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Homocysteine: a risk factor for cardiovascular disease in subclinical hypothyroidism?
Robert Deicher1, Heinrich Vierhapper
1Universitätsklinik für Innere Medizin III, Klinische Abteilung für Endokrinologie und Stoffwechsel, Allgemeines Krankenhaus der Stadt Wien, Wien, Austria. robert.deicher@nephro.imed3.akh-wein.ac.at
Insights
Subclinical hypothyroidism does not elevate homocysteine levels, a risk factor for cardiovascular disease. Treatment with levothyroxine did not alter homocysteine in patients with subclinical hypothyroidism.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Clinical Chemistry
Background:
- Cardiovascular disease (CVD) risk is linked to homocysteine levels, but its causal role is debated.
- Subclinical hypothyroidism is an emerging CVD risk factor, particularly in elderly women.
- Elevated homocysteine has been observed in overt hypothyroidism, suggesting a potential link.
Purpose of the Study:
- To investigate plasma homocysteine levels in individuals with newly diagnosed subclinical hypothyroidism.
- To determine the effect of levothyroxine supplementation on homocysteine levels in this population.
Main Methods:
- Prospective measurement of fasting total plasma homocysteine in 37 subjects with subclinical hypothyroidism.
- Homocysteine levels were assessed at baseline and after 3-4 months of levothyroxine treatment.
- Thyrotropin (TSH), serum folate, and vitamin B12 levels were also monitored.
Main Results:
- Baseline homocysteine levels were not elevated (9.9 +/- 2.9 micromol/L) and remained unchanged after treatment (9.6 +/- 3.5 micromol/L).
- Levothyroxine treatment effectively normalized TSH levels (from 10.1 +/- 5.8 to 1.5 +/- 1.8 mU/L).
- Serum folate and vitamin B12 levels showed no significant changes.
Conclusions:
- Subclinical hypothyroidism is not associated with hyperhomocysteinemia.
- Levothyroxine therapy does not impact plasma homocysteine levels in subclinical hypothyroidism.
- Homocysteine likely does not contribute to the increased atherosclerotic risk observed in subclinical hypothyroidism.
Abstract:
The role of homocysteine as a causal risk factor for cardiovascular disease remains controversial. Moderately elevated total plasma homocysteine levels have been reported in patients with overt hypothyroidism, a condition that is associated with an increased risk for cardiovascular disease. Recently, subclinical hypothyroidism has been identified as an independent risk factor for atherosclerosis and myocardial infarction in elderly women. Therefore, we measured prospectively total fasting plasma homocysteine levels in 37 consecutive subjects (6 males, 31 females, mean age 50 +/- 18 standard deviation [SD] years) with newly diagnosed subclinical hypothyroidism at baseline and after 3-4 months of levothyroxine supplementation. During levothyroxine treatment concentrations of thyrotropin (TSH) decreased from 10.1 +/- 5.8 (SD) to 1.5 +/- 1.8 mU/L. Fasting total plasma homocysteine levels were not elevated at baseline (9.9 +/- 2.9 micromol/L) and remained unchanged (9.6 +/- 3.5 micromol/L) after levothyroxine treatment. Serum folate or vitamin B(12) levels also remained unchanged. We conclude that subclinical hypothyroidism is not associated with hyperhomocysteinemia. Levothyroxine supplementation has no influence on total plasma homocysteine levels in subclinical hypothyroidism. Hence, total plasma homocysteine does not appear to contribute to the increased risk for atherosclerotic disease and myocardial infarction in patients with subclinical hypothyroidism.