Mean platelet volume (MPV), a determinant of platelet function, is a newly emerging risk factor for atherothrombosis. The present study was designed to evaluate MPV in patients with obesity compared with non-obese control subjects. We selected 100 non-obese subjects and 100 subjects with obesity [body mass index (BMI) > or =30 kg/m(2)] matched for age and gender. The MPV was significantly higher in obese group than in non-obese control group (10.3 +/- 1.2 vs. 9.0 +/- 0.8 fl, p < 0.01). MPV was positively correlated with BMI in obese group (p < 0.05). Increased MPV may be a possible cause for increased cardiovascular risk in patients with obesity.

Numerous clinical and experimental reports suggest that a high von Willebrand factor (vWf) level reflects endothelial damage or endothelial dysfunction. The present study was designed to evaluate vWf in subclinical hyperthyroidic subjects compared with euthyroidic subjects. We selected 20 subclinical hyperthyroidic subjects and 20 euthyroidic control subjects matched for age, gender and body mass index. The level of vWf was significantly higher in the subclinical hyperthyroidic group than in the euthyroidic group (42.9+/-9.6 vs 37.6+/-6.4%, p=0.026). In conclusion, our results suggest that subjects with subclinical hyperthyroidism tend to have an endothelial dysfunction. Endothelial dysfunction could contribute to increasing the cardiovascular risk in subclinical hyperthyroidism.

Mean platelet volume (MPV), a determinant of platelet function, is a newly emerging risk factor for atherothrombosis. The risk profile of white coat hypertension has not yet been completely clear. The present study was designed to evaluate MPV in white coat hypertensive subjects compared with essential hypertensive patients and normotensive subjects. We selected 36 essential hypertensive patients, 36 white coat hypertensive subjects and 36 normotensive control subjects matched for age, gender, and body mass index. MPV was very significantly higher in essential hypertensives and white coat hypertensives than in normotensives (P < 0.00); it was also higher in essential hypertensives than in white coat hypertensives (P < 0.05). Platelet counts were not different among the study groups (P > 0.05). MPV was positively correlated with ambulatory diastolic blood pressure in essential hypertension and white coat hypertension groups (P < 0.05). In conclusion, our data suggests one possible mechanism by which white coat hypertensive subjects may be at increased cardiovascular risk.

Hypocalcemic cardiomyopathy due to hypoparathyroidism is a very rare condition which is usually refractory to conventional treatment for cardiac failure but which responds favorably to restoration of normocalcemia. A 55-year-old man and a 46-year-old woman with a history of postoperative hypoparathyroidism presented with symptoms of cardiac failure and hypocalcemia. A presumptive diagnosis of dilated cardiomyopathy was considered by echocardiography and endomyocardial biopsies were consistent with cardiomyopathy. The coronary angiograms were normal and there was no apparent cause for dilated cardiomyopathy in these patients. The history of the patients and partial recovery of cardiac function after restoration of normocalcemia suggest that hypocalcemia was the cause of dilated cardiomyopathy.

Insulin resistance (IR), glucose intolerance and diabetes mellitus are commonly associated with cirrhosis. The exact pathogenetic mechanisms responsible are still unknown; however, they may be related to both hepatitis C virus itself and to liver injury. IR may be the earliest abnormality, which in the following years may progress to clinical diabetes mellitus. The aim of this study was to investigate the presence of IR by euglycaemic hyperinsulinemic clamp technique, in chronic hepatitis C patients. 15 patients and nine healthy controls without any known condition that may affect IR were enrolled to the study. Chronic hepatitis C was diagnosed by liver biopsy (hepatic activity index was also determined in 10 patients) and appropriate viral and biochemical tests. Eight patients were given interferon therapy, which had been stopped for at least 3 months before the study. Euglycaemic hyperinsulinemic clamp technique was performed as previously described and peripheral glucose utilisation rate, M value, was calculated in mg/kg/min by infusion of 40 IU/m2/min regular insulin. M value of the control group was significantly higher than that of chronic hepatitis C patients (M = 5.1+/-1 vs. 3.7+/-1; p = 0.004), which was consistent with IR in the patient group. There was no significant correlation between the M value and alanine aminotransferase, aspartate aminotransferase and hepatic activity index (p = 0.621, 0.549, 0.479, respectively). Our results suggest that IR is present in chronic hepatitis C patients; it is not directly related to hepatic injury, moreover, it may be associated with some component(s) inherent to hepatitis C virus.

BACKGROUND AND AIM:Orlistat and metformin are the currently used drugs for weight loss. We aimed to compare the effect of orlistat and orlistat plus metformin combination therapy on weight loss and insulin resistance in obese women. PATIENTS AND METHODS:In all, 57 obese women (body mass index Z30 kg/m 2 and normal glucose tolerance) were included. All subjects took the same content and caloric diet therapy during the study. After a month of diet period, each individual was randomly assigned to receive 360 mg orlistat per day (group 1; n ¼ 30) or 360 mg orlistat plus 1700 mg metformin per day (group 2; n ¼ 27) during the next 3 months. Body weight and insulin resistance by the homeostasis model assessment model (HOMA-IR) was measured at baseline, first month and fourth month. RESULTS: The mean weight loss in groups 1 and 2 was 1.3670.8 kg (1.470.7%) and 1.1170.7 kg (1.170.7%) from baseline to first month; 4.872.9 kg (5.2873.0%) and 5.7772.5 kg (6.1772.9%) from first month to fourth month. Body weight was decreased in groups 1 (Po 0.001) and 2 (Po 0.001), but there was no statistically significant difference between groups. Change of HOMA-IR in groups 1 and 2 was 0.4170.4 (14.9710.1%) and 0.2370.7 (8.16712.3%) from baseline to first month; 0.4970.77 (22.0726%) and 0.9570.88 (34.8729.1%) from first month to fourth month. HOMA-IR value was decreased in groups 1 (Po 0.001) and 2 (Po 0.001) but was not different between groups during the study period. CONCLUSIONS: Combination of orlistat with metformin did not result in an additional effect on weight loss and insulin resistance when compared to orlistat alone in our study. However, new studies which have more sample sizes and the longer study period are necessary for this purpose.

We describe a 52-year-old woman with pancytopenia associated with Sheehan's syndrome, whose presenting feature was severe malaise and syncope after a psychological stress. Hormonal replacement therapy alone (with L-thyroxine and prednisolone) produced clinical and full haematological recovery. This is a very rare case of Sheehan's syndrome because the diagnosis was delayed for 27 years after delivery, and it was associated with pancytopenia.

It is now well documented that hypertension is associated with a chronic low-grade inflammatory state. Levels of high-sensitivity C-reactive protein (hs-CRP), a marker of systemic inflammation and a mediator of atherothrombotic disease, have been shown to correlate with cardiovascular disease risk. Our objective was to evaluate the effect of fenofibrate on the levels of hs-CRP in dyslipidaemic hypertensive patients. We selected 30 dyslipidaemic hypertensive patients and 20 normolipidemic normotensive healthy subjects. Dyslipidaemic hypertensive patients were treated with fenofibrate 200 mg/day for 3 months. Serum hs-CRP and metabolic parameters were evaluated at baseline in both groups and after fenofibrate treatment in dyslipidaemic hypertensive patients. At baseline, significantly higher hs-CRP levels were found in dyslipidaemic hypertensive patients than normal subjects (0.48 +/- 0.3 vs. 0.15 +/- 0.1 mg/dl, p < 0.01). Total cholesterol, low-density lipoprotein cholesterol and triglyceride significantly decreased (p < 0.05, p < 0.05 and p < 0.01, respectively), and levels of high-density lipoprotein cholesterol significantly increased (p < 0.05) after treatment with fenofibrate in dyslipidaemic hypertensive group. Levels of hs-CRP significantly decreased after fenofibrate treatment from a mean of 0.48 +/- 0.3 mg/dl to vs. 0.16 +/- 0.2 mg/dl, p < 0.01). Our findings suggest that fenofibrate may be used as a first-line therapy for improving the plasma lipids profile as well as the chronic low-grade inflammatory state in dyslipidaemia and hypertension.