Overweight and obesity are health problems of epidemic proportions, increasing the risk not only of cardiovascular disease and type 2 diabetes mellitus but also of various types of cancer. Obesity is strongly associated with changes in the physiological function of adipose tissue, leading to insulin resistance, chronic inflammation, and altered secretion of adipokines. Several of these factors, such as insulin resistance, increased levels of leptin, plasminogen activator inhibitor-1, and endogenous sex steroids, decreased levels of adiponectin, and chronic inflammation, are involved in carcinogenesis and cancer progression. This article reviews these mechanisms, focusing on adipose tissue dysfunction as a unifying causal factor. Although understanding of the link between obesity and cancer might provide therapeutic targets, preventing overweight and obesity still remains number one priority. (Cancer Epidemiol

Background: Patients with vascular disease may be at increased risk of cancer because of shared risk factors and common pathogenesis.Methods: Patients with vascular disease (n ¼ 6,172) were prospectively followed for cancer incidence. Standardized incidence ratios (SIRs) were calculated to compare the cancer incidence of the study population with that of the general population. Multivariable-adjusted hazard ratio's (HRs) of cancer were estimated for smoking status, pack-years, body mass index, waist circumference and visceral adipose tissue (VAT), and metabolic syndrome (MetS).Results: During a median follow-up of 5.5 years, 563 patients were diagnosed with cancer. Patients with vascular disease were at increased risk of cancer [SIR ¼ 1.19; 95% confidence interval (CI), 1.10-1.29]. Specifically, risk of lung cancer (SIR ¼ 1.56; 95% CI, 1.31-1.83), as well as bladder cancer (SIR ¼ 1.60; 95% CI, 1.11-2.24) and cancer of the lip, oral cavity, or pharynx in men (SIR ¼ 1.51; 95% CI, 0.89-2.39), and colorectal (SIR ¼ 1.71; 95% CI, 1.11-2.53) and kidney cancer (SIR ¼ 2.92; 95% CI, 1.05-6.38) in women was increased. A relation between smoking and cancer risk was observed (HR for current smokers ¼ 1.37; 95% CI, 1.05-1.73), whereas an increase in VAT was associated with higher breast cancer risk in women (HR ¼ 1.42; 95% CI, 1.03-1.96). No relation between MetS and cancer risk was found.Conclusions: Patients with vascular disease have a 19% higher cancer risk compared to the general population. Smoking increased cancer risk and abdominal obesity is a risk factor for breast cancer in female patients with vascular disease.Impact: These results call for awareness of the increased cancer risk in patients with vascular disease among physicians and underline the necessity of lifestyle improvement not only for reducing cardiovascular risk. Cancer Epidemiol Biomarkers Prev; 22(7); 1267-77. Ó2013 AACR.

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Background The value of aspirin in primary prevention of cancer and cardiovascular disease (CVD) remains unclear. The aim of this study was to identify women who benefit from alternate-day aspirin with regard to all relevant outcomes, including cancer, CVD and major gastro-intestinal bleeding. Methods Long-term follow-up data of 27,939 healthy women with baseline plasma samples in the Women's Health Study, a randomized trial of 100mg alternate-day aspirin vs. placebo, were used to develop competing risks models for individualized prediction of absolute risk reduction (ARR) of the combination of CVD, cancer and major gastro-intestinal bleeding by aspirin. Results Although aspirin was associated with a modestly decreased 15-year risk of colorectal cancer, CVD, and in some women non-colorectal cancer, aspirin treatment resulted in a negative treatment effect in the majority of women if gastro-intestinal bleeding was also taken into account. The excess risk of major gastro-intestinal bleeding by aspirin increased with age, but the benefits for colorectal cancer and CVD risk were also greater at higher age. Decision curves indicated that selective treatment of women ≥65 years may improve net benefit compared to treating all, none and prediction-based treatment. The observed 15-year number-needed-to-treat to prevent one event among women ≥65 years was 29 (95% confidence interval:12–102). Conclusion Concurrent evaluation of the absolute effects on cancer, CVD and major gastro-intestinal bleeding showed that alternate-day use of low-dose aspirin is ineffective or harmful in the majority of women in primary prevention. Selective treatment of women ≥65 years with aspirin may improve net benefit.

A 56-year-old man was admitted on our intensive care unit with septic shock after 10 days of diarrhea, shortly after he had visited India. He had no relevant previous medical history. Blood and fecal cultures grew various pathogens, including Shigella flexneri. ECG showed diffuse ST elevation with PR depression (Figure 1), and laboratory results revealed significant troponin (peak level of 5.72 ng/mL) and creatine phosphokinase-MB (peak level of 117 ng/mL) release, most likely caused by a perimyocarditis in the setting of Shigella sepsis. Further diagnostic evaluation revealed hairy cell leukemia. After initial improvement of his clinical condition and treatment with rituximab and prednisolone, he was readmitted to the intensive care unit with respiratory failure and new-onset left ventricular dysfunction as was observed with echocardiography. Compared with the prior tracing, his ECG now showed microvoltages in the extremity leads, this time with normal ST segments ( Figure 2). Computed tomographic imaging revealed extensive myocardial calcification of the left ventricle that was not seen on previous computed tomographic images (Figures 3 and 4). Comparable images of a pronounced dense myocardium with normal aspect of the endocardial layer were observed with transesophageal echocardiography (Figure 5). Serum levels of calcium were repeatedly not elevated during the admittance.Localized myocardial calcification is commonly observed after myocardial infarction. Diffuse calcification, however, is a rare phenomenon. Interestingly, similar cases of extensive left ventricular calcification after a period of severe sepsis have been described previously. 1-3 Two different pathophysiological mechanisms resulting in calcium deposition in cardiac myocytes can be distinguished. 4 First, significant disturbances in calcium metabolism can lead to metastatic calcification, as is occasionally observed in patients with chronic renal failure. Furthermore, calcium may accumulate in necrotized cardiac myocytes, which is known as dystrophic calcification. The latter mechanism is believed to underlie myocardial calcification in the setting of myocardial infarc-Figure 1. ECG at day 1 of admission showing diffuse concave ST elevation with PR depression (arrow).