Homocysteine, Folate and Cobalamin Levels in Hypothyroid Women before and after Treatment

Abstract

Abstract. Hypothyroidism may result in accelerated atherosclerosis. Hyperhomocysteinaemia is an independent risk factor for premature atherosclerotic vascular disease. The aim of the present study was to assess plasma total homocysteine (tHcy), folate and cobalamin concentrations in hypothyroid patients before and after treatment. Thirty-one hypothyroid and thirty health young women were studied. The hypothyroid patients were investigated in the untreated state and again after restoration of euthyroidism. The levels of homocysteine, folate, cobalamin and thyroid stimulating hormone (TSH), free thyroxine (fT 4 ), free triiodothyronine (fT 3 ) and renal function were measured before and after treatment. In hypothyroidism tHcy was higher but not statistically significant than in control group. Serum level of folate was higher and serum cobalamin was lower in the hypothyroid state. Following L-thyroxine therapy tHcy significantly decreased as well as the concentration of cobalamin. Level of folate remained unchanged. Univariate analysis in hypothyroid group indicated that tHcy negative correlated with creatinine clearance, fT 3 , fT 4 , cobalamin and positive with TSH. In multivariate analysis tHcy correlated with creatinine clearance, cobalamin and fT 4 . Thyroid status influences the plasma tHcy. Free triiodothyronine and next free thyroxine have the greatest negative influence. This would account for hyperhomocysteinemia in the hypothyroid state and premature atherogenesis.

Potential harmful correlation between homocysteine and low-density lipoprotein cholesterol in patients with hypothyroidism

“…L-T4 treatment significantly reduced the BMI, TC, HDL-C, LDL-C, TG, Hcy, and ApoB in our patients. In accordance with our results, Orzechowska-Pawilojc et al [27] also reported a significant decrease in the Hcy levels following L-T4 treatment in women with HO. Thyroid hormone replacement is a routine and conventional clinical practice for patients with HO and has been shown to ameliorate the lipid profiles in patients with atherosclerosis.…”

“…In our observations, the subjects in the HO group had higher Hcy and LDL-C levels than the subjects in the SHO and control groups. Our results were consistent with the findings of previous studies, [23–26] but were not in agreement with those reported by Orzechowska-Pawilojc et al, [27] who observed that the Hcy levels were nonsignificantly higher in patients with HO compared to healthy subjects. In HO patients, we found that the Hcy levels were positively correlated with the LDL-C level after adjustment for sex, BMI, FT4, and FBG.…”

Evaluation of plasma homocysteine level according to the C677T and A1298C polymorphism of the enzyme MTHRF in type 2 diabetic adults

“…Epidemiological studies of genetic polymorphism require large samples, especially for the evaluation of hyperhomocysteinemia as a risk factor for chronic complications (2,7,10). On the other hand, even when conducted on a reduced number of patients, clinical studies can point out changes in the metabolic pathways of homocysteine (4,28).…”

“…Several factors have been pointed out as determinants of hyperhomocysteinemia, such as folate, vitamin B 6 and vitamin B 12 deficiencies (5), impaired renal function (6), hypothyroidism (7), as well as genetic predisposition. Hy perhomocysteinemia has been attributed to genetic defects of the remethylation pathway responsible for the conversion of homocysteine to methionine, or of the transsulfuration pathway, which converts homocysteine to cysteine.…”

Thyroid Hormone and Vascular Remodeling

“…An elevation of serum homocysteine levels in patients with overt hypothyroidism was reported (12.4 vs. 8.8 mmol/L in non-hypothyroid group, P 0.05) 42,43) . Thyroid hormone supplementation successfully reduced serum homocysteine levels 44,45) . In contrast, it was shown that subclinical hypothyroidism did not affect serum homocysteine level 44,46) .…”