Association of metabolic syndrome in polycystic ovarian syndrome: an observational study

Objectives

To find out the prevalence of metabolic syndrome (MBS) in women with PCOS and assess their strength of association. Methods: Total 50 apparently healthy non-pregnant PCOS subjects of 15 to 35 years were studied for having the features of MBS from May 2006 to April 2007. MBS was diagnosed by National Cholesterol Education Program’s Adult Treatment Panel III 2001 criteria. Student’s t test & Mann-Whitney U test were used for statistical analysis.

Results

21 subjects out of 50 (42%) met criteria for the MBS. 15(71.5%) belonged to 26–35 years and six (20.7%) in 15–25 years. Prevalence of waist circumference > 88 cm were noted in 34%, HDL cholesterol< 50 mg/dl in 50%, triglycerides ≥ 150 mg/dl in 40%, BP ≥130/85 mm Hg in 50% and FBS≥ 110 mg/dl in 16%. Women with higher insulin resistance and free testosterone levels significantly (P<0.01) correlated with higher prevalence of MBS.

Conclusion

The metabolic syndrome and its individual components are common in PCOS, particularly among women with hyperinsulinemia and hyperandrogenism.     

CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice

Tubular damage following ischemic renal injury is often reversible, and tubular epithelial cell (TEC) proliferation is a hallmark of tubular repair. Macrophages have been implicated in tissue repair, and CSF-1, the principal macrophage growth factor, is expressed by TECs. We therefore tested the hypothesis that CSF-1 is central to tubular repair using an acute renal injury and repair model, ischemia/reperfusion (I/R). Mice injected with CSF-1 following I/R exhibited hastened healing, as evidenced by decreased tubular pathology, reduced fibrosis, and improved renal function. Notably, CSF-1 treatment increased TEC proliferation and reduced TEC apoptosis. Moreover, administration of a CSF-1 receptor–specific (CSF-1R–specific) antibody after I/R increased tubular pathology and fibrosis, suppressed TEC proliferation, and heightened TEC apoptosis. To determine the contribution of macrophages to CSF-1–dependent renal repair, we assessed the effect of CSF-1 on I/R in mice in which CD11b⁺ cells were genetically ablated and determined that macrophages only partially accounted for CSF-1–dependent tubular repair. We found that TECs expressed the CSF-1R and that this receptor was upregulated and coexpressed with CSF-1 in TECs following renal injury in mice and humans. Furthermore, signaling via the CSF-1R stimulated proliferation and reduced apoptosis in human and mouse TECs. Taken together, these data suggest that CSF-1 mediates renal repair by both a macrophage-dependent mechanism and direct autocrine/paracrine action on TECs.     

LDL-receptor gene mutations and the hypocholesterolemic response to statin therapy

Studies of the cholesterol lowering effect of statin therapy as a function of low-density lipoprotein (LDL)-receptor mutation type have not produced a clear picture, possibly because they included patients with several different kinds of LDL-receptor mutations. We studied the response to treatment with fluvastatin in 28 patients with heterozygous familial hypercholesterolemia as a result of a receptor-negative mutation (Trp23-stop) and in 30 patients with a receptor-binding defective mutation (Trp66-Gly) to test the hypothesis that response to treatment depends on the type of mutation. Patients were randomized to 12 weeks of treatment with fluvastatin 40 mg daily and 12 weeks of placebo treatment, preceded by a placebo run-in period of 8 weeks in a double-blind, cross-over design. Untreated plasma concentrations of lipids and lipoproteins were similar in the two groups of patients. Plasma cholesterol and LDL cholesterol response to therapy tended to be less marked in receptor-binding defective patients, but the differences were not statistically significant. A tabulation of the results of the present and earlier studies suggests that differences in treatment response as an apparent function of LDL-receptor gene mutational type occur mainly in populations with recent genetic admixture (<400 years). In such populations, persons with the same mutation in the LDL-receptor gene are more likely to share other but undetermined genetic variations affecting the pharmacology of statins.     

Oral lesions of HIV infection in developing countries

HIV infection has spread rapidly within developing countries since it was first recognized in the early 1980s. The purpose of this paper is to review the prevalence of oral lesions associated with HIV infection (oral HIV) in the developing world, and to identify additional factors that may complicate the presentation of these lesions. Direct comparison of regional and local prevalence studies within Africa, India and Thailand is speculative because there are few reports available. Furthermore, inherent differences in study design, data collection, standardization and calibration of health workers make any inferences inconclusive. Additional prevalence studies of oral HIV lesions associated with systemic disease or social conditions, such as poverty or malnutrition, are needed. In order to provide a basis for the diagnosis and treatment of HIV-associated oral lesions in the developing world, it is important to recognize any confounding factors that may impact on their presentation and management. Elucidation of these various factors may provide a basis for treatment within the developing and developed world.