Hassan Kahal

Glucagon-like peptide-1 analogue, liraglutide, improves liver fibrosis markers in obese women with polycystic ovary syndrome and nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) has been linked to polycystic ovary syndrome (PCOS) and carries an increased risk of liver cirrhosis. Procollagen type 3 amino‐terminal peptide (PIIINP) is an independent predictor of liver cirrhosis.

The effect of parathyroidectomy on neuropsychological symptoms and biochemical parameters in patients with asymptomatic primary hyperparathyroidism

Backgroundu2002 With increased biochemical screening, primary hyperparathyroidism (pHPT) is often discovered incidentally whilst patients are asymptomatic.

Polycystic ovary syndrome has no independent effect on vascular, inflammatory or thrombotic markers when matched for obesity

Previous studies investigating cardiovascular (CV) risk in obese women with polycystic ovary syndrome (PCOS) have been potentially confounded by not adequately accounting for body weight.

The effects of treatment with liraglutide on atherothrombotic risk in obese young women with polycystic ovary syndrome and controls

BackgroundPolycystic ovary syndrome (PCOS) is associated with obesity and increased cardiovascular (CV) risk markers. In this study our aim was to assess the effects of six months treatment with liraglutide 1.8xa0mg od on obesity, and CV risk markers, particularly platelet function, in young obese women with PCOS compared to controls of similar age and weight.MethodsCarotid intima-media wall thickness (cIMT) was measured by B-mode ultrasonography, platelet function by flow cytometry, clot structure/lysis by turbidimetric assays and endothelial function by ELISA and post-ischaemic reactive hyperemia (RHI). Data presented as mean change (6-month – baseline)u2009±u2009standard deviation.ResultsNineteen obese women with PCOS and 17 controls, of similar age and weight, were recruited; baseline atherothrombotic risk markers did not differ between the two groups. Twenty five (69.4%) participants completed the study (13 PCOS, 12 controls). At six months, weight was significantly reduced by 3.0u2009±u20094.2 and 3.8u2009±u20093.4xa0kg in the PCOS and control groups, respectively; with no significant difference between the two groups, Pu2009=u20090.56. Similarly, HOMA-IR, triglyceride, hsCRP, urinary isoprostanes, serum endothelial adhesion markers (sP-selectin, sICAM and sVCAM), and clot lysis area were equally significantly reduced in both groups compared to baseline. Basal platelet P-selectin expression was significantly reduced at six months in controls −0.17u2009±u20090.26 but not PCOS −0.12u2009±u20090.28; between groups difference, 95% confidence intervalu2009=u2009−0.14 – 0.26, Pu2009=u20090.41. No significant changes were noted in cIMT or RHI.ConclusionsSix months treatment with liraglutide (1.8xa0mg od) equally affected young obese women with PCOS and controls. In both groups, liraglutide treatment was associated with 3–4% weight loss and significant reduction in atherothrombosis markers including inflammation, endothelial function and clotting. Our data support the use of liraglutide as weight loss medication in simple obesity and suggest a potential beneficial effect on platelet function and atherothrombotic risk at 6xa0months of treatment.Trial registrationClinical trial reg. no. ISRCTN48560305. Date of registration 22/05/2012.

Pharmacological Treatment of Obesity in Patients with Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is a common disorder affecting women of reproductive age and it is associated with increased cardiovascular risk. Obesity plays an important role in the pathogenesis of PCOS, and the majority of patients with PCOS are obese. Over the last 20 years, the prevalence of obesity has dramatically increased, with probable associated increase in PCOS. Weight reduction plays an integral part in the management of women with PCOS. In this paper, current available weight reduction therapies in the management of PCOS are discussed.

Obstructive Sleep Apnoea and Polycystic Ovary Syndrome; a comprehensive review of clinical interactions and underlying pathophysiology.

Polycystic ovary syndrome (PCOS) is the most prevalent endocrine disorder in women of reproductive age. PCOS is associated with multiple comorbidities including, obesity, insulin resistance and type 2 diabetes, as well as mood disorders and impaired quality of life (QoL). Obstructive sleep apnoea (OSA) is also a common medical condition that is often undiagnosed, particularly in women. OSA is associated with a similar spectrum of comorbidities to that observed in PCOS, including manifestations of the metabolic syndrome and impaired QoL, whilst obesity frequently constitutes a common denominator in the pathophysiology of both OSA and PCOS. Hence, it is not surprising that OSA and PCOS may coexist in women of reproductive age, and the current clinical guidelines on the management of PCOS recommend screening for OSA symptoms in overweight/obese women with PCOS. In this review, we examine the relationship between OSA and PCOS and explore the potential underlying mechanisms that link these two conditions.

The association between obstructive sleep apnea and metabolic abnormalities in women with polycystic ovary syndrome : a systematic review and meta-analysis

Study ObjectivesnIn this systematic review and meta-analysis, we aimed to examine the relationship between obstructive sleep apnea (OSA) and metabolic abnormalities in women with polycystic ovary syndrome (PCOS).nnnMethodsnElectronic databases (Medline, Embase, Cinahl, PsycInfo, Scopus, Web of Science, Opengrey, and CENTRAL), conference abstracts, and reference lists of relevant articles were searched. No restriction was applied for language or publication status.nnnResultsnSix studies involving 252 participants were included. Women with PCOS and OSA had significantly higher body mass index (mean difference [MD]: 6.01 kg/m2, 95% confidence intervals [CI]: 4.69-7.33), waist circumference (MD: 10.93 cm, 95% CI: 8.03-13.83), insulin resistance, systolic and diastolic blood pressure, and worse lipids profile and impaired glucose regulation compared with women with PCOS without OSA. Most studies did not adjust for weight in their between-groups analysis. Total and free testosterone levels were not significantly different between the two groups. The majority of studies were found to be at high risk of selection bias, did not account for important confounders, were conducted in one country (United States), and used different methodologies to assess testosterone levels (preventing a meta-analysis for this specific outcome).nnnConclusionsnOSA is associated with obesity and worse metabolic profiles in women with PCOS. However, whether the effects of OSA are independent of obesity remain unclear. As OSA is a treatable condition, research focused on the independent effects of OSA on key clinical outcomes in women with PCOS, including fertility, psychological health, type 2 diabetes, and cardiovascular risk, is lacking and needed. PROSPERO registration number: CRD42016048587.

Platelet function following induced hypoglycaemia in type 2 diabetes

AIMnStrict glycaemic control has been associated with an increased mortality rate in subjects with type 2 diabetes (T2DM). Here we examined platelet function immediately and 24hours following induced hypoglycaemia in people with type 2 diabetes compared to healthy age-matched controls.nnnMETHODSnHyperinsulinaemic clamps reduced blood glucose to 2.8mmol/L (50mg/dl) for 1hour. Sampling at baseline; euglycaemia 5mmol/L (90mg/dl); hypoglycaemia; and at 24 post clamp were undertaken. Platelet function was measured by whole blood flow cytometry.nnnRESULTSn10 subjects with T2DM and 8 controls were recruited. Platelets from people with T2DM showed reduced sensitivity to prostacyclin (PGI2, 1nM) following hypoglycaemia. The ability of PGI2 to inhibit platelet activation was significantly impaired at 24hours compared to baseline in the T2DM group. Here, inhibition of fibrinogen binding was 29.5% (10.3-43.8) compared to 50.8% (36.8-61.1), (P<0.05), while inhibition of P-selectin expression was 32% (16.1-47.6) vs. 54.4% (42.5-67.5) (P<0.05). No significant changes in platelet function were noted in controls.nnnCONCLUSIONnInduced hypoglycaemia in T2DM enhances platelet hyperactivity through impaired sensitivity to prostacyclin at 24hours.

A reversible rise in the total cholesterol to HDL ratio in a body builder

Introduction Low HDL-cholesterol concentration is one of the defining abnormalities of metabolic syndrome1 and an independent risk factor for CHD. Total cholesterol/HDL ratio is regarded as a better cardiovascular risk indicator than sole total cholesterol concentrations. The JBS-2 guidelines identify patients with an elevated total cholesterol to HDL cholesterol ratio ≥6.0, as a threshold for initiation of lipid lowering therapy in combination with intensive lifestyle changes. We report a case of raised cholesterol/HDL ratio, in which treating the underlying aetiology led to the resolution of the biochemical abnormality.