Amiodarone-induced changes in lipid metabolism

Siddika E Karakas, N. Bagchi, T. R. Brown, S. Khilnani, K. Jackson, R. T. Steinman, M. H. Lehmann

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Hypotheroidism is a major cause of secondary hypercholesterolemia. Amiodarone treatment alters both the levels of serum lipids and thyroid hormones. We investigated whether the amiodarone-induced changes in lipid metabolism are related to the changes in thyroid hormone levels. Eighteen patients received amiodarone (31 ± 3 g cumulative dose) for six weeks. Serum triglyceride, total-cholesterol, high density lipoprotein-cholesterol and its subfractions, apolipoproteins B and AI, and plasma post-heparin lipoprotein lipase and hepatic triglyceride lipase activities were determined. Amiodarone treatment caused significant increases in serum total-cholesterol (baseline 4.4 ± 0.21 (SE), 6 weeks 5.12 ± 0.26 mmol/P < 0.01), in low density lipoprotein cholesterol (baseline 2.61 ± 0.26, 6 weeks 3.36 ± 0.21 mmol/l, P < 0.05) and in apolipoprotein B (baseline 1.95 ± 0.15, 6 weeks 2.26 ± 0.13 mmol/l, P < 0.01) concentrations. Serum high density lipoprotein and its subfractions, or apolipoprotein AI levels did not change. Plasma post-heparin lipoprotein lipase activity increased (baseline 137 ± 21, 6 weeks 168 ± 21 U/ml, P < 0.01) while hepatic triglyceride lipase did not change. Amiodarone also caused an increase in serum thyroxine (baseline 110 ± 8, 6 weeks 136 ± 6 mmol/l, P < 0.05), although values remained in euthyroid range. In summary, amiodarone therapy increased the concentrations of atherogenic lipoproteins in the serum similar to that seen in hypothyroidism. On the other hand the effect of amiodarone on lipoprotein lipase was opposite to that seen in hypothyroidism. Therefore, amiodarone-induced changes in lipid metabolism cannot be explained solely on the basis of the changes in circulating thyroid hormone levels.

Original languageEnglish (US)
Pages (from-to)385-388
Number of pages4
JournalHormone and Metabolic Research
Volume22
Issue number7
StatePublished - 1990
Externally publishedYes

Fingerprint

Amiodarone
Lipid Metabolism
Lipoprotein Lipase
Serum
Thyroid Hormones
Apolipoprotein A-I
Apolipoproteins B
Hypothyroidism
Lipase
Heparin
Cholesterol
Plasmas
Liver
HDL Lipoproteins
Hypercholesterolemia
Thyroxine
LDL Cholesterol
HDL Cholesterol
Lipoproteins
Triglycerides

Keywords

  • amiodarone
  • hepatic lipase
  • lipids
  • lipoprotein lipase
  • thyroid hormones

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Karakas, S. E., Bagchi, N., Brown, T. R., Khilnani, S., Jackson, K., Steinman, R. T., & Lehmann, M. H. (1990). Amiodarone-induced changes in lipid metabolism. Hormone and Metabolic Research, 22(7), 385-388.

Amiodarone-induced changes in lipid metabolism. / Karakas, Siddika E; Bagchi, N.; Brown, T. R.; Khilnani, S.; Jackson, K.; Steinman, R. T.; Lehmann, M. H.

In: Hormone and Metabolic Research, Vol. 22, No. 7, 1990, p. 385-388.

Research output: Contribution to journalArticle

Karakas, SE, Bagchi, N, Brown, TR, Khilnani, S, Jackson, K, Steinman, RT & Lehmann, MH 1990, 'Amiodarone-induced changes in lipid metabolism', Hormone and Metabolic Research, vol. 22, no. 7, pp. 385-388.
Karakas SE, Bagchi N, Brown TR, Khilnani S, Jackson K, Steinman RT et al. Amiodarone-induced changes in lipid metabolism. Hormone and Metabolic Research. 1990;22(7):385-388.
Karakas, Siddika E ; Bagchi, N. ; Brown, T. R. ; Khilnani, S. ; Jackson, K. ; Steinman, R. T. ; Lehmann, M. H. / Amiodarone-induced changes in lipid metabolism. In: Hormone and Metabolic Research. 1990 ; Vol. 22, No. 7. pp. 385-388.
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AB - Hypotheroidism is a major cause of secondary hypercholesterolemia. Amiodarone treatment alters both the levels of serum lipids and thyroid hormones. We investigated whether the amiodarone-induced changes in lipid metabolism are related to the changes in thyroid hormone levels. Eighteen patients received amiodarone (31 ± 3 g cumulative dose) for six weeks. Serum triglyceride, total-cholesterol, high density lipoprotein-cholesterol and its subfractions, apolipoproteins B and AI, and plasma post-heparin lipoprotein lipase and hepatic triglyceride lipase activities were determined. Amiodarone treatment caused significant increases in serum total-cholesterol (baseline 4.4 ± 0.21 (SE), 6 weeks 5.12 ± 0.26 mmol/P < 0.01), in low density lipoprotein cholesterol (baseline 2.61 ± 0.26, 6 weeks 3.36 ± 0.21 mmol/l, P < 0.05) and in apolipoprotein B (baseline 1.95 ± 0.15, 6 weeks 2.26 ± 0.13 mmol/l, P < 0.01) concentrations. Serum high density lipoprotein and its subfractions, or apolipoprotein AI levels did not change. Plasma post-heparin lipoprotein lipase activity increased (baseline 137 ± 21, 6 weeks 168 ± 21 U/ml, P < 0.01) while hepatic triglyceride lipase did not change. Amiodarone also caused an increase in serum thyroxine (baseline 110 ± 8, 6 weeks 136 ± 6 mmol/l, P < 0.05), although values remained in euthyroid range. In summary, amiodarone therapy increased the concentrations of atherogenic lipoproteins in the serum similar to that seen in hypothyroidism. On the other hand the effect of amiodarone on lipoprotein lipase was opposite to that seen in hypothyroidism. Therefore, amiodarone-induced changes in lipid metabolism cannot be explained solely on the basis of the changes in circulating thyroid hormone levels.

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