Adiponectin levels, insulin resistance and their relationship with serum levels of inflammatory cytokines in patients with Behçet's disease.

AIM: Increased frequency of cardiovascular disease and its possible relations with insulin resistance have been reported in patients with inflammatory diseases. The aim of our study was to investigate insulin resistance and serum adiponectin levels as cardiovascular risk markers in patients with Behçet's disease. METHOD: Study population consisted of 40 patients with Behçet's disease (BD) and a control group composed of age, gender, body mass index-matched 46 healthy individuals. All patients were examined for signs of Behçet's disease. Body mass index, waist and hip circumference were measured. Insulin resistance was evaluated using the homeostasis model assessment-insulin resistance method. Erythrocyte sedimentation rate (ESR), lipid profile, high sensitive CRP (hsCRP), adiponectin, TNF-α, IL-6 and IL-8 levels were measured. RESULTS: Erythrocyte sedimentation rate, serum hsCRP and IL-6 levels were significantly higher in patients with BD than those in the controls (P=0.001, P=0.001, P=0.001, respectively). Fasting plasma glucose, insulin levels and lipid profile were not different between the two groups. Insulin resistance and decreased levels of the serum adiponectin were not detected in the patients. There was no relationship between insulin resistance, adiponectin levels and inflammatory markers. Active and inactive patients did not differ in respect of any parameters. CONCLUSION: Being a systemic vasculitis, BD may cause cardiovascular involvement. In this study, dyslipidemia, insulin resistance and low adiponectin levels were not detected among our patients with Behçet's disease. Our results suggest that there exists no increased risk for atherosclerotic cardiovascular disease associated with adiponectin levels and insulin resistance in patients with Behçet's disease.

Protective effects of silymarin against doxorubicin-induced toxicity.

OBJECTIVES: The aim of the present study was to investigate the effect of silymarin on doxorubicin-induced toxicity to the rat kidney, heart, and liver. MATERIALS AND METHODS: A single dose of 10 mg/kg doxorubicin was injected intraperitoneally (ip) in the doxorubicin group. The silymarin group received silymarin (100mg/kg) every other day. In the doxorubicin + silymarin group, silymarin was injected ip at 100 mg/kg dose for 5 days before doxorubicin administration (10 mg/kg, single ip injection) and then continued daily thereafter until euthanization. On the seventh day after doxorubicin injection, eight animals from each group were decapitated and liver and heart samples were obtained. The remaining eight animals of each group continued to receive silymarin every other day, till euthanized on the twenty first day. Serum was separated for determination of superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT), malondialdehyde (MDA), nitric oxide (NO), creatinine, urea, AST, ALT, lactate dehydrogenase (LDH) and creatinine phosphokinase (CPK) activities. Histopathological and electron microscopic examinations of heart, kidney and liver sections were also performed. RESULTS: Doxorubicin caused a significant increase in serum NO levels compared to controls. Silymarin pretreatment group lowered these. Histopathological and electron microscopic examinations of kidney, heart, and liver sections showed doxorubicin to cause myocardial and renal injury which was levv evident in silymarin treated rats. CONCLUSION(S): Results of the present study indicate that silymarin significantly protected doxorubicin-induced toxicities to the rat kidney, heart, and liver, thus suggesting its administration as a supportive care agent during anti-cancer treatment featuring doxorubicin.

Evaluation of serum cystatin-C in dogs with visceral leishmaniasis.

Serum Cystatin C (sCys-C) is one of the most important serum markers of renal function assessment in dogs. The purpose of this study was to determine the sCys-C concentration in dogs with visceral leishmaniasis (VL). In the study, 16 dogs with VL and 10 clinical healty dogs (control) were used. Mean sCys-C concentration of the infected dogs was significantly higher than that of the control group (p < 0.05). Mean serum creatinine concentration was lower and mean blood urea nitrogen, albumin and globulin concentrations were higher in dogs with VL; however, these changes were not statistically significant. Mean total protein and phosphorus concentrations were found to be higher in dogs with VL than healthy dogs (p < 0.05). No significant correlation had been determined between sCys-C and other variables. Visceral leishmaniasis in dogs has increased sCys-C concentration indicating a possible renal impairment; however, further studies are needed to be performed together with renal biopsies in the investigation sCys-C in dogs with VL.

Sex hormone alterations and systemic inflammation in chronic obstructive pulmonary disease.

OBJECTIVE: Decreased anabolic hormone levels are described in chronic obstructive pulmonary disease (COPD), leading to important clinical consequences. The aim of this study was to evaluate the alterations in sex hormone levels in men with COPD to compare with age-matched control subjects, the determinants of these alterations, the relationship between hypogonadism and markers of systemic inflammation [interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha)] and the androgen status during an acute exacerbation of COPD. METHODS: A total of 103 COPD patients and 30 control subjects were admitted to the study. 83 stable COPD patients and 30 control subjects were evaluated as outpatients. 20 patients with COPD exacerbation were hospitalised and evaluated before discharge and after 1 month. RESULTS: Testosterone and dehydroepiandrosteronesulphate (DHEAS) levels of both COPD groups were lower than that of the control group. Luteinizing hormone (LH), follicle stimulating hormone (FSH) levels were increased during exacerbation. Testosterone and DHEAS levels increased and LH decreased in follow-up measurements of COPD exacerbation group. Testosterone and DHEAS levels were lower in severe COPD [forced expiratory volume in 1 s (FEV(1)) < 50%], in patients with severe hypoxaemia (PaO(2) < 60 mmHg) and in hypercapnic patients. Circulating IL-6 and TNF-alpha concentrations were higher in both stable and exacerbation phase COPD groups than controls. There was no correlation between sex hormones and TNF-alpha or IL-6. CONCLUSION: The alterations in sex hormone levels in COPD are particularly related to FEV(1), hypoxaemia and hypercapnia. There are significant differences in hormone levels during stable and exacerbation phases of COPD; the hormonal changes are marked during exacerbation and partially regress after 1 month when the disease is stabilised.

Circulating leptin and body composition in chronic obstructive pulmonary disease.

Nutritional depletion and weight loss are two features of chronic obstructive pulmonary disease (COPD), and the association between low body mass index (BMI) and poor prognosis in patients with COPD is a common clinical observation. Mechanisms of weight loss are still unclear in COPD. Excessive energy expenditure partly due to increased work of breathing was shown, but other mechanisms have been searched for. Leptin is a hormone secreted by adipocytes that plays an important role in energy homeostasis and regulates body weight through control of appetite and energy expenditure. The aim of this study was to evaluate the association of circulating leptin levels and measures of body composition in COPD patients. Thirty male COPD outpatients (mean age 66.3 +/- 8.4) and 20 controls (mean age 65.9 +/- 10.8) were included in the study. After standard spirometry and body composition measurements, serum leptin concentration was measured by ELISA assay. COPD patients were grouped according to BMI. Mean BMI was 19.01 +/- 2.26 kg/m2 in group 1 (COPD patients with low BMI), 26.85 +/- 4.51 in group 2 COPD (COPD patients with normal/high BMI) and 27.64 +/- 2.75 kg/m2 in healthy controls (group 3). Mean serum leptin concentration was 1.41 +/- 1.86 ng/ml in group 1, 2.60 +/- 1.38 ng/ml in group 2 and 2.82 +/- 1.46 ng/ml in group 3 (p = 0.002). Leptin correlated to not only BMI but also body weight, waist circumference, triceps and biceps skinfold thickness and body fat percent (p < 0.05 for all). Results of this study suggest that the cause of weight loss is not increased circulating leptin in COPD. Instead, leptin remains regulated in COPD and further decreased in patients with low BMI, probably as a compensatory mechanism to preserve body fat content, which should be evaluated in further studies.