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.

Intra-individual biological variation contributes to the variation in serial results and should therefore be included in the criteria for serum tumour marker assessment.

Abstract. Subclinical hypothyroidism is a frequent disorder in populations and has been shown to be a risk factor for coronary heart disease (CHD). Less is known about the contribution of lipoprotein (a) [Lp(a)] to the development of CHD in this disorder. Therefore this study was designed to evaluate Lp(a) and other lipoprotein concentrations before and after L-T4 therapy in 20 patients with subclinical hypothyroidism and 20 normal healthy subjects matched for sex, age and BMI. In the basal state of subclinical hypothyroidism, a significant increase in total cholesterol, LDL-cholesterol and apolipoprotein (apo) B concentrations was observed in patients compared with those in the control group. The mean Lp(a) concentration before treatment was 163 ± 15 mg/L. This is slightly but not significantly higher than those in the control group (131 ± 15 mg/L). Treatment of subclinical hypothyroidism with a low dose of L-T4 (25 ug daily) for 3 months after restoration of euthyroidism led to decreases in levels of Lp(a) from 163 mg/L to 126 mg/L (23% reduction, P<0.001), total cholesterol from 5.5 mmol/L to 5.1 mmol/L (7% reduction, P<0.001), LDL-cholesterol from 4.14 mmol/L to 3.63 mmol/L (12%, P<0.001), and apo B from 98 mg/dL to 86 mg/dL (12% reduction, P<0.05), but triglyceride, HDL-cholesterol and apo A-I concentrations were unchanged. These data suggest that L-T4 replacement therapy in patients with subclinical hypothyroidism has beneficial effects on the lipid profile since L-T4 replacement therapy lowered the concentrations of Lp(a) and other atherogenic lipid particles. [7,8]. The Lp(a) lipid composition is similar to that of LDL, but the protein composition is different, consisting of two major proteins, apolipoproteins (apo) B 100 and apo (a) attached to each other by a disulfide bridge [9]. Lp(a) is closely correlated with a high risk for CHD [10,11]. Metabolism of Lp(a) is largely unknown; its sites of degradation and the factors affecting its plasma levels are not fully understood. Diets and most drugs that decrease LDL cholesterol levels do not substantially alter Lp(a) levels [12] except the use of neomycin in combination with nicotinic acid [13].Recently, several reports have been published

Elevated SUA level on admission independently predicts impaired myocardial flow and poor prognosis in STEMI patients undergoing primary PCI.

It is known that lipoprotein(a) [Lp(a) is an independent risk factor for developing atherosclerosis, whereas the LpA-I particle of high density lipoprotein (HDL) is an antiatherogenic factor. The effects of androgen replacement therapy on lipid and lipoproteins have previously been reported in male hypogonadism. However, no study reported the effect of gonadotropin or testosterone treatment on Lp(a), LpA-I, or LpA-I;A-II levels in make hypogonadism. We, therefore, determined Lp(a), LpA-I, LpA-I:A-II, and other lipoprotein levels before and 3 months after treatment in 22 patients with idiopathic hypogonadotropic hypogonadism (IHH) and in 9 patients with Klinefelter's syndrome. All patients had been previously untreated for androgen deficiency. Plasma FSH, LH, PRL, testosterone (T), estradiol, and dehydroepiandrosterone sulfate levels were also determined before and 3 months after treatment. Patients with IHH were treated with hCG/human menopausal gonadotropin, whereas patients with Klinefelter's syndrome received T treatment. Three months after treatment, mean T levels role to low normal levels in both groups. Triglyceride, LpA-I:A-II, Lp(a), HDL cholesterol, HDL3 cholesterol, and apolipoprotein (apo) A-I concentrations did not change significantly after treatment, whereas total cholesterol, low density lipoprotein cholesterol, LpA-I, and HDL2 concentrations were significantly increased 3 months after treatment in both groups. The apo B concentration significantly increased in patients with klinefelter's syndrome, whereas no change was observed in the IHH group. Lp(a) concentrations were not related to all hormonal and clinical parameters in both groups. LpA-I concentrations were significantly and negatively correlated with free T (r = -0.80; P = 0.010) in patients with Klinefelter's syndrome and were not correlated with all hormonal and clinical parameters in the IHH group. The LpA-I:A-II concentration was only correlated with body mass index (r = -0.83; P = 0.005) in patients with Klinefelter's syndrome, whereas it was correlated negatively with dehydroepiandrosterone sulfate (r = -0.57; P = 0.005) in the IHH group.2 Overall, our study demonstrates that gonadotropin or T treatment has a complex effect on lipids and lipoproteins. This complexity will be resolved when sufficient large scale androgen treatment data are available for assessment of the long term outcome of androgen treatment. The increases in total cholesterol and low density lipoprotein cholesterol concentrations after treatments are the adverse effects of these treatments, whereas the increases in HDL2 and LpA-I concentrations and the lack of changes in Lp(a) are the beneficial effects. Gonadotropin or T treatment did not modify the Lp(a) concentration, indicating that it is not affected by the hormonal milieu in male hypogonadism. Our study also showed that LpA-I, but not LpA-I:A-II, particles could be modified by androgen replacement therapy.