PROJECT:Noninsulin dependent diabetes mellitus is supposed to be associated with fluctuations in the plasma levels of several trace elements. There is accumulating evidence that the metabolism of several trace elements is altered in patients with noninsulin dependent diabetes mellitus and that these nutrients might have specific roles in the pathogenesis and progression of this disorder.PROCEDURE:The aim of the present study is to compare the levels of essential trace and toxic elements including lead (Pb), arsenic (As), cadmium (Cd), chromium (Cr), aluminium (Al), nickel (Ni), cobalt (Co), iron (Fe), copper (Cu), selenium (Se), zinc (Zn), vanadium (V), manganese (Mn), barium (Ba), silver (Ag), and mercury (Hg) in patients with noninsulin dependent diabetes mellitus (n = 31), impaired glucose tolerance (n = 20), impaired fasting glucose (n = 14), and healthy controls (n = 22). Plasma concentrations of the elements were measured by using inductively coupled plasma mass spectrometry.RESULTS:The results indicated that values of lead, nickel, aluminium, copper, and chromium were significantly higher, but not above toxic levels, in the plasma of nonsmoker patients with noninsulin dependent diabetes mellitus (P < 0.05). The values for these elements were found to be significantly higher (P < 0.05) in patients with impaired fasting glucose than in controls. Moreover, a statistically significant correlation was found between plasma levels of glycated hemoglobin and of some trace elements like lead, nickel, aluminium, copper, chromium, cadmium, and mercury.CONCLUSIONSThus, it was concluded that chronic complications of glucose metabolism disorders might be associated with alterations in the levels of some trace elements. Nevertheless, some more timely and extensive studies are required to clarify the exact mechanisms of each of these changes.

Intrauterine growth retardation/restriction (IUGR) is associated with fetal malnutrition. It has consequences for later life including increased incidence of obesity, diabetes mellitus, cardiovascular disease (CVD), and metabolic syndrome. Adipokines (adiponectin and leptin), adropin, and endothelin-1 are associated with obesity and metabolic syndrome regulation. Intrauterine changes in these mediators could affect programming of later adult obesity and metabolic syndrome. Our objectives were to compare the levels of these mediators in both cord and maternal blood between IUGR pregnancies and control, healthy pregnancies, and to study the correlation of adipokines with adropin and endothelin-1 in maternal and cord blood in IUGR pregnancies as well as in healthy control pregnancies. Maternal and cord blood samples were taken from 16 women with IUGR pregnancies and 16 women with healthy pregnancies. Serum levels of leptin, adiponectin, adropin, and endothelin-1 were measured by ELISA. Maternal blood adropin levels were significantly lower in the IUGR group than in the control group; the other mediators did not differ significantly. There was a positive correlation between maternal blood adropin and endothelin levels. (r=0.731, P=0.001) in the control but not the IUGR group. Cord blood adropin and adiponectin levels were significantly lower in the IUGR group compared with the control group, while leptin or endothelin-1 did not differ significantly. There was a negative correlation between adropin and leptin (r=-0.704, P=0.001) in the IUGR but not the control group cord blood. There were also positive correlations between endothelin and adropin for both groups (r=0.594, P=0.006; r=0.560, P=0.010, respectively); to the best of our knowledge, this is the first report of such a correlation. Differences in fetal expression of adropin and adiponectin in IUGR could influence programming of obesity, metabolic syndrome, diabetes, and CVD in later life.

Serum ADA levels were found to be elevated in UC patients in active state suggesting a partial role of activated T-cell response in the disease pathophysiology. Further randomized controlled studies are warranted to demonstrate the role of ADA in UC patients, with a special interest in specifically targeted therapies against ADA for achieving disease remission.

Purpose: Atrial fibrillation (AF) is the most common form of arrhythmia. AF leads to electrical remodelling and fibrosis of the atria; however, the mechanism(s) remain poorly understood. Galectin-3 is a potential mediator of cardiac fibrosis. The present study aimed to examine the relationship between serum galectin-3 levels and paroxysmal AF.Methods: Forty-six patients with paroxysmal AF and preserved left ventricular systolic function, and 38 age-and gender-matched control subjects, were involved in the study. Serum galectin-3 levels were analyzed with an enzyme-linked immunosorbent assay (ELISA).Results: Serum galectin-3 levels (median 1.38 ng/mL; 1.21 ng/mL-1.87 ng/mL; p< 0.001) were significantly elevated in patients with paroxysmal AF compared with the control. Left atrial diameter was significantly higher in patients with paroxysmal AF (41.2±3.0 mm vs. 39.6±3.3 mm). Left atrial diameter was found to be significantly correlated with serum galectin-3 levels in patients with paroxysmal AF (r= 0.378, p= 0.001).Conclusion: Serum galectin-3 levels are significantly elevated and significantly correlated with left atrial diameter in patients with paroxysmal AF.SUPPLEMENT

Background and aims: Hepatitis B virus (HBV) infection is a public health problem and affects nearly 350 million people worldwide. The present study was conducted in order to investigate the role of circulating angiotensin-converting enzyme (ACE) in the context of renin-angiotensin-aldosterone in newly diagnosed chronic hepatitis B infection. Moreover the association between liver fibrosis and serum ACE levels was also investigated. Materials and methods:The study was performed on 50 chronic hepatitis B (CHB) patients (24 males, 26 females; median age 39.4 years, range 18-63) and 20 healthy controls. The clinical features of CHB patients including demographics, laboratory and liver biopsy findings were summarized. Serum ACE levels were measured by using commercially available kits. Results: Serum median ACE levels were 48.4 (14-83) U/L and 26.2 (12-48) U/L for the CHB patients and controls, respectively. Serum ACE levels were significantly higher in patients with CHB compared with the control group (p<0.001). Twenty-two patients (44%) had advanced liver fibrosis (Ishak score >2) and 28 patients (56%) had mild liver fibrosis (Ishak score ≤ 2). Mean serum levels of ACE were significantly higher among patients with advanced fibrosis as compared with those without advanced fibrosis (60.3±14.2 U/L vs. 39.0±10.5 U/L, p<0.001). Receiver operating characteristic (ROC) curve analysis suggested that the optimum ACE level cut-off point for advanced fibrosis was 52.5 U/L (sensitivity: 81.8%, specificity: 82.1%, PPV 78.3%, NPV 85.2%, accuracy 82%, AUC: 0.890). Conclusions: Our study showed that elevated circulating ACE levels are commonly observed in CHB patients. This finding was more prominent in patients with advanced fibrosis in liver. When evaluating a patient along with other parameters, the inclusion of ACE levels in the evaluation of CHB patients may grant additional prognostic information.