Endocrine Abstracts

Background: Hyperhomocysteinemia is an independent risk factor for
atherosclerosis (1,2). Elevated plasma total homocysteine(t-Hcy) levels have
been described in primary hypothyroidism (3,4). Subclinical hypothyroidism
has also been found to be associated with atherosclerosis (5).
Hypothyroidism decreases hepatic levels of enzymes involved in the
remethylation pathway of homocysteine and renal excretion of t-Hcy (6,7).
The present study evaluates t-Hcy in subclinical hypothyroid patients.
Methods: 52 patients with persistent subclinical hypothyroidism and 52
controls were included in a prospective case control study. The two tailed
student's t test was used to compare patient findings with control subjects.
Results: Mean (m), fasting plasma total homocysteine levels were higher in
subclinical hypothyroidism subjects m=10.4 mmol/L with standard error of
mean (SE) 0.51 and in control subjects, (m=7.7 mmol/L, SE 0.26, P < 0.0008).
The serum creatinine level was in the upper normal range in the patient
group, (m=83.7 mmol/L, SE,1.2) and in control group (m=73 mmol/L,SE1.2,
P<0.0001). We also found lower level of serum folate in patients (m=7.02
ng/ml, SE0.4) than in control subjects, (m=9.81ng/L, SE 0.26, P<0.001).
There was a statistically significant lower level of serum vitamin B12,
(m=362 pg/ml, SE 22), in patients than in the control group, (m=424 pg/ml,
SE 24.5, P<0.05).
Conclusion: Elevated levels of plasma total homocysteine were found in
subclinical hypothyroidism. This is most probably due to reduced renal
excretion and metabolism of homocysteine. The other possible mechanism could
be deficiency of serum folate and vitamin B12. These are essential
co-factors for methionine synthase and methyl tetrahydrofolate reductase
which converts homocysteine to methionine. Hyperhomocysteinemia may be a
risk factor for atherosclerosis in patients with subclinical hypothyroidism.
Whether thyroxine replacement will normalise homocysteine or not needs
further studies.