Small Number Of Epidemiological Studies Research Articles

Abstract 2796: Circulating 25-hydroxyvitamin D and prostate cancer risk in a large male cohort

Abstract Vitamin D compounds have been shown to inhibit prostate tumorigenesis experimentally, but based on the small number of epidemiological studies conducted to date, the relation between vitamin D status and prostate cancer risk remains unclear. We investigated the association between 25-hydroxyvitamin D [25(OH)D] and prostate cancer in a nested case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of 50-69 year old Finnish men. To 1,000 cases diagnosed during up to 20 years of follow-up, we matched 1,000 controls on age (within 1 year) and baseline blood collection date (within 30 days). Serum samples were assayed for 25(OH)D using the DiaSorin LIAISON 25(OH)D method (intra-batch and inter-batch CVs, 10.5% and 12.3%), and conditional multivariate logistic regression models estimated odds ratios (OR) and 95% confidence intervals (CI) for the prostate cancer-25(OH)D association, conditioned on the matching factors and adjusted for body mass index, residence, benign prostatic hyperplasia, and the trial supplements. 25(OH)D concentrations were categorized according to quintiles based on control cut-points of <18.6, −28.3, −39.7, >53.3 nmol/L. ORs (95% CIs) for Q1-Q5 were 1.00 (reference), 1.39 (1.04-1.86), 1.54 (1.14-2.08), 1.20 (0.88-1.62), and 1.41 (1.03-1.93)(p-trend=0.06). These findings were similar for subgroups of age, season of blood draw, time from blood draw to diagnosis, body mass index, vitamin D intake, and disease stage. Analyses of 25(OH)D based on clinically-defined categories, season-adjusted (by regression residual method), and season-specific cut-points yielded similar results. Our findings suggest that men with lower serum 25(OH)D levels may be at lower risk of developing prostate cancer compared to men with higher levels. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2796.

Cereal grains and legumes in the prevention of coronary heart disease and stroke: a review of the literature

A number of reviewers have examined studies investigating the relationship between coronary heart disease and stroke prior to 2000. Since then, several key studies have been published. Five studies have examined the relationship between wholegrain consumption, coronary heart disease (CHD) and cardiovascular (CVD) disease and found protection for either or both diseases. The researchers concluded that a relationship between wholegrain intake and CHD is seen with at least a 20% and perhaps a 40% reduction in risk for those who eat wholegrain food habitually vs those who eat them rarely. Notwithstanding the fact that fibre is an important component of wholegrains, many studies have not shown an independent effect of fibre alone on CHD events. Thus in terms of CHD prevention, fibre is best obtained from wholegrain sources. Wholegrain products have strong antioxidant activity and contain phytoestrogens, but there is insufficient evidence to determine whether this is beneficial in CHD prevention. Soluble fibre clearly lowers cholesterol to a small but significant degree and one would expect that this would reduce CHD events. There have been a small number of epidemiological studies showing soy consumption is associated with lower rates of heart disease. Countering the positive evidence for wholegrain and legume intake has been the Nurses Health Study in 2000 that showed women who were overweight or obese consuming a high glycaemic load (GL) diet doubled their relative risk of CHD compared with those consuming a low GL diet. Although the literature relating GL with CHD events is somewhat mixed, the relationship with risk factors such as HDL cholesterol, triglyceride and C reactive protein is relatively clear. Thus, carbohydrate-rich foods should be wholegrain and, if they are not, then the lowest glycaemic index (GI) product should be used. Promotion of carbohydrate foods should be focused on wholegrain cereals because these have proven to be associated with health benefits. There is insufficient evidence about whether the addition of other components of wholegrains such as polyphenolics or minerals (such as magnesium or zinc) would improve the health benefits of refined grain foods and this needs investigation. Whether adding bran to refined carbohydrate foods can improve the situation is also not clear, and it was found that added bran lowered heart disease risk in men by 30%. This persisted after full adjustment (including GL) suggesting, at least in men, that fibre may be more important than GI. Thus there are two messages: The intake of wholegrain foods clearly protects against heart disease and stroke but the exact mechanism is not clear. Fibre, magnesium, folate and vitamins B6 and vitamin E may be important. The intake of high GI carbohydrates (from both grain and non-grain sources) in large amounts is associated with an increased risk of heart disease in overweight and obese women even when fibre intake is high but this requires further confirmation in normal-weight women. Carbohydrate-rich foods should be wholegrain and if they are not, then the lowest GI product available should be consumed. Glycemic index is largely irrelevant for foods that contain small amounts of carbohydrate per serve (such as most vegetables).

Drug-Induced Immune Thrombocytopenia

Thrombocytopenia can have several causes, including the use of certain drugs. The mechanism behind drug-induced thrombocytopenia is either a decrease in platelet production (bone marrow toxicity) or an increased destruction (immune-mediated thrombocytopenia). In addition, pseudothrombocytopenia, an in vitro effect, has to be distinguished from true drug-induced thrombocytopenia. This article reviews literature on drug-induced immune thrombocytopenia, with the exception of thrombo-haemorrhagic disorders such as thrombotic thrombocytopenic purpura and heparin-induced thrombocytopenia and thrombosis. A literature search in PubMed combined with a check of the reference lists of all the retrieved articles resulted in 108 articles relevant to the subject. The drug classes that are most often associated with drug-induced immune thrombocytopenia are cinchona alkaloid derivatives (quinine, quinidine), sulfonamides, NSAIDs, anticonvulsants, disease modifying antirheumatic drugs and diuretics. Several other drugs are occasionally described in case reports of thrombocytopenia; an updated review of these case reports can be found on the internet. A small number of epidemiological studies, differing largely in the methodology used, describe incidences in the magnitude of 10 cases per 1 000 000 inhabitants per year. No clear risk factors could be identified from these studies. The underlying mechanism of drug-induced immune thrombocytopenia is not completely clarified, but at least three different types of antibodies appear to play a role (hapten-dependent antibodies, drug-induced, platelet-reactive auto-antibodies and drug-dependent antibodies). Targets for drug-dependent antibodies are glycoproteins on the cell membrane of the platelets, such as glycoprotein (GP) Ib/IX and GPIIb/IIIa. Diagnosis of drug-induced immune thrombocytopenia may consist of identifying clinical symptoms (bruising, petechiae, bleeding), a careful evaluation of the causal relationship of the suspected causative drug, general laboratory investigation, such as total blood count and peripheral blood smear (to rule out pseudothrombocytopenia), and platelet serology tests. The sensitivity of these tests is dependent on factors such as the concentration of the drug in the test and the potential sensitisation of the patient by metabolites instead of the parent drug. Drug-induced immune thrombocytopenia can be treated by withholding the causative drug and, in severe cases associated with bleeding, by platelet transfusion. Although drug-induced thrombocytopenia is a relatively rare adverse drug reaction, its consequences may be severe. Therefore it is important to extend our knowledge on this subject. Future research should focus on the identification of potential risk factors, as well as the exact mechanism underlying drug-induced thrombocytopenia.

Socioeconomic variation in incidence of epilepsy: prospective community based study in south east England

Objective: To determine the incidence of epilepsy in a general practice population and its variation with socioeconomic deprivation.Design: Prospective surveillance for new cases over an 18 or 24 month period.Participants:...

Prevalence of hepatitis B and C virus infection in barbers in the Sivas region of Turkey.

Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are among the most devastating health problems in the world, including Turkey. The route of transmission of HBV and HCV is mainly parenteral, a small number of epidemiological studies demonstrating that perinatal, sexual, household and occupational transmission occurs. Contact of a patient's blood or bodily fluids with non-intact skin is another mode of HBV and HCV transmission. Barbers in Turkey may often be exposed accidentally to the blood and bodily fluids of their customers. The aim of this study was to determine the prevalence of HBV and HCV infection in barbers. We conducted a study to determine the prevalence of antibodies against HBV and HCV among 176 barbers and 180 control subjects in the Sivas region of Turkey. The prevalence of HBV and HCV was found to be higher in barbers (39.8 and 2.8%, respectively) than in a comparison group (28.3 and 1.1%, respectively). No significant relationship was found with the duration of occupation. Among the seropositive subjects, it was found that most had been exposed to needle pricks or scissor cuts. Our data suggest that both HBV and HCV infections may constitute occupational hazards for barbers. The sources of infection could be not only such personal risk factors as 'sharps' injuries and scissor cuts, but may also include other unknown factors.

Epidemiology of organic solvents and connective tissue disease

Case reports suggest that solvents are associated with various connective tissue diseases (systemic sclerosis, scleroderma, undifferentiated connective tissue disease, systemic lupus erythematosis, and rheumatoid arthritis), particularly systemic sclerosis. A small number of epidemiological studies have shown statistically significant but weak associations between solvent exposure, systemic sclerosis, and undifferentiated connective tissue disease. However, the interpretation of these positive findings is tempered by a lack of replication, an inability to specify which solvents convey risk, and an absence of increasing risk with increasing exposure. Existing studies, on aggregate, do not show conclusively that solvents (either as a group of chemicals or individual chemicals) are causally associated with any connective tissue disease. Further investigations should be carried out to replicate the positive existing findings and to specify the solvents and circumstances of exposure that carry risk.

Occupational Heat Exposure and Male Fertility: A Review

In humans, as in most mammals, spermatogenesis is temperature dependent. This temperature dependence has been clearly demonstrated by several experimental studies showing that artificial increases in scrotum or testicle temperature in fertile men reduce both sperm output and quality. Our knowledge of the effects of occupational heat exposure on male fertility comes mostly from a small number of epidemiological studies. We conducted an extensive review of these published reports, focusing on methodology and design (retrospective or prospective; reference group; number of subjects) and principal results (using several indicators such as the time taken to obtain a pregnancy or sperm characteristics). We concluded that occupational heat exposure is a significant risk factor for male infertility, affecting sperm morphology and resulting in delayed conception. The limits and biases involved in this type of research are also discussed.

Occupational heat exposure and male fertility: a review.

In humans, as in most mammals, spermatogenesis is temperature dependent. This temperature dependence has been clearly demonstrated by several experimental studies showing that artificial increases in scrotum or testicle temperature in fertile men reduce both sperm output and quality. Our knowledge of the effects of occupational heat exposure on male fertility comes mostly from a small number of epidemiological studies. We conducted an extensive review of these published reports, focusing on methodology and design (retrospective or prospective; reference group; number of subjects) and principal results (using several indicators such as the time taken to obtain a pregnancy or sperm characteristics). We concluded that occupational heat exposure is a significant risk factor for male infertility, affecting sperm morphology and resulting in delayed conception. The limits and biases involved in this type of research are also discussed.

Formate-Induced Alterations in Retinal Function in Methanol-Intoxicated Rats

Formic acid is the toxic metabolite in methanol poisoning. Permanent visual damage in methanol-intoxicated humans and nonhuman primates has been associated with prolonged exposures (>24 hr) to blood formate concentrations in excess of 7 mM; however, little information is available on the toxicity associated with chronic low-level or repeated exposure to methanol. The present studies compared the effects on retinal function and structure of rapidly increasing formate concentrations typical of acute methanol intoxication with low-level plateau formate concentrations more likely to be generated by subacute or chronic methanol exposure. Rats that accumulated formate concentrations of 8–15 mMdeveloped metabolic acidosis, retinal dysfunction, and retinal histopathologic changes. Retinal dysfunction was measured as reductions in thea- andb-waves of the electroretinogram that occurred coincident with blood formate accumulation. Histopathologic studies revealed vacuolation in the retinal pigment epithelium and photoreceptor inner segments. Rats exposed to formate concentrations ranging from 4 to 6 mMfor 48 hr showed evidence of retinal dysfunction in the absence of metabolic acidosis and retinal histopathology. These data indicate that formic acid generated from methanol oxidation acts as a direct retinal toxin. Formate-induced retinal dysfunction in methanol-intoxicated rats can be produced by steadily increasing concentrations of formate and importantly can also be produced by prolonged exposure to lower concentrations of formate. Our findings substantiate evidence based on clinical case reports and a small number of epidemiological studies and support the hypothesis that the visual system toxicity produced by acute, subacute, or chronic methanol poisoning share a common mechanism.