Comparison of advanced glycation endproducts on haemoglobin (Hb-AGE) and haemoglobin A1c for the assessment of diabetic control.

Glycation process in vivo results in two different products: early and advanced glycation endproducts (AGEs). The mechanism of early product formation has been well described, with HbA1c as the best-studied example. The finding that advanced glycation endproducts are also formed on haemoglobin suggests that HbA1c is a precursor for Hb-AGE formation. HbA1c has been well established as an important indicator for glycaemia monitoring, but the diagnostic role of Hb-AGE has not yet been clarified. A question is whether HbA1c and Hb-AGE are competitive or complementary parameters. In our study, Hb-AGE was quantified by the competitive ELISA technique using polyclonal anti-AGE-RNase antibodies to detect AGE immunoreactivities of proteins precipitated in red cell hemolysate. Results are expressed as AGE units/mg Hb. Hb-AGE was analysed in three groups of patients divided according to HbA1c values as follows: group I (n = 25) HbA1c < 7%, Hb-AGE = 6.93 (5.7-7.3) U/mg; group II (n = 25) HbA1c = 7-10%, Hb-AGE = 8.62 (7.7-10.2) U/mg; and group III (n = 25) HbA1c > 10%, Hb-AGE = 12.47 (10.8-13.9) U/mg (median (interquartile range)). A close relation between the amounts of red cell HbA1c and Hb-AGE was observed in all diabetic subjects (n = 75) r = 0.77, P < 0.001. Patients with HbA1c level > 8% were considered to be in poor glycaemic control and those with HbA1c < 8% in good control. In the well-controlled subgroup (n = 33), HbA1c and Hb-AGE were less tightly correlated (r = 0.37, P <0.001). However, in those patients with a higher level of HbA1c = 12.55 (8.9-13.3)% (n = 42), the related Hb-AGE was 11.5 (10.3-12.8) U/mg Hb, yielding a more significant correlation (r = 0.51, P < 0.001). The content of Hb-AGE did not correlate with age (r = 0.09), diabetes duration (r = 0.05) or severity of retinopathy and/or nephropathy. The observed difference may reflect a different kinetic rate of HbA1c production and subsequently the rate of Hb-AGE formation. The discrepancy in the correlation between HbA1c and Hb-AGE suggests that they are complementary rather than opposed parameters. The amount of haemoglobin-linked AGEs does not correlate with the presence or absence of retinopathy and/or nephropathy. It seems that Hb-AGE represents only the metabolic status, equally in the subjects with and without diabetic microangiopathy.

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).