Objectives: Most patients with polycystic ovary syndrome (PCOS) are obese and known to have insulin resistance. Obesity per se is a cause of insulin resistance. This study was performed to determine whether insulin resistance occurs in patients with PCOS in the absence of obesity and acanthosis nigricans. Method: For this purpose, an euglycemic hyperinsulinemic clamp study was performed in 12 nonobese patients with PCOS and in 10 healthy control subjects matched for age and weight. Results: The mean serum testosterone and luteinizing hormone (LH) levels were significantly elevated (4.09 ± 1.32 vs. 1.18 ± 0.53 pg/ml, p < 0.001, and 11.63 ± 5.37 vs. 4.98 ± 2.73 mIU/ml, p < 0.001, respectively), and the serum sex hormone binding globulin level was significantly reduced (40.96 ± 14.94 vs. 73.98 ± 30.40 nmol/l, p < 0.001) in patients with PCOS as compared with the values in control subjects. The mean serum insulin level was also elevated in patients with PCOS as compared with control subjects (32.33 ± 4.98 vs. 19.56 ± 2.21 µU/ml, p < 0.05). The insulin sensitivity was lower in patients with PCOS as compared with the control subjects (200 ± 27.8 vs. 427.8 ± 88.9 µmol kg–1min–1, p < 0.001). In patients with PCOS, the serum levels of free testosterone (r = –0.89, p < 0.001) and LH were inversely correlated with the insulin sensitivity (r = –0.63, p < 0.05). Serum follicle-stimulating hormone, prolactin, and dehydroepiandrosterone sulfate levels were similar in both groups. Conclusions: These results indicate that a significant degree of insulin resistance exists in nonobese patients with PCOS and that this insulin resistance is significantly related to serum LH and free testosterone levels. Thus, measures to decrease insulin resistance may have to be considered earlier to decrease the potential risks of developing diabetes mellitus and coronary artery disease at later ages of life in these patients.
Although G-CSF improves neutrophil function as well as increasing the absolute numbers, this improvement is not associated with shortening of duration of antibiotic administration, duration of hospital stay or need for amputation in diabetic foot infection.
Background: The obese are usually protected against osteoporosis and have increased bone mineral density and plasma leptin concentrations. A recent in vitro study demonstrated that leptin acts on human marrow stromal cells to enhance differentiation to osteoblasts, suggesting an influence of leptin on bone mass. However, little is known about the relationship between plasma leptin and bone mass in postmenopausal women with osteoporosis. Objective: To investigate plasma leptin concentrations in postmenopausal women with osteoporosis to improve the understanding of the role of leptin in determining bone mass. Methods: Fifty postmenopausal women with osteoporosis (ages 61.18 Ϯ 6.51 years; body mass index (BMI) 28.91 Ϯ 3.44 kg/m
Smell and taste are known to be influenced by thyroid function changes. However, many hypothyroid patients and physicians are unaware of their dysosmia and dysgeusia. The present study was performed to shed more light on the relation between hypothyroidism and olfactory loss. 32 primary hypothyroid patients and 31 controls enrolled in the prospective randomized interventional study. Newly diagnosed Primary hypothyroid patients were treated with L-thyroxine for 3-6 months. The control group was selected on the basis of the biochemical evidence of a normal thyroid function. Psychophysiological olfactory testing was performed using odor dispensers similar to felt-tip pens ("Sniffin' Sticks", Burghart, Wedel, Germany). Taste function tests were made using "Taste Strips" (Burghart, Wedel, Germany) which are basically tastant adsorbed filter paper strip. Smell identification, threshold, discrimination, TDI scores, bitter and sweet taste scores were significantly lower in untreated hypothyroid patients compared to controls (12.31±1.09 vs. 14.03±1.05, p<0.001; 7.09±1.15 vs. 8.89±1.12, p<0.001; 11.47±0.95 vs. 13.06±0.85, p<0.001; 30.90±2.70 vs. 35.89±2.07, p<0.001; 4.88±1.6 vs. 6.64±0.96, p<0.001; and 5.5±2.22 vs. 6.58±1.28, p=0.021) respectively. Comparison of scores at the third month of treatment and before treatment of hypothyroid patients revealed significant improvement in smell and taste functions in terms of identification, threshold, discrimination, TDI scores, bitter, sweet and salty tastes (12.31±1.09 vs. 13.84±1.22, p<0.001; 7.09±1.15 vs. 8.02±1.16, p<0.001; 11.47±0.95 vs. 12.41±1.21, p<0.001; 30.90±2.70 vs. 34.27±3.25, p<0.001; 4.88±1.6 vs. 6.06±1.4, p<0.001; 5.5±2.22 vs. 6.38±1.28, p<0.001; and 6.12±2.32 vs. 6.62±1.48, p=0.044) respectively. On correlation analysis, there was a negative correlation between TPO-Ab levels and discrimination, identification and TDI scores (r=-0.409, p=0.02; r=-0.424, p=0.016; r=-0.532, p=0.002), and also between Tg-Ab levels and identification, TDI, and bitter scores (r=-0.423, p=0.016; r=-0.468, p=0.007; r=-0.409, p=0.02) respectively. Primary hypothyroidism was found to have a negative effect on smell and taste. RAI treatment was found to be most destructive on smell and taste compared to surgical and autoimmune hypothyroidism. Treatment of hypothyroidism was positively correlated with an improvement of both senses. Thus, the future workup of patients with smell/taste loss should include investigations for thyroid functions.
Background/Aim: Intercellular adhesion molecule 1 (ICAM-1) is a mediator in the recruitment of leukocytes in the glomerular cells. The role of ICAM-1 in diabetic complications is still a matter of debate. This study was performed to investigate the relation of plasma soluble ICAM-1 (sICAM-1) to nephropathy in patients with type 2 diabetes mellitus. Methods: Ninety-three patients (24 males and 69 females) with type 2 diabetes mellitus were included into the study. Fifty patients had nephropathy, and 43 were free from nephropathy. Fifty healthy subjects (14 males and 36 females) served as the control group (group 1). Twenty-five of the diabetic patients had microalbuminuria (group 2), 25 had macroalbuminuria (group 3), and 43 had neither micro- nor macroalbuminuria (group 4). The plasma sICAM-1 levels were measured in blood samples drawn after fasting. Results: The mean plasma sICAM-1 levels were not different in the 93 diabetic patients as compared with the healthy controls (392.7 ± 119.5 vs. 350.1 ± 90.2 ng/ml, p > 0.05). The mean sICAM-1 level was significantly higher in the diabetic patients with nephropathy than in those without nephropathy (430.3 ± 78.2 vs. 368.2 ± 122.5 ng/ml, p = 0.03) and in the controls (430.3 ± 78.2 vs. 350.1 ± 90.2 ng/ml, p = 0.016). The difference in sICAM-1 levels between groups 2 and 3 was not significant (p > 0.05). The plasma sICAM-1 levels were significantly higher in both groups 2 and 3 than in both groups 1 and 4 (434.5 ± 129.2 vs. 427.2 ± 113.7 ng/ml and 368.2 ± 122.5 vs. 350.1 ± 90.2 ng/ml, respectively). Conclusions: The plasma sICAM-1 levels in patients with type 2 diabetes mellitus are not significantly different from those in nondiabetic subjects. High levels of sICAM-1 suggest that sICAM-1 may play a role in the development of nephropathy in patients with type 2 diabetes mellitus.
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