Vit D & Thyroid

Vitamin D & Thyroid Status

What regulates Vitamin D metabolism?

Arlet P, Latorzeff S, Bayard F, Le Tallec Y - "Bone and calcium metabolism in adult hypothyroidism" Sem Hop 55(33-34):1488-92 (1979)

    A study of blood and urinary calcium and phosphorus, 25 hydroxyvitamin D plasma level (25 OH D3), bone radiology and hystology was performed in 12 hypothyroid adult patients. This study confirms the notion of myxoedematous osteopetrosis. Radiologic and histologic findings shows an osteocondensation, more important on the skull, and augmentation of cortical thickness of the bones is noted. Quantitative histologic findings show some signs of diminution of bone cellular activity. Low plasma level of 25 OH D3 in these patients is discussed in the view of an event of disturbance in the metabolism of D-vitamin in hypothyroidism.

Barsony J, Lakatos P, Foldes J, Feher T - "Effect of vitamin D3 loading and thyroid hormone replacement therapy on the decreased serum 25-hydroxyvitamin D level in patients with hypothyroidism" Acta Endocrinol (Copenh) 113(3):329-34 (1986)

    Twelve hypothyroid subjects, 13 healthy and 12 healthy women with a slight deficiency of vitamin D were studied to distinguish seasonal changes from the thyroxine-dependent ones. Serum 25-hydroxyvitamin D levels of hypothyroid patients were lower than those of healthy individuals when the sera were obtained in the autumn. In hypothyroid patients a single oral dose of 100,000 IU vitamin D3 resulted in a smaller increase in 25-hydroxyvitamin D concentration than in controls having subclinical exogenous vitamin D deficiency. Substitution therapy with thyroid hormone, started in our study always in autumn, increased the 25-hydroxyvitamin D concentration in hypothyroid patients, which was opposite to the autumn-to-spring variation of this hormone observed in healthy controls. The increase of 25-hydroxyvitamin D, dehydroepiandrosterone and its sulphate values following substitution therapy in the hypothyroid patients may indicate that thyroid hormone(s) is (are) involved in the regulation of steroid hormone synthesis.

Bouillon R, Muls E, De Moor P - "Influence of thyroid function on the serum concentration of 1,25-dihydroxyvitamin D3" J Clin Endocrinol Metab 51(4):793-7 (1980)

    The serum concentrations of parathyroid hormone, 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 were measured in patients with untreated thyroid disorders. The serum concentration of parathyroid hormone was decreased in hyperthyroidism [20 +/- 10 mU/liter, (mean +/- SD); n =23; P < 0.01] and increased in hypothyroidism (53 +/- 17 mU/liter; n = 12; P < 0.001) compared to that in normal subjects (26 +/- 9 mU/liter; n = 81). The concentration of 25-hydroxyvitamin D3 was not altered, but the concentration of 1,25-dihydroxyvitamin D3 was significantly lower in the serum of hyperthyroid patients (28 +/- 11 ng/liter) than in the serum of normal subjects (42 +/- 13 ng/liter). On the contrary, an increased concentration of 1,25-dihydroxyvitamin D3 was observed in the serum of hypothyroid patients (73 +/- 28 ng/liter; P <0.001 vs. normal subjects). The abnormal serum concentrations of 1,25-dihydroxyvitamin D3 in thyroid disorders cannot be explained by differences in serum binding because the serum vitamin D-binding protein was unaltered in hyperthyroid subjects and only slightly increased (+17%) in hypothyroid subjects. These changes in the serum concentration of 1,25-dihydroxyvitamin D3 are compatible with previous data on altered intestinal calcium absorption in thyroid disorders.

Gasinska T, Kierat A, Kochanska-Dziurowicz A, Izbicka M - "TSH secretion stimulated by thyroliberin in patients with hypothyroidism receiving 1,25-hydroxyvitamin D3" Endokrynol Pol 44(1):47-55 (1993)

    The effect of 1,25-hydroxy vitamin D3 on the secretion of TSH was studied in 49 patients with primary hypothyroidism. The vitamin D3 metabolite did not cause any significant changes in the secretion of TSH both basal and stimulated with TRH in patients with untreated hypothyroidism. In those treated with the synthetic L-thyroxine it produced a significant increase in basal TSH secretion.

Leger J, Tau C, Garabedian M, Farriaux JP, Czernichow P - "Prophylaxis of vitamin D deficiency in hypothyroidism in the newborn infant" Arch Fr Pediatr 46(8):567-71 (1989)

    This study deals with the relationship between the occurrence of hypercalcemia and the administration of prophylactic doses of vitamin D in children with hypothyroidism, before and during L-thyroxine (LT4) treatment. The goal of the study was to determine the dosage of vitamin D necessary to prevent rickets without inducing hypercalcemia. There was a 23% prevalence of hypercalcemia at the time of the diagnosis of hypothyroidism by screening whereas it was 21% in the children who were not given vitamin D during the first 3 months of LT4 treatment. This figure was significantly higher in those who were given vitamin D during the first 3 months of treatment and reached 70%. However, one of the 19 children not given vitamin D presented with biological signs evoking vitamin D deficiency. In conclusion, in hypothyroid infants, vitamin D should be administered carefully during the first 6 months of treatment and restricted to children at risk for developing vitamin D deficiency.

Kashio Y, Iwasaki J, Chihara K, Kaji H, Kita T, Okimura Y, Fujita T - "Pituitary 1,25-dihydroxyvitamin D3 receptors in hyperthyroid- and hypothyroid-rats" Biochem Biophys Res Commun 131(1):122-8 (1985)

    The binding of 1 alpha,25-dihydroxy (26,27-methyl-[3H]) cholecalciferol ([3H]1,25-(OH)2D3) to its receptor in cytosol of the anterior pituitary cells was examined in hyperthyroid- and hypothyroid rats, as well as in normal rats. The binding capacity increased by 41% in L-Thyroxine-treated hyperthyroid rats and decreased by 49% in propylthiouracil-ingested hypothyroid rats as compared with normal control rats, whereas the affinity of the receptor for [3H]-1,25(OH)2D3 showed no difference among these 3 animal groups. These findings indicate that the number of 1,25(OH)2D3 receptors in the pituitary may be regulated by thyroid hormone, and further suggest that 1,25-(OH)2D3 may play some role in regulating functions of the anterior pituitary.

Sakai Y, Fukuda T, Takayanagi R, Sekiya K, Ohashi M, Nawata H - "A case of thyrotoxicosis with prolonged muscle cramp and hypocalcemia after treatment with methimazole" Fukuoka Igaku Zasshi 82(8):458-60 (1991)

    We report a case of thyrotoxicosis with prolonged post-treatment muscle cramp and hypocalcemia. A 36 year-old woman with hyperthyroidism was treated with Methimazole (MMI). As plasma levels of T4 and T3 were normalized, hypocalcemia was noted and severe cramp of skeletal muscle appeared so that the patient was unable to walk. The cramp was gradually relieved as the levels of thyroid hormones re-increased by discontinuance of MMI, and recurred as the hormone levels were normalized by readministration of MMI. The plasma levels of free calcium ion was positively correlated with those of thyroid hormones, and the muscle cramp was worsened with lowering of the calcium level. Serum examination also revealed vitamin D-deficiency, which was probably due to an unbalanced diet of the patient. A therapeutic trial with 1 alpha-vitamin D3 and calcium lactate in addition to MMI improved both thyrotoxicosis and muscle cramp. These findings suggested that hypocalcemia due to vitamin D-deficiency was involved in the exceptionally prolonged muscle cramp associated with the treatment of hypothyroidism in this patient.

Tau C, Garabedian M, Farriaux JP, Czernichow P, Pomarede R, Balsan S - "Hypercalcemia in infants with congenital hypothyroidism and its relation to vitamin D and thyroid hormones" J Pediatr 109(5):808-14 (1986)

    The circulating concentrations of calcium, phosphorus, and vitamin D metabolites were measured in 25 infants (fifteen to 30 days of age) with congenital hypothyroidism before treatment or during the first 6 months of thyroxine therapy. Five of the children before treatment and four during the early 3 months of treatment had mild hypercalcemia (10.8 to 12.4 mg/dl). Hypercalcemia before treatment did not appear to be related to the vitamin D status of the infant nor to an alteration in vitamin D metabolism, but to the presence of a residual thyroid secretion. In contrast, hypercalcemia during thyroxine therapy was related to vitamin D supplementation, even though the serum calcium concentration could not be correlated with the circulating concentration of any of the vitamin D metabolites assayed and obvious changes in vitamin D metabolism could not be demonstrated.

Zaloga GP, Eil C, O'Brian JT - "Reversible hypocalciuric hypercalcemia associated with hypothyroidism"  Am J Med 77(6):1101-4 (1984)

    Hypothyroidism is known to affect calcium homeostasis by decreasing bone turnover and serum calcium level, and by increasing parathyroid hormone and 1,25-dihydroxyvitamin D concentrations. A 52-year-old hypothyroid woman is described who had hypercalcemia associated with elevated parathyroid hormone and 1,25-dihydroxyvitamin D levels, but decreased 24-hour urinary calcium excretion and ratio of calcium to creatinine clearance. These parameters normalized following thyroid hormone replacement therapy. Hypercalcemia appeared to result from a combination of reduced renal calcium excretion and a change in the "set point" for calcium feedback inhibition of the parathyroid glands. These data suggest that thyroid hormone has a direct effect on the parathyroid glands, regulating parathyroid hormone secretion, and on the kidney's ability to excrete calcium. It is recommended that parathyroid hormone, 1,25-dihydroxyvitamin D, and urinary calcium excretion values be interpreted in light of thyroid hormone status.


Gouveia CH, Christoffolete MA, Zaitune CR, Dora JM, Harney JW, Maia AL, Bianco AC - “Type 2 iodothyronine selenodeiodinase is expressed throughout the mouse skeleton and in the MC3T3-E1 mouse osteoblastic cell line during differentiation” Endocrinology 146(1):195-200 (2005) 1965

    “Treatment with vitamin D [1,25(OH)2VD]-induced D2 activity by 2- to 3-fold as early as 24 h...”