Objective: The significance of dyslipidemia in subclinical hypothyroidism (SH) and the effect of thyroid substitution on lipids remain controversial. The present study aimed to assess the association of SH with lipid abnormalities and to quantify the effect of L-thyroxine therapy on serum lipid profiles. Design: Serum lipid parameters of 66 patients with SH and 75 age-and sex-matched euthyroid controls were evaluated in a cross-sectional study. Results: Patients with SH had higher total cholesterol (TC) ð222^45 (S.D.) vs 190^32 mg=dlÞ; lowdensity lipoprotein cholesterol (LDL-C) ð139^28 vs 118^39 mg=dlÞ; apolipoprotein B ð149^21 vs 139^18 mg=dlÞ and lipoprotein (a) (Lp(a)) (median 12.5 (0.8-101) mg/dl vs 7 (0.8 -44) mg/dl) levels compared with euthyroid controls (P , 0:05 for all comparisons). In a follow-up study including 37 patients with SH, all measurements were repeated after restoration of a euthyroid state with incremental doses of L-thyroxine. No significant changes in serum lipid profiles were observed except for a decrease in high-density lipoprotein cholesterol ð59^15 to 55^14 mg=dl; P , 0:05Þ: However, patients with high pre-treatment TC ($240 mg/dl) showed a significant reduction in both TC ð278^28 vs 257^36 mg=dl; P , 0:05Þ and LDL-C ð192^23 vs 173^28 mg=dl; P , 0:01Þ levels. Similar but more pronounced changes were observed in a subgroup of patients with pre-treatment levels of TSH $10 mU/ml. Thyroid autoimmunity had no effect on either the baseline or the posttreatment lipid profile. Conclusion: Although patients with subclinical hypothyroidism exhibit increased levels of the atherogenic parameters (mainly LDL-C and Lp(a)), thyroid substitution therapy does not seem to significantly improve dyslipidemia in the whole group of patients.
This study was performed to examine the contribution of genetic polymorphism of oestrogen and androgen receptor (AR) genes in male infertility. We have studied in total 173 Greek men, 109 infertile patients and 64 controls (group A). Patients were divided in to three subgroups: group B (n=29) with idiopathic moderate oligospermia, group C (n=42) with azoospermia or idiopathic severe oligospermia and group D (n=38) with azoospermia or oligospermia of various known aetiologies. All patients and controls were genotyped for two polymorphisms of the oestrogen receptor alpha (ERalpha) gene and also for the (CAG)n repeat length polymorphism of the X-linked androgen receptor (AR)gene. The control group had statistically significant difference from group C regarding the XbaI polymorphism of ERalpha gene. Despite the fact that we did not observe any statistically significant differences in the mean and range of the CAG repeat number, the frequency of the higher repeats of the nucleotide repeat sequence (CAG)n of the AR gene was 2-4 times higher in groups B and C compared with the control group A. Our results indicate that both ERalpha and AR gene play significant role in male fertility. It is possible that a synergy may exist between unfavourable genotypes of these two genes in male infertility.
Our study suggests that adiponectin polymorphisms are not causatively involved in the metabolic disturbances of PCOS, but that an interaction between adiponectin and steroid synthesis or action might exist.
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