24-25-dihydroxyvitamin-d-3 and Hyperthyroidism

Serum levels of 25-hydroxyvitamin DF, 24,25-dihydroxyvitamin D and 1,25-dihydroxyvitamin D were measured in 25 untreated hyperthyroid patients in whom histomorphometric evaluations of iliac crest bone biopsies were performed after in vivo tetracycline doublelabeling. The serum concentration of 25-hydroxyvitamin D was normal. The serum concentration of 1,25-dihydroxyvitamin D was reduced (p less than 0.02) compared to normal whereas the serum concentration of 24,25-dihydroxyvitamin D was increased (p less than 0.02). The bone changes were characterized by an enhanced turn-over in trabecular and cortical bone leading to an increased porosity of cortical bone and mobilisation of bone mineral. The observed changes in vitamin D metabolism could be explained by a reduced renal 1-alpha-hydroxylase activity secondary to hypercalcaemia with suppressed parathyroid secretion and hyperphosphataemia. The bone changes were unrelated to the serum levels of vitamin D metabolites. In trabecular bone the appositional rate and mineralization rates of osteoid were increased and the mineralization lag time was shortened showing that the mineralization and formation of osteoid in the hyperthyroid state can progress with an enhanced rate in spite of a reduced mean serum level of the active vitamin D metabolite, 1,25-dihydroxyvitamin D.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Aged; Alkaline Phosphatase; Bone and Bones; Calcitriol; Calcium; Dihydroxycholecalciferols; Female; Humans; Hydroxycholecalciferols; Hydroxyproline; Hyperthyroidism; Male; Middle Aged; Phosphorus; Vitamin D

The serum concentrations of 25-hydroxycholecalciferol (25 OH D3), 24,25-dihydroxycholecalciferol [24,25(OH)-2D3] and 1,25-dihydroxycholecalciferol [1,25(OH)2D3] were measured in twenty-one patients with untreated hyperthyroidism. Compared with control subjects, 25 OH D3 concentrations were not altered, 24,25(OH)2D3 concentrations were increased, although not significantly and 1,25(OH)2D3 concentrations were decreased (P = 0.01). Following oral carbimazole therapy, 24,25(OH)2D3 concentrations fell (P less than 0.01), 1,25(OH)2D3 concentrations increased (P less than 0.01) and 25 OH D3 concentrations were unchanged. The altered 1,25(OH)2D3 and 24,25(OH)2D3 concentrations found in hyperthyroidism are probably due to the effects of thyroid hormone on bone and mineral metabolism. Increased serum calcium and phosphate concentrations with secondary hypoparathyroidism result in stimulation of the renal 24-hydroxylase and suppression of the 1-hydroxylase enzymes. In addition, serum 24,25(OH)2D3 concentrations were significantly correlated with serum triiodothyronine levels (T3) (r = 0.66, P less than 0.002) before treatment. This may indicate a direct stimulatory effect of T3 on 24-hydroxylase activity. No relationship was found between serum 1,25(OH)2D3 concentrations before therapy and serum T3.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Calcitriol; Calcium; Carbimazole; Dihydroxycholecalciferols; Female; Humans; Hyperthyroidism; Male; Middle Aged; Phosphates; Thyroxine; Triiodothyronine; Vitamin D

The effect of thyroxine on the metabolism of vitamin D was investigated in rats. Vitamin D depleted rats were repleted by injections of radiolabelled cholecalciferol or 25-hydroxycholecalciferol (25OHD3). After 3 weeks, a state of hyperthyroidism was induced by daily injections of L-thyroxine for 21 days. The lipid extracts of the Plasma and tissues were analyzed by successive Sephadex LH-20 and high pressure liquid chromatography. The concentrations of 25OHD3 and of 24,25-dihydroxycholecalciferol (24,25 (OH)2D3) were significantly higher and those of cholecalciferol and of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were significantly lower in the plasma and tissues of animals treated with thyroxine than in controls. The present study suggests that alterations in the metabolism of vitamin D may be involved in the disturbances of calcium metabolism observed in hyperthyroidism.

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Calcifediol; Calcitriol; Cholecalciferol; Dihydroxycholecalciferols; Hydroxycholecalciferols; Hyperthyroidism; Intestinal Mucosa; Kidney; Liver; Male; Rats; Rats, Inbred Strains; Thyroxine