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Departments of Biochemistry A, INSERM XR308 (F.B., A.C., S.F., P.G., J.-P.N.) and INSERM 0014 (P.G., J.-L.G.). and Department of Endocrinology (M.K., G.W.), Centre Hospitalier Universitaire de Nancy, Hôpital de Brabois–Hôpital d’Adultes 54511 Vandoeuvre-les-Nancy, France
To the editor:
In the March 2000 issue of this journal, Lien et al. (1) reported a transient increase in both plasma homocysteine and serum cholesterol during short-term iatrogenic hypothyroidism, which may confer increased cardiovascular risk. The observations of Lien et al. (1) are in accordance with the results of our previous preliminary study (2).
We now repeat plasma homocysteine, serum folate, and vitamin B12
in patients with successive hypo- and hyperthyroid states.
Cobalamin-binding proteins, transcobalamins, were also determined to
explain changes in vitamin B12 concentrations. Forty-five patients
[age, 44.5 ± 12.3 yr (23–78); sex ratio M/F, 11/34] who had
undergone total thyroidectomy for well-differentiated thyroid carcinoma
were studied 4 weeks after the withdrawal of thyroïdal hormone
therapy and then 14 weeks after the resumption of treatment to suppress
the thyrotropin concentration. Hypo- and thyrotoxic states were
evidenced by TSH concentrations (Table 1
). Total EDTA-plasma homocysteine, serum
folate, cobalamin, serum total B12 binding capacity, apo-haptocorrin,
and apo-transcobalamin II were measured by methods described previously
(4).
|
). Furthermore, moderate hyperhomocysteinemia was observed for
10 of 45 patients (22%) with hypothyroidism [range, 17.5–27.2
µmol/L; reference range, 6.0–16.0 µmol/L (5)].
Homocysteinemia was normal in all patients in the hyperthyroid state.
On univariate analysis, homocysteine was inversely related to folate
(Rho, -0.33; P = 0.02). Our results suggested that
folate levels may account in determining homocysteine as we confirmed
the observation (1) of a moderate decline in serum folate
in hypothyroid state, with a P value at the limit of
significance (P = 0.07). Vitamin B12 was significantly
higher in the hypothyroid state than in the hyperthyroid state, as
found by Lien et al. (1). Transcobalamin levels
were determined attempting to explain changes in vitamin B12
concentrations. Except in two cases, apo-haptocorrin was low in all
patients in the two states whereas apo-transcobalamin II was not
significantly decreased in hypothyroid patients. Vitamin B12 was not
correlated to transcobalamins. We concluded that the increased vitamin
B12 observed in hypothyroid state could not be explained by changes in
transcobalamins. Lien et al. (1) have compared the results at 2-week intervals during two phases. We compared the results between two states, hypo- and hyperthyroidism, in a larger cohort of patients. The increase in homocysteine concentrations during hypothyroidism may be explained by changes in folate status and also by modifications in enzymes involved in homocysteine metabolism, distribution or clearance (1, 6), and/or by concurrent changes in renal function (1). Changes in activities of 5,10-methylenetetrahydrofolate reductase and methionine synthase have been reported during both hyper- and hypothyroid states in an animal model (7). Data about normalization of hyperhomocysteinemia with levothyroxine are conflicting. Normalization was obtained after 3–9 months in a study of 14 patients (8), but failed after 2 months in a cohort of 14 patients (9).
In conclusion, homocysteine was increased in 22% of our patients in the hypothyroidism stage. This mild hyperhomocysteinemia was rather explained by a modification of folates status, with a mild decrease of blood concentration and a negative correlation between folates and homocysteinemia, than by a modification of vitamin B12 status and transport.
References
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  A. Squizzato, V.E.A. Gerdes, D.P.M. Brandjes, H.R. Buller, and J. Stam Thyroid Diseases and Cerebrovascular Disease Stroke, October 1, 2005; 36(10): 2302 - 2310. [Abstract] [Full Text] [PDF]
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 H. Refsum, A. D. Smith, P. M. Ueland, E. Nexo, R. Clarke, J. McPartlin, C. Johnston, F. Engbaek, J. Schneede, C. McPartlin, et al. Facts and Recommendations about Total Homocysteine Determinations: An Expert Opinion Clin. Chem., January 1, 2004; 50(1): 3 - 32. [Abstract] [Full Text] [PDF]
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 A. R. Cappola and P. W. Ladenson Hypothyroidism and Atherosclerosis J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2438 - 2444. [Full Text] [PDF]
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