There is a high prevalence of HP infection in diabetic patients and it is correlated with dyspeptic symptoms. Diabetic subjects complicated with cardiovascular autonomic neuropathy and dyspepsia are at high risk of HP infection and should be carefully investigated and considered for eradication therapy.

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The aim of our study was to assess the changes in serum lipid profiles after replacement therapy with L-T4 in patients with subclinical hypothyroidism (SCH), and to see whether there is an improvement in dyslipidemia based cardiovascular risk. Thirty non-smoker pre-menopausal women with newly diagnosed SCH (TSH between 4 and 10 microIU/ml) were involved in our study; twenty-six euthyroid healthy subjects were used as control group. TSH, free T3 (FT3), free T4 (FT4), total cholesterol (TC), triglyceride (TG), HDL cholesterol (HDL-C) and LDL cholesterol (LDL-C) levels were measured before and after 6 months of L-T4 (50-100 microg/ day) therapy. TSH levels were targeted as < 2.0 microIU/ml. LDL-C was calculated using the Friedewald formula, while the cardiovascular risk was assessed with the TC/HDL-C ratio. Pre-treatment serum TC and LDL-C concentrations in SCH patients were significantly higher than those of euthyroid subjects (199.8 +/- 22.2 vs 181.5 +/- 24.6 mg/dl, p < 0.01; 146.3 +/- 26.1 vs 124.8 +/- 12 mg/dl, p < 0.001, respectively). TC, LDL-C levels and the TC/HDL-C ratio were reduced significantly after 6-month replacement therapy (-21.1 +/- 34.4 mg/dl or -10.5%, p < 0.01; -21.5 +/- 30.3 mg/dl or -14.7%, p < 0.001, respectively; and TC/HDL-C from 4.8 +/- 0.6 to 4.1 +/- 0.5 mg/dl, p < 0.01), while body mass index (BMI) values did not change. In conclusion, even mild elevations of TSH are associated with changes in lipid profile significant enough to raise the cardiovascular risk ratio, and these changes are corrected once the patients have been rendered euthyroid.

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.

The aim of the present study was to evaluate plasma total homocysteine (Hcys) and serum fibrinogen concentrations in subclinical hypothyroid (SH) and overt hypothyroid patients before and after L-thyroxine (LT4) replacement and to compare them in euthyroid subjects. Fifteen SH and 20 hypothyroid premenopausal women were recruited in the study. We measured fasting plasma levels of Hcys and serum levels of free thyroxine (fT4), free triiodothyronine (fT3), thyrotropin (TSH), folate, vitamin B12, fibrinogen, renal functions, and lipid profiles in patients with SH and overt hypothyroid patients before and after LT4 treatment. Eleven healthy women were included in the study as a control group. Pretreatment Hcys levels were similar in SH and control subjects, whereas mean fibrinogen level of SH patients was higher than that of control subjects (p<0.05). Baseline Hcys (p<0.01) and fibrinogen (p<0.001) levels of the overt hypothyroid patients were significantly higher than those of the healthy subjects, and the pretreatment Hcys levels decreased with LT4 treatment (p<0.001). In conclusion, our data support that SH is not associated with hyperhomocysteinemia and Hcys does not appear to contribute to the increased risk for atherosclerotic disease in patients with SH.

In this study we investigated whether leptin and TNFα levels change with improvement in body weight with antituberculotic therapy in active tuberculosis patients. 30 patients (8 females and 22 males) with active pulmonary tuberculosis formed the patient group, and 25 sex- and age-matched healthy subjects (8 females and 17 males) served as the control group. Body weight, body mass index (BMI) and serum leptin and plasma TNFα levels are measured before and in the sixth month of therapy in all patients. Before the initiation of therapy, BMI of the patients was significantly lower than BMI of the controls (20.2 ± 1.6 vs. 25.2 ± 2.7 kg/m², respectively; p < 0.05). After treatment, BMI of the patients increased significantly to 21.4 ± 1.9 kg/m² (p < 0.05), but was still lower than that of the controls (p < 0.05). Pretreatment serum leptin (4.5 ± 0.9 vs. 2.1 ± 0.2 ng/ml, respectively; p < 0.05) and plasma TNFα (27.9 ± 3.4 vs. 23.9 ± 3.0 pg/ml, respectively; p < 0.05) levels of the patients were significantly higher than those of the controls. After treatment, serum leptin levels increased to 6.7 ± 2.2 ng/ml, but this rise was not statistically significant (p > 0.05). Treatment did not result in any significant change in TNFα levels, either. Δ leptin was highly related to Δ BMI in patients with tuberculosis (r = 0.68, p = 0.02). In the pretreatment period, there was a significant correlation between leptin and TNFα levels in the whole patient group (r = 0.78, p < 0.001), and in female (r = 0.74, p < 0.001) and male patients separately (r = 0.74, p = 0.035). In conclusion, leptin and TNFα may be responsible for the weight loss in pulmonary tuberculosis patients, but their levels do not change with improvement in body weight with antituberculotic treatment.