Topic Resources Vitamin D has 2 main forms: D2 (ergocalciferol) D3 (cholecalciferol): The naturally occurring
form and the form used for low-dose supplementation Vitamin D3 is synthesized in skin by exposure to direct sunlight (ultraviolet B radiation) and obtained in the diet chiefly in fish liver oils and salt water fish (see table ). In some countries, milk and other foods are fortified with vitamin D. Human breast milk is low in vitamin D, containing an average of only 10% of the amount in fortified cow’s milk. Vitamin D levels may decrease with age because skin synthesis declines. Sunscreen use and dark skin pigmentation also reduce skin synthesis of vitamin D. Vitamin D is a prohormone with several active metabolites that act as hormones. Vitamin D is metabolized by the liver to 25(OH)D (calcifediol, calcidiol, 25-hydroxycholecalciferol, or 25-hydroxyvitamin D), which is then converted by the kidneys to 1,25-dihydroxyvitamin D (1,25-dihydroxycholecalciferol, calcitriol, or active vitamin D hormone). 25(OH)D, the major circulating form, has some metabolic activity, but 1,25-dihydroxyvitamin D is the most metabolically active. The conversion to 1,25-dihydroxyvitamin D is regulated by its own concentration, parathyroid hormone (PTH), and serum concentrations of calcium and phosphate. Vitamin D affects many organ systems (see table ), but mainly it increases calcium and phosphate absorption from the intestine and promotes normal bone formation and mineralization. Vitamin D and related analogs may be used to treat psoriasis Psoriasis Psoriasis is an inflammatory disease that manifests most commonly as well-circumscribed, erythematous papules and plaques covered with silvery scales. Multiple factors contribute, including... read more , hypoparathyroidism Hypoparathyroidism Hypoparathyroidism is a deficiency of parathyroid hormone often caused by an autoimmune disorder or by iatrogenic damage or removal of the glands during thyroidectomy or parathyroidectomy. Symptoms... read more , and renal osteodystrophy Calcium and phosphate . Vitamin D's usefulness in preventing leukemia and breast, prostate, colon, or other cancers has not been proved, nor has its efficacy in treating various other nonskeletal disorders in adults (1–3 Physiology references Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more ). Vitamin D supplementation does not effectively treat or prevent depression or cardiovascular disease (4, 5 Physiology references Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more ). Some evidence suggests that taking the combined recommended daily allowance of both vitamin D and calcium reduces the risk of fractures (6, 7 Physiology references Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more ) and falls (8 Physiology references Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more ), but primarily in patients who are vitamin D deficient. As the causes of falls are multifactorial, other studies have not found that vitamin D supplements alone reduce falls in older adults (9 Physiology references Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more ).
Symptoms and Signs of Vitamin D ToxicityThe main symptoms of vitamin D toxicity result from hypercalcemia Hypercalcemia Hypercalcemia is a total serum calcium concentration > 10.4 mg/dL (> 2.60 mmol/L) or ionized serum calcium > 5.2 mg/dL (> 1.30 mmol/L). Principal causes include hyperparathyroidism... read more . Anorexia, nausea, and vomiting can develop, often followed by polyuria, polydipsia, weakness, nervousness, pruritus, and eventually renal failure. Proteinuria, urinary casts, azotemia, and metastatic calcifications (particularly in the kidneys) can develop.
A history of excessive vitamin D intake may be the only clue differentiating vitamin D toxicity from other causes of hypercalcemia. Elevated serum calcium levels of 12 to 16 mg/dL (3 to 4 mmol/L) are a constant finding when toxic symptoms occur. Serum 25(OH)D levels are usually elevated to > 150 ng/mL (> 375 nmol/L). Levels of 1,25-dihydroxyvitamin D, which need not be measured to confirm the diagnosis, may be normal. Serum calcium should be measured often (weekly at first, then monthly) in all patients receiving large doses of vitamin D, particularly the potent 1,25-dihydroxyvitamin D.
After stopping vitamin D intake, hydration (with IV normal saline) and corticosteroids or bisphosphonates (which inhibit bone resorption) are used to reduce blood calcium levels. Kidney damage or metastatic calcifications, if present, may be irreversible. Click here for Patient Education Copyright © 2022 Merck & Co., Inc., Rahway, NJ, USA and its affiliates. All rights reserved. |