Horm Metab Res 1998; 30(4): 217-221
DOI: 10.1055/s-2007-978869
Originals Clinical

© Georg Thieme Verlag Stuttgart · New York

The Effects of Thyroid Status on Serum Apolipoprotein A-I-Containing Lipoprotein Particles*

M. Ozata1 , M. Yildrimkaya2 , K. Yilmaz2 , T. Kutluay2 , A. Çorakci2 , Z. Beyhan2 , M. A. Gundogan2
  • 1Department of Endocrinology and Metabolism, Gulhane School of Medicine, Etlik, Ankara, Turkey
  • 2Department of Biochemistry, Gulhane School of Medicine, Etlik, Ankara, Turkey
* This work was supported by Research Center of Gulhane School of Medicine
Further Information

Publication History

1997

1997

Publication Date:
20 April 2007 (online)

Alterations of lipid profile are a well-known phenomenon in thyroid dysfunction. However, little is known about the influence of thyroid hormone on Lp A-I and LpA-I:A-II particles. We have, therefore, studied LpA-I and LpAI:A-II concentrations in a group of 20 patients with hyperthyroidism and in a group of 15 patients with hypothyroidism before and one month after attainment of euthyroidism. In hypothyroid patients, LDL-cholesterol and apo B concentrations decrease significantly after L-T4 replacement treatment (from 4.49 ± 2.51 to 2.76 ± 0.70 mmol/L, P = 0.036 and from 89.4 ± 16.1 to 78.3 ± 13.3 mg/dL, P = 0.05, respectively), whereas no significant change was observed in the total cholesterol, HDL-C, LpA-I, LpA-I:A-II and apo A-I concentrations. In hyperthyroid patients, total cholesterol (from 3.58 ± 0.72 to 4.74 ± 1.39 mmol/L, P = 0.0025), HDL-C (from 1.19 ± 0.23 to 1.41 ± 0.27 mmol/L, P = 0.0084), LDL-C (from 1.83 ± 0.69 to 2.96 ± 1.20 mmol/l, P = 0.0025), apo A-I (from 85.6 ± 12.5 to 91.7 ± 18.1 mg/dL, P = 0.05) and apo B (from 52.7 ± 8.2 to 65.6 ± 16.5 mg/dL, P = 0.0013) increased after restoration of euthyroidism while triglycerides, LpA-I and LpA-I: A-II concentrations were unchanged. LpA-I and LpA-I:A-II concentrations were not related to thyroid hormones in both groups. Our study suggests that LpA-I and LpA-I:A-II particles are not under the direct control of thyroid hormones.

    >