Oncogenic osteomalacia - detection of the tumour site upon physical examination.

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Homocysteine, folate, and cobalamin levels in hyperthyroid women before and after treatment.

INTRODUCTION: Hyperhomocysteinaemia is an independent risk factor for premature atherosclerotic vascular disease and venous thrombosis. Hypothyroidism is associated with mild hyperhomocysteinaemia. The aim of the present study was to assess plasma total homocysteine (tHcy) and its determinants (folate, cobalamin) in hyperthyroid patients before and after treatment. MATERIAL AND METHODS: Thirty hyperthyroid and thirty healthy premenopausal women were studied. The hyperthyroid 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. RESULTS: In hyperthyroidism, tHcy was lower than in the control group. The serum level of folate was higher and serum cobalamin was lower in the hyperthyroid state. Following antithyroid drug therapy, tHcy significantly increased and folate decreased. The level of cobalamin remained unchanged. Univariate analysis in the hyperthyroid group indicated that tHcy significantly negatively correlated only with fT(3). CONCLUSIONS: Lower homocysteine levels in hyperthyroid state can be explained by the influence of thyroid hormone. High level of folate is only partially responsible for these changes.

Homocysteine, folate and cobalamin levels in hypothyroid women before and after treatment.

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.

[The influence of thyroid hormones on homocysteine and atherosclerotic vascular disease]. / Wplyw hormonów tarczycy na poziom homocysteiny w aspekcie ryzyka rozwoju zmian miazdzycowych.

Several reports have appeared in the literature proving that hypothyroidism is associated with increased risk for cardiovascular disease, especially coronary heart disease. This increased risk for premature atherosclerosis is supported by autopsy and epidemiological studies in patients with thyroid hormone deficiency. Hypothyroid patients have increased diastolic blood pressure (as a result of increased systemic vascular resistance), altered lipid profile (elevated levels of total cholesterol, LDL-cholesterol and apolipoprotein B). More recently homocysteine, C-reactive protein, increased arterial stiffness, endothelial dysfunction and altered coagulation parameters have been recognized as a "new" risk factors for atherosclerosis in patients with thyroid hormone deficiency. The plasma total homocysteine concentration, an independent risk factor for atherosclerosis, is moderately elevated in overtly hypothyroid patients and it decreases with thyroid replacement therapy. Several experimental study have shown that hypothyroidism affects folate metabolism and the enzymes involved in the remetylation pathway of homocysteine (particularly 5,10-methylenotetrahydrofolate reductase - MTHFR). In hypothyroid condition the hepatic activity of flavoenzyme - MTHFR, is decreased. Thyroid hormone may affect the availability of FMN and FAD - necessary for stabilizing MTHFR. An impairment of enzyme involved in transsulfuration pathway is suggested. The increased serum creatinine level in hypothyroidism probably reflects a reduced glomerular filtration rate, which is linked to impaired renal homocysteine clearance and hyperhomocysteinemia.