Serum sialic acid in subjects with impaired glucose tolerance and in newly diagnosed type 2 diabetic patients.

Several general population studies and those carried out in diabetic patients with complications have pointed to serum sialic acid as a marker of inflammation in atherosclerosis. In this study we examined whether total sialic acid (TSA) was changed in the sera of 28 newly diagnosed subjects with type 2 diabetes (type 2 DM), 47 subjects with impaired glucose tolerance (IGT) and 72 subjects with normal glucose tolerance (NGT). The associations between sialic acid and other atherosclerotic risk factors such as lipid profile, baseline diene conjugates in low-density lipoproteins (LDL-BDC) and fasting insulin were also investigated. We found a trend to TSA increase in subjects with impaired glucose tolerance and a significant increase in TSA in newly diagnosed patients with type 2 DM (2.2+/-0.3 vs. 1.9+/-0.3 mmol/l; p<0.03) when compared to subjects with NGT. Lipid profile and LDL-BDC, as a marker of circulating oxidized LDL, did not differ among glucose tolerance categories. Significant associations between total sialic acid and 2-h post-load glucose level, fasting insulin, insulin sensitivity, HDL-cholesterol and log of triglycerides were found in the examined subjects. Multiple regression analysis showed significant correlations between serum sialic acid and 2-h post-load glucose levels and insulin sensitivity. This study indicates that measurement of TSA as a marker of subclinical inflammation may be valuable as an independent parameter in identifying subjects at higher risk of developing type 2 diabetes and those who might benefit from anti-inflammatory treatment.

Lipoprotein (a) levels in thyroid dysfunction before and after treatment.

AIM: To investigate the possible effects of thyroid hormones on the lipoprotein (a) (Lp(a)) serum concentration. METHODS: Eleven patients with hyperthyroidism (Grave's disease), 18 patients with hypothyroidism and low Lp(a) (Hashimoto's disease), and 13 patients with hypothyroidism (Hashimoto's disease) and elevated Lp(a) were examined before and after thyroid hormone normalization. The measurements included total cholesterol, HDL cholesterol (including HDL2 and HDL3 subfractions), LDL cholesterol, VLDL cholesterol, triglycerides, apoproteins A1 and B, and Lp(a), thyrotropin (TSH) and thyroid hormones/total thyroxine (T4), triiodothyronine (T3), free thyroxine (FT4), and free triiodothyronine (FT3). RESULTS: In patients with hyperthyroidism, serum concentrations of total cholesterol, LDL cholesterol, and apo B significantly increased (p<0.05) after the treatment, whereas a moderate increase in HDL (HDL2 subfraction), triglyceride, and Lp(a) concentrations did not reach statistical significance. In both groups of patients with hypothyroidism, concentrations of total cholesterol, LDL cholesterol, apo B, and triglycerides significantly decreased after the treatment, whereas the changes in HDL (HDL2 and HDL3 subfractions), VLDL cholesterol, apo A1, and Lp(a) were not significant. CONCLUSION: Thyroid hormones had only a moderate effect on the metabolism of Lp(a).

Nevo syndrome.

We report on a patient with Nevo syndrome manifesting intrauterine and postpartum overgrowth, accelerated osseous maturation, dolichocephaly, highly arched palate, large, low-set ears, cryptorchidism, delayed neuropsychological development, hypotonia, adema, contractures of the hands and feet, a single a transverse palmar crease, and tapering digits. After meningococcal sepsis at age 6 months, he remained decerebrate. Thereafter, overgrowth and especially weight gain were extremely accelerated until his death at age 18 months, at which time his height was 103 cm and his weight was 23 kg. In addition to low plasma concentrations of growth hormone and insulin-like growth factor, severe insulin resistance was observed. It is presumed that a selective defect in insulin-stimulated glucose uptake, with preservation of anabolic effect, was one of the causes of his "overgrowth without growth hormone," at least in the last 12 months of life after severe brain damage.