Few large-scale epidemiologic studies have quantified the possible link between obesity and chronic renal failure (CRF). This study analyzed anthropometric data from a nationwide, population-based, case-control study of incident, moderately severe CRF. Eligible as cases were all native Swedes who were aged 18 to 74 yr and had CRF and whose serum creatinine for the first time and permanently exceeded 3.4 mg/dl (men) or 2.8 mg/dl (women) during the study period. A total of 926 case patients and 998 control subjects, randomly drawn from the study base, were enrolled. Face-to-face interviews, supplemented with self-administered questionnaires, provided information about anthropometric measures and other lifestyle factors. Logistic regression models with adjustments for several co-factors estimated the relative risk for CRF in relation to body mass index (BMI). Overweight (BMI > 25 kg/m 2 ) at age 20 was associated with a significant three-fold excess risk for CRF, relative to BMI <25. Obesity (BMI >30) among men and morbid obesity (BMI > 35) among women anytime during lifetime was linked to three-to four-fold increases in risk. The strongest association was with diabetic nephropathy, but two-to three-fold risk elevations were observed for all major subtypes of CRF. Analyses that were confined to strata without hypertension or diabetes revealed a three-fold increased risk among patients who were overweight at age 20, whereas the two-fold observed risk elevation among those who had a highest lifetime BMI of >35 was statistically nonsignificant. Obesity seems to be an important-and potentially preventable-risk factor for CRF. Although hypertension and type 2 diabetes are important mediators, additional pathways also may exist.

Background:Venous thromboembolism (VTE) frequently complicates cancer. Data on tumour-specific VTE predictors are limited, but may inform strategies to prevent thrombosis.Methods:We computed incidence rates (IRs) with 95% confidence intervals (CIs) for VTE hospitalisation in a cohort of cancer patients (n=57 591) and in a comparison general-population cohort (n=287 476) in Denmark. The subjects entered the study in 1997–2005, and the follow-up continued through 2006. Using Cox proportional-hazards regression, we estimated relative risks (RRs) for VTE predictors, while adjusting for comorbidity.Results:Throughout the follow-up, VTE IR was higher among the cancer patients (IR=8.0, 95% CI=7.6–8.5) than the general population (IR=4.7, 95% CI=4.3–5.1), particularly in the first year after cancer diagnosis (IR=15.0, 95% CI=13.8–16.2, vs IR=8.6, 95% CI=7.6–9.9). Incidence rates of VTE were highest in patients with pancreas (IR=40.9, 95% CI=29.5–56.7), brain (IR=17.7, 95% CI=11.3–27.8) or liver (IR=20.4, 95% CI=9.2–45.3) tumours, multiple myeloma (IR=22.6, 95% CI=15.4–33.2) and among patients with advanced-stage cancers (IR=27.7, 95% CI=24.0–32.0) or those who received chemotherapy or no/symptomatic treatment. The adjusted RR (aRR) for VTE was highest among patients with pancreas (aRR=16.3, 95% CI=8.1–32.6) or brain cancer (aRR=19.8 95% CI=7.1–55.2), multiple myeloma (aRR=46.1, 95% CI=13.1–162.0) and among patients receiving chemotherapy, either alone (aRR=18.5, 95% CI=11.9–28.7) or in combination treatments (aRR=16.2, 95% CI=12.0–21.7).Conclusions:Risk of VTE is higher among cancer patients than in the general population. Predictors of VTE include recency of cancer diagnosis, cancer site, stage and the type of cancer-directed treatment.

Bone metastasis and skeletal related events predict poor prognosis in men with prostate cancer.

MDS patients in the United States have substantial transfusion needs, and use of erythropoiesis-stimulating agents and are seldom considered for bone marrow transplantation or clinical trials. These data may be useful in characterizing the health care resource use and pharmacoeconomic impact of MDS in the United States.

Hydroxymethylglutaryl-CoA reductase inhibitors (statins) have been linked with potential chemopreventive effects; however, the data are conflicting. We conducted a population-based cohort study using data from the Prescription Database of North Jutland County and the Danish Cancer Registry for the period 1989 -2002. In a study population of 334,754 county residents, we compared overall and site-specific cancer incidence among 12,251 statin users (>2 prescriptions) with cancer incidence among nonusers and users of other lipid-lowering drugs (n ‫؍‬ 1,257). Statistical analyses were based on age-standardization and Poisson regression analysis, adjusting for age, gender, calendar period and use of NSAIDs, hormone replacement therapy and cardiovascular drugs. We identified 398 cancer cases among statin users during a mean follow-up period of 3.3 years (range 0 -14 years). The age-and gender-standardized incidence rates of cancer overall were 596 per 100,000 Key words: statins; cancer incidence; risk; epidemiology; cohort study Inhibitors of hydroxymethylglutaryl-CoA reductase (statins) have been linked with several beneficial effects beyond their effect on cardiovascular disease, including reductions in risk of dementia, 1-3 fractures 4 -7 and cancer. 8,9 However, the data on cancer risk are conflicting. In a review of rodent carcinogenicity tests, Newman and Hulley reported that statins and fibrates initiate or promote cancer in rats and mice. 10 In most of the reviewed studies, however, the doses used were substantially higher than the recommended maximum doses for humans, and the employed bioassays were criticised for being inadequate to predict carcinogenicity in humans. 11 In contrast, several recent studies of human cancer cell lines and animal tumour models indicate that statins may have chemopreventive properties by inducing apoptosis and inhibiting tumour growth and metastasis. 12-21 Although a growing body of laboratory data thus indicate that statins may protect against cancer, 8,9 the clinical relevance of these data remain unclear. Results of clinical trials and observational studies of the association between statin use and cancer are inconsistent. [22][23][24][25][26][27][28][29][30][31][32][33][34] A few studies lend some support to a cancer-protective effect, 27,31,33,34 but the majority of the studies do not point to any substantially increased or decreased cancer risk among statin users. The reasons for the varying results are unclear but may relate to methodologic issues, including small sample sizes and short follow-up periods.Given the uncertainty about the effect of statins on cancer development and their widespread and long-term use, more data are needed on the relationship between statins and cancer. Thus, we examined cancer incidence among statin users in a populationbased cohort study in Denmark.

Inverse associations between dairy consumption and CVD have been reported in several epidemiological studies. Our objective was to conduct a meta-analysis of prospective cohort studies of dairy intake and CVD. A comprehensive literature search was conducted to identify studies that reported risk estimates for total dairy intake, individual dairy products, low/full-fat dairy intake, Ca from dairy sources and CVD, CHD and stroke. Random-effects meta-analyses were used to generate summary relative risk estimates (SRRE) for high v. low intake and stratified intake dose-response analyses. Additional dose-response analyses were performed. Heterogeneity was examined in sub-group and sensitivity analyses. In total, thirty-one unique cohort studies were identified and included in the meta-analysis. Several statistically significant SRRE below 1.0 were observed, namely for total dairy intake and stroke (SRRE = 0·91; 95 % CI 0·83, 0·99), cheese intake and CHD (SRRE = 0·82; 95 % CI 0·72, 0·93) and stroke (SRRE = 0·87; 95 % CI 0·77, 0·99), and Ca from dairy sources and stroke (SRRE = 0·69; 95 % CI 0·60, 0·81). However, there was little evidence for inverse dose-response relationships between the dairy variables and CHD and stroke after adjusting for within-study covariance. The results of this meta-analysis of prospective cohort studies have shown that dairy consumption may be associated with reduced risks of CVD, although additional data are needed to more comprehensively examine potential dose-response patterns.

There is a wide variation in both prevalence and incidence estimates observed across European data sources. Carefully designed studies, with standardized definitions of MPNs and complete ascertainment of patients including both primary and secondary MFs, should be conducted so that estimates of the population aimed to receive novel treatments for these neoplasms are better understood assist public health planning and provide valuable information about the burden of illness to policy makers, funding agencies, resource planners, healthcare insurers, and pharmaceutical manufacturers.

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