cholecalciferol and Hyperthyroidism

There has been accumulating evidence that various diseases and drugs cause increased risk of fracture. Although the treatment of primary diseases and discontinuation of drugs are the first and ideal option for the cure of secondary osteoporosis, medical intervention for osteoporosis is often necessary. The mechanisms, which induce bone fragility, are supposed to be different, depending on diseases and drugs. Guidelines for the evaluation and treatment of secondary osteoporosis have not been established except glucocorticoid-induced osteoporosis. In patients with osteoporosis caused by primary hyperparathyroidism, hyperthyroidism, diabetes mellitus as well as hormone deprivation therapy, bisphosphonate is effective in increasing bone mineral density but no data have been available about the fracture risk. Guidelines on the management and treatment of each secondary osteoporosis are desirable.

Topics: Aromatase Inhibitors; Bone Density Conservation Agents; Cholecalciferol; Diabetes Complications; Diphosphonates; Glucocorticoids; Humans; Hyperparathyroidism; Hyperthyroidism; Osteoporosis; Parathyroidectomy; Risk; Vitamin K 2

Topics: Calcium; Calcium Metabolism Disorders; Cholecalciferol; Cushing Syndrome; Diagnosis, Differential; Fanconi Syndrome; Fractures, Bone; Glomerular Filtration Rate; Humans; Hypercalcemia; Hyperparathyroidism; Hyperthyroidism; Kidney Calculi; Nephrocalcinosis; Osteitis Deformans; Osteoporosis; Parathyroid Hormone; Sarcoidosis

This trial aimed to analyze the relationship between hyperthyroidism and the morbidity rate of hypercalcemia in the Xindu district, Chengdu, Sichuan province. We observed the level of serum calcium, the bone metabolic and thyroid autoimmune-related antibodies index during vitamin D3 treatment combined with traditional antithyroid drugs (ATD).. Our research included hyperthyroid patients with a first-time diagnosis of Graves diseases (GD) combined with hypercalcemia on the basis of conventional anti-hyperthyroidism therapy, which were randomized into a vitamin D3 group (vitamin D3, 800-1,200 IU/day) and an ATD group (methimazole, 15-30 mg/day). All hyperthyroidism patients with hypercalcemia were analyzed, and changes in serum calcium (Ca2+), parathyroid hormone (PTH), thyroid function, thyroid autoimmune-related antibodies, and 25-dihydroxyvitamin D (25-OHVit D) levels during treatment of thyrotoxicosis with added vitamin D3 were explored.. In total, 184 patients with hyperthyroidism were observed, including 36 (19.57%) patients associated with hypercalcemia, with an age of onset of (56.39±5.80) years old. Twelve (6.52%) of these 36 cases reported digestive symptoms as the first manifestation, and four (2.17%) patients presented with a hypercalcemia crisis as the first manifestation. Serum Ca2+, free triiodothyronine (FT3), free thyroxine (FT4), and thyrotropin hormone receptor antibody (TRAb) levels increased in patients with hypercalcemia. Following the addition of vitamin D3 treatment, serum Ca2+, FT3, FT4, and TRAb levels were significantly decreased relative to the ATD group, while the thyroid-stimulating hormone (TSH), PTH, and 25-OHVit D levels were normalized.. Our study highlighted the importance of taking functional digestive disturbance into consideration in hyperthyroidism diagnosis, even in the absence of the typical symptoms. The level of thyroid related antibodies, thyroid function, and bone metabolism in hyperthyroidism patients combined with hypercalcemia could be improved by vitamin D3 adjuvant therapy.. Chinese Clinical Trial Registry: ChiCTR2100047870.

Topics: Cholecalciferol; Graves Disease; Humans; Hypercalcemia; Hyperthyroidism; Middle Aged; Prevalence

The relationship between parathyroid hormone (PTH) secretion and extracellular calcium (Ca) level is reciprocal causality. The equilibrium operating point determines basal PTH secretion rate and basal extracellular Ca level. We studied how this equilibrium was achieved in the subjects with decreased PTH secretion or decreased parathyroid glands number. Basal/maximum ratio of serum PTH, which reflects the basal secretory state of parathyroid glands, was increased in 9 hypoparathyroid patients treated with vitamin D3 (VD3) [7 patients with idiopathic hypoparathyroidism] and in seven of nine parathyroid adenectomized patients. There was a negative correlation between the ratio and basal serum Ca level in the patients with IHP after VD3 treatment (r = 0.7167, P < 0.05) and in the patients after parathyroid adenectomy (r = 0.7760, P < 0.05). The regression curves in these two groups coincided regardless of the difference in maximum PTH secretion rate, which suggested that the basal secretory state of parathyroid glands was determined by extracellular Ca level in a similar manner in these subjects. There was a sigmoidal relationship between basal/maximum ratio of serum PTH and basal serum Ca level, when the data were collected from 15 hypoparathyroid patients before or after VD3 treatment, 9 parathyroid adenectomized patients, and 10 normal subjects (r = 0.9057, P < 0.001). This sigmoidal curve is thought to represent the fundamental relationship between the basal secretory state of parathyroid glands and extracellular Ca level.

Topics: Adenoma; Adolescent; Adult; Aged; Calcium; Child; Cholecalciferol; Humans; Hyperthyroidism; Hypoparathyroidism; Middle Aged; Parathyroid Hormone; Parathyroid Neoplasms; Parathyroidectomy

25 OH D3 plasma levels were measured in thyrotoxic patients and in euthyroid subjects before and after the intravenous injection of vitamin D3. In thyrotoxic subjects the transformation of injected vitamin D3 into 25 OH D3 had already begun six hours after the injection, reached a maximum between the twelfth and thirty-sixth hour and decreased thereafter. In contrast, in euthyroid healthy subjects the increase in 25 OH D3 plasma levels starts 96 hours after the vitamin D3 injection. On the basis of these data it may be estimated that hepatic hydroxylation of vitamin D3 in thyrotoxicosis is 2.5 faster than in euthyroid healthy subjects. This finding may explain the variability in 25 OH D3 plasma levels reported in thyrotoxicosis, the final value depending on degree of acceleration of the hepatic hydroxylation of vitamin D3 and on the vitamin D3 status of the organism.

Topics: Cholecalciferol; Female; Humans; Hydroxylation; Hyperthyroidism; Liver; Male; Time Factors

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