI) were calculated to estimate cancer risk among 1634 patients with acromegaly. RESULTS: The patterns of cancer risk in Sweden and Denmark were similar. After excluding the first year of follow-up, 177 patients with acromegaly had a diagnosis of cancer compared with an expected number of 116.5 (SIR = 1.5. 95% CI = 1.3-1.8). Increased risks were found for digestive system cancers (SIR = 2.1, 95% CI = 1.62.7), notably of the small intestine (SIR = 6.0, 95% CI = 1.2-17.4), colon (SIR = 2.6, 95% CI = 1.6-3.8), and rectum (SIR = 2.5, 95% CI= 1.3-4.2). Risks were also elevated for cancers of the brain (SIR = 2.7, 95% CI= 1.2-5.0). thyroid (SIR = 3.7, 95% CI = 1.8-10.9), kidney (SIR = 3.2, 95% CI = 1.6-5.5), and bone (SIR= 13.8, 95% CI= 1.7-50.0). CONCLUSIONS: The increased risk for several cancer sites among acromegaly patients may be due to the elevated proliferative and anti-apoptotic activity associated with increased circulating levels of insulin-like growth factor-1 (IGF-1). Pituitary irradiation given to some patients may have contributed to the excess risks of brain tumors and thyroid cancer. Our findings indicate the need for close medical surveillance of patients with acromegaly, and further studies of the IGF-I system in the etiology of various cancers.
BACKGROUND: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. METHODS: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer among patients admitted to hospital for alcoholism (n=178 688), alcoholic chronic pancreatitis (n=3500), non-alcoholic chronic pancreatitis (n=4952), alcoholic liver cirrhosis (n=13 553), or non-alcoholic liver cirrhosis (n=7057) from 1965 to 1994. Follow up through to 1995 was accomplished by linkage to nationwide registers. Standardised incidence ratios (SIRs) express the relative risks by taking the general Swedish population as reference. To minimise the possible influence of selection bias, we excluded the first year observations. RESULTS: Alcoholics had only a modest 40% excess risk of pancreatic cancer (SIR 1.4, 95% confidence interval (CI) 1.2-1.5). Overrepresented smokers among alcoholics might confound a true SIR of unity among alcoholics to approximately 1.4. SIR among alcoholic chronic pancreatitis patients (2.2, 95% CI 0.9-4.5) was considerably lower than that among non-alcoholic chronic pancreatitis patients (8.7, 95% CI 6.8-10.9), and decreased with increasing duration of follow up in both groups, indicating that most of the excess might be explained by reversed causation from undiagnosed cancers. Among patients with alcoholic liver cirrhosis, the increased risk of pancreatic cancer was also moderate (SIR 1.9, 95% CI 1.3-2.8) while no significant excess risk was found among non-alcoholic liver cirrhosis patients (SIR 1.2, 95% CI 0.6-2.2). CONCLUSIONS: The excess risk for pancreatic cancer among alcoholics is small and could conceivably be attributed to confounding by smoking.
A population-based cohort study of 36 856 women diagnosed with alcoholism in Sweden between 1965 and 1995 found that alcoholic women had only a small 15% increase in breast-cancer incidence compared to the general female population. It is therefore apparent, contrary to expectation, that alcoholism does not increase breast-cancer risk in proportion to presumed ethanol intake.
We conducted a population-based cohort study to analyze the risk of developing cancers of the female genitals among 36,856 patients with a hospital discharge diagnosis of alcoholism (ICD-7: 307, 322; ICD-8: 291, 303; ICD-9: 291, 303, 305A) in Sweden between 1965 and 1995. The follow-up was done by linkages of national registries. Standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were computed based on nationwide specific cancer rates. The first year of follow-up was excluded from all analyses to minimize the impact of selection bias. We found that alcoholic women had excess risks for in situ cervical cancer (SIR, 1.7; 95% CI, 1.6-1.9), for invasive cervical cancer (SIR, 2.9; 95% CI, 2.4-3.5), and for cancer of the vagina (SIR, 4.6; 95% CI, 2.2-8.5) but not for cancer of the vulva (SIR, 1.0; 95% CI, 0.4-2.0). The fact that alcoholics had an excess risk also for the in situ cancer suggests that the observed excess in invasive cervical cancer may not only be attributable to less use of Pap smear screening among them. The alcoholic women may be at higher risk for the progression from human papillomavirus infection to a malignant lesion for lifestyle-related reasons (promiscuity, smoking, use of contraceptive hormones, and dietary deficiencies). We conclude that alcoholic women are at high risk for in situ and invasive cervical cancer and for cancer of the vagina.
Endogenous estrogens increase the risk of endometrial cancer and are also elevated among women with high alcoholic intake. It is incompletely known, however, whether alcohol intake in general and alcohol abuse in particular increases risk for endometrial cancer. We thus analyzed prospectively the risk for endometrial cancer among 36,856 women hospitalized with alcoholism between 1965 and 1994 through linkages between several national Swedish registers. Compared with the general population, women who were alcoholics had an overall 24% lower risk of developing endometrial cancer, a finding challenging our a priori hypothesis. However, among women below the age of 50 years at follow-up, the mean age of menopause among Swedish women, the risk was 70% higher, whereas the risk among women aged 50 years or more at follow-up was 40% lower compared with the general population. Hence, the effect of alcoholism on endometrial cancer appears to be age dependent.
Sun exposure is associated with risk of several chronic diseases including cancer. The study aim is to investigate whether sun behaviors are related to other lifestyle risk factors of cancer.
We analyzed data collected in 2003-2004 by self-completed questionnaire from 34,402 Swedish women aged 40-61 years, who comprised 70% of a cohort of originally recruited from a population registry in 1991-1992 (n = 49,259). Participants were asked about annual number of sunburns and annual number of weeks of swimming and sunbathing during 1991-2002, solarium use during 1991-1998 and current sunscreen use.
Compared to non-drinkers, the prevalence ratio (95% CI) in women who drank >10 g of alcohol per day was 1.64 (1.49, 1.81) for having >1 sunburn per year, 1.39 (1.29, 1.51) for swimming and sunbathing >2.5 weeks per year and 1.55 (1.41, 1.70) for using a solarium >1 time per 2 months, adjusting for demographic and lifestyle variables. Tobacco smokers were less likely to report sunburn and to use sunscreen, and more likely to sunbath and use solaria, compared with non-smokers. Physical activity was associated positively with swimming and sunbathing, and with the separate use of solaria and sunscreens, but not with number of sunburns. The lifestyle variables that explained most of the variation in sun behavior were alcohol and smoking.
Our results suggest that alcohol consumption and tobacco smoking are potential lifestyle confounders which should be adjusted in studies investigating the association that sun and/or solarium exposure may have with risk of several cancer sites.
OBJECTIVE: To measure the association between endometrial cancer risk and obesity at age 18 and recently, adult weight gain, diabetes mellitus and hypertension. METHODS: We performed a population-based, nationwide case-control study among postmenopausal women aged 50-74 years in Sweden, including 709 incident cases with histopathologically verified endometrial cancer and 3368 controls. RESULTS: Compared to lean women (recent body mass index (BMI), i.e. kg/m2 below 22.5), overweight women (recent BMI 28-29.99) had a 50% increase in risk for endometrial cancer (OR 1.5, 95% CI 1.0-2.1). Obese women (recent BMI 30-33.99) had a 3-fold increased risk (OR 2.9, 95% CI 2.0-4.0), and markedly obese women (recent BMI > or = 34) a 6-fold increased risk (OR 6.3, 95% CI 4.2-9.5). The OR for Type 2 diabetes mellitus was 1.5 (95% CI 1.0-2.1) and for Type 1 diabetes mellitus it was 13.3 (3.1-56.4). The effect of recent BMI was similar for tumors having different degrees of differentiation and myometrial invasion, and did not vary with age, time since menopause, smoking status, diabetes mellitus, and use of contraceptives. Hypertension increased risk only among obese women. BMI at age 18, height, and adult weight change were not independent risk factors. CONCLUSIONS: Recent overweight/obesity and diabetes mellitus (Types 1 and 2) are associated with endometrial cancer risk. Hypertension increases risk among obese women.
The etiology of breast cancer is not fully understood. Environmental and occupational exposures may contribute to breast cancer risk.
We linked 324 job titles from the 1970 census of 892,591 Finnish women with incidence of breast cancer (23,638 cases) during 1971-1995. We converted job titles to 31 chemical and two ergonomic agents through a measurement-based, period-specific, national job-exposure matrix. Poisson regression models were fit to the data, with adjustment for birth cohort, follow-up period, socioeconomic status, mean number of children, mean age at first delivery, and turnover rate.
For premenopausal breast cancer, medium/high level of occupational exposure to ionizing radiation was associated with a standardized incidence ratio (SIR) of 1.3 (95% confidence interval (CI) 0.7-2.5; trend P = 0.03). For postmenopausal breast cancer, we found on SIR of 1.2 (1.1-1.3) for low level and 1.4 (1.1-1.8) for medium/high level of ionizing radiation (trend P = 0.001); and an SIR 1.3 (1.1-1.7) for medium/high levels of both asbestos and man-made vitreous fibers. Aromatic hydrocarbon solvents showed a significant trend for a modest excess of postmenopausal breast cancer.
Our study indicates that occupational exposure to ionizing radiation may be associated with an increased risk of female breast cancer. High-quality studies on environmental and occupational etiology of breast cancer are needed for further elucidation of risk factors.
OBJECTIVE: To investigate the association between alcoholism and risk of male breast cancer. METHODS: We conducted a retrospective population-based cohort study in Sweden of men diagnosed with alcoholism between 1965 and 1995. The cohort was followed up through interlinkages with nationwide registries (the national cancer registry, immigration registry, causes of death registry, and population registry), using the national registration numbers. Standardized incidence ratios (SIRs), calculated using the Swedish national cancer incidence rate as reference, were used as estimates of relative risks. RESULTS: A total of 145,811 men were enrolled into the cohort, contributing 1,499,504 person-years of follow-up. Sixteen incident breast cancer cases were identified, and the mean age at diagnosis was 68 years. We excluded the first year of follow-up (cases and person-years) from the analysis to avoid detection bias. The overall SIR (excluding the first year of follow-up) was 1.1 (95% CI 0.6-2.0). Although based on small numbers we found no indication of a differential SIR according to duration of follow-up, age at cohort enrolment, or age at follow-up (attained age or age at cancer diagnosis). CONCLUSION: The observed associations are not compatible with an increase in breast cancer risk among male alcoholics.
A cohort of patients with diabetes mellitus hospitalised in Sweden from 1965 to 1983 was followed up until 1989, by linkages of population-based registers. Standardised mortality ratios (SMR), adjusted for confounding variables, and 95% confidence intervals (CIs) were calculated. After exclusion of the first year of follow-up (to reduce the effect of selection bias), the cohort consisted of 144,427 patients, of whom 92,248 patients died during follow-up. The SMR for all causes of death combined was 2.62 (95% CI 2.58-2.67) among men and 3.23 (95% CI 3.18-3.28) among women. The excess mortality was still evident 20 years after first hospitalisation, but became less marked with longer follow-up time. Patients with presumably insulin-dependent diabetes mellitus (IDDM) had the highest SMRs (10.2; CI 9.5-11.0); however, there was a significant (34%) improvement over time in their mortality risk. We conclude that excess mortality persisted throughout all calendar periods and at all ages, indicating the need for health care prevention measures.