Biological variation of cardiovascular risk factors in patients with diabetes

Biological variation refers to the natural fluctuations found when repeated measurements are made in a biological system. Generally, biological variation remains within narrow boundaries in health, but may differ in pathological states, with implications for the diagnosis and monitoring of disease processes. In disease, biological variation may alter such that any subsequent measurement may need to have a greater difference compared with a healthy control to be biologically relevant. Treatments such as insulin or anti‐hypertensive therapy have been shown to reduce biological variability closer to normal levels and theoretically this may help prevent complication development or progression in conditions such as diabetes. This article reviews how biological variation can influence our identification and assessment of vascular risk factors in a person with diabetes. The role of biological variation in the diagnosis of diabetes (glucose and HbA_1c) is then examined. Finally, the influence that common treatments in diabetes have in modifying biological variation is described.     

Laboratory evaluation of some larvicidal agents against Anopheles culicifacies in Pune.

A laboratory study to evaluate some larvicidal agents against Anopheles culcifacies was carried out. The findings of this study brought out that the larvae of this species were highly susceptible to temephos, fenthion, Paris green and Mosquito Larvicidal Oil (MLO) in that order. The LC50 values in respect of these larvicides were 0.0009 ppm, 0.0081 ppm, 0.029 ppm and 0.015 ml respectively and LC90 values were 0.0018 ppm, 0.022 ppm, 0.11 ppm and 0.046 ml respectively.     

Soy isoflavones improve cardiovascular disease risk markers in women during the early menopause

Background

Hormone replacement therapy may be beneficial for cardiovascular disease risk (CVR) in post-menopausal women. Soy isoflavones may act as selective estrogen receptor modulators. The aim of this study was to evaluate whether soy isoflavones had an effect on CVR markers.

Recent advances in cardiovascular aspects of polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) has been associated with increased cardiovascular risk (CVR) markers, but population studies have not clarified whether there is an increase in cardiovascular morbidity and mortality. Four different PCOS phenotypes resulted from the Rotterdam criteria that may differ in their CVR potential, thus introducing further complexity. This has led to studies using surrogate CVR markers including biomarkers in blood and imaging such as flow-mediated vasodilatation. In PCOS, both peripheral and central insulin resistance (IR) have been shown. Weight loss has been shown to improve IR and visceral fat, while insulin sensitizer therapies with metformin or thiazolidinediones improve IR and endothelial dysfunction. IR is also found in non-alcoholic fatty liver disease that in turn is very common in PCOS; studies have suggested that IR may be improved by treatment with metformin and omega-3 fish oils. PCOS patients have a more dyslipidemic phenotype that is worse in 'classical PCOS' associated with a higher CVR. Studies with atorvastatin and simvastatin have reported a decrease in the lipid parameters and an improvement in CVR indices including IR, but it is unclear whether this is due to their lipid-lowering action or a pleiotropic effect of the statin. In this expert opinion review, the relevant literature published during the last 2 years was considered. It focuses on some recent important data that has emerged while also exposing the gaps that remain in our knowledge that need to be addressed.     

Variability of lipids in patients with Type 2 diabetes taking statin treatment: implications for target setting

Aims To determine the biological variability of lipids in patients with Type 2 diabetes (T2DM) who are on statin treatment and then to assess any implications for current lipid targets. Methods A cross‐over study of biological variation of lipids in 26 patients with T2DM taking either simvastatin 40 mg or atorvastatin 10 mg. After 3 months on one statin, fasting lipids were measured on 10 occasions over a 5‐week period. Following 3 months on the other statin, 10 further samples were taken over 5 weeks. The main outcome measures were biological variability of total cholesterol (TC), low‐density lipoprotein (LDL) cholesterol, high‐density lipoprotein (HDL) cholesterol and triglycerides. Results The coefficient of variation (CV) of TC, LDL, HDL and triglycerides on simvastatin was 8.17, 13.11, 7.95 and 12.06%, respectively, whereas the CV on atorvastatin was 6.92, 10.30, 5.13 and 19.71%, respectively, with no statistically significant differences between statins. Treating to sustain a target TC < 5.0 mmol/l or LDL < 3.0 mmol/l means needing to maintain a mean TC of 4.3–4.4 mmol/l or LDL of 2.4–2.5 mmol/l. Treating to consistently achieve an LDL < 2.0 mmol/l means aiming for a mean of only 1.5–1.6 mmol/l. Conclusion In patients with T2DM taking either simvastatin or atorvastatin, the mean TC and LDL concentrations needed to consistently remain below a target are much lower than the target value itself. This means that guideline target limits extrapolated from the mean values of patients participating in clinical studies may overestimate the lipid reductions required.