Polycystic ovary syndrome (PCOS) is a common endocrine disorder predominantly affecting women of reproductive age. Clinical manifestations are diverse including hyperandrogenism, anovulation, infertility and increased risk of metabolic diseases besides psychosocial dysfunction. This review provides information on the problem of PCOS in India, its pathophysiology, genetics and an overview of current management options to instigate further research in this field. Prevalence of PCOS in India ranges from 3.7 to 22.5 per cent depending on the population studied and the criteria used for diagnosis. Abnormalities in leptin-adiponectin (adipocyte biology), oxidative stress and autoimmunity are among the mechanisms studied regarding pathogenesis of PCOS. Many candidate gene studies have shown associations with PCOS in various studies. Studies have consistently demonstrated the relationship between the well-known manifestation of hyperandrogenism among Indian PCOS women and the metabolic morbidities including insulin resistance, glucose intolerance and cardiovascular risk. Management of individual components of PCOS can be achieved by medications or surgical methods, though further clarification regarding pathogenesis of PCOS is needed to sharpen our therapeutic armamentarium.

Sheehan syndrome (SS) caused by postpartum hemorrhage leads to partial or complete pituitary hormone deficiency. In addition to lipid and glucose abnormalities, patients with SS have increased body fat, insulin resistance (IR), coagulation abnormalities, increased leptin concentration, low-grade inflammation, and endothelial dysfunction that predispose them to cardiovascular diseases. Untreated growth hormone (GH) deficiency, hypogonadism, and excess glucocorticoid use are considered risk factors for these abnormalities. Compared to other hypopituitary subjects, patients with SS are younger and have a longer duration of disease and severe GH deficiency. Replacement with GH in addition to standard hormone replacement improves their cardiometabolic profile.

Vitamin D (VD) deficiency [serum 25(OH)D concentration of <20 ng/ml], in endemic proportions, demands a supplementation strategy with optimal dosing regimens. A randomised parallel-group, active-controlled trial was conducted among apparently healthy, VD deficient subjects, age 18-60 years who received 600 IU/day (Group A), 1000 IU/day (Group B), 2000 IU/day (Group C) and 60,000 IU/month (Group D) of oral cholecalciferol. The intervention was carried in two phases (I&II) of 12 weeks each, with same dose, separated by a washout phase of 12 weeks. Serum 25(OH)D, iPTH, calcium (Ca), phosphorous (PO4), alkaline phosphatase (ALP), spot urine calcium/creatinine (Ca/Cr) was measured at baseline, 12, 24 and 36 weeks following the intervention and adverse events were recorded at each occurrence and at 12, 24 and 36 weeks. A statistically significant time-group interaction was found in serum 25(OH)D concentration (P<0.05). Serum 25(OH)D concentration increased significantly from baseline to 12 weeks (P<0.05) in all the groups with no change at 24 weeks but further increase at 36 weeks (P<0.05). At the end of study, group C had maximum increment in serum 25(OH)D concentration while as groups C and D (95%, and 90%) had higher proportion of subjects VD sufficient than groups A and B (65% and 78%) (Table 3) (P<0.05). No significant time-dose interactions were observed in serum iPTH, Ca, PO4 and ALP or Urine Ca/Cr ratio. Three subjects (two in group C and one in group D) developed transient hypercalciuria. Supplementation with daily 2000IU or monthly 60,000IU oral cholecalciferol among adults seems optimal and safe.

Objective Patients with Sheehan syndrome (SS) are predisposed to coronary artery disease (CAD) due to risk factors like abdominal obesity, dyslipidemia and chronic inflammation. In addition to estimate CAD risk enhancers like high sensitive C reactive protein (hsCRP), apolipoprotein B (ApoB) and lipoprotein A [Lp(a)], this study applies Framingham risk score (FRS) and coronary artery calcium (CAC) score to compute a 10‐year probability of cardiovascular (CV) events in SS patients. Design Case–control study Sixty‐three SS patients, on a stable hormonal replacement treatment except for growth hormone and 65 age, body mass index and parity‐matched controls. Measurements Measurement of serum hsCRP, ApoB and Lp(a) and estimation of CAC with 16‐row multislice computed tomography scanner. Results The concentrations of hsCRP, ApoB and Lp(a) were significantly higher in SS patients than in controls (p < .01). After calculating FRS, 95.2% of SS patients were classified as low risk, 4.8% as intermediate risk and all controls were classified as low risk for probable CV events. CAC was detected in 50.7% SS patients and 7.6% controls (p = .006). According to the CAC score, 26.9% SS patients were classified as at risk (CAC > 10) for incident CV events as against 1.6% controls. The mean Multi‐Ethnic Study of Atherosclerosis (MESA) score was significantly higher in patients with SS than controls. CAC corelated significantly with fasting blood glucose (r = .316), ApoB (r = .549), LP(a) (r = .310) and FRS (r = .294). Conclusion Significant number of asymptomatic SS patients have high coronary artery calcium score and are classified at risk for CAD.

Background: Hyperprolactinemia is associated with obesity, dyslipidemia, insulin resistance, and low-grade inflammation which may promote endothelial dysfunction (EnD). Limited work has been done on EnD in prolactinomas and we, therefore, studied serum markers of inflammation and EnD in patients with prolactinomas before and after treatment with dopamine agonists. Methodology: Fifty-six treatment naïve patients with prolactinomas and fifty-three (apparently healthy age and sex-matched) controls were enrolled in the study and subjected to clinical assessment and laboratory investigations including blood glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, urea, creatinine, uric acid, erythrocyte sedimentation rate (ESR), highly sensitive C-reactive protein (hsCRP) and markers of EnD i.e., intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Patients were treated with a dopamine agonist (cabergoline) and parameters (like ESR, hsCRP, ICAM-1, and VCAM-1) were measured at 12 weeks. Results: The majority of the patients (84%) were female, more than half (52%) had metabolic syndrome and over a third (36%) were obese. Blood glucose fasting, HbA1c, lipid fractions, ESR, hsCRP, ICAM-1, and VCAM-1 were significantly higher in patients than in controls. Median ICAM-1 was 1331.95 ng/ml (IQR 803.43-1825.99) in patients vs 753.04 ng/ml (IQR 402.04-871.55) in controls, P < 0.001 and median VCAM-1in patients was 971.35 ng/ml (IQR 695.03-1285.23) as against 634.56 ng/ml (IQR 177.49-946.50) in controls, p0.001. Serum ICAM-1 and VCAM-1 correlated positively with hsCRP. On multivariate regression analysis, serum hsCRP was the only significant predictor of change in ICAM-1 and VCAM-1. Normalization of serum PRL with CAB resulted in a significant decrease in metabolic parameters, ESR, hsCRP, ICAM-1, and VCAM-1. Conclusion: Hyperprolactinemia because of prolactinoma is associated with EnD secondary to systemic inflammation and metabolic abnormalities which improve after treatment with DA.