Hypervitaminosis D

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-in-Chief:

Hypervitaminosis D is a state of Vitamin D toxicity.

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Overdose occurs at more than 100 times the recommended daily allowance (roughly one bottle of vitamin D tablets per day), over a period of months. Acute overdose requires over 50mg (ten thousand times the RDA). Foods contain low levels, and have not been known to cause overdose. Overdose has occurred due to industrial accidents, for example when incorrectly formulated pills were sold or missing industrial concentrate cans misused as cans of milk.

Symptoms and presentation

Symptoms of vitamin D poisoning include:

An excess of vitamin D causes abnormally high blood concentrations of calcium (hypercalcemia) which can eventually cause severe damage to the bones, soft tissues, and kidneys. It can also damage the kidney and produce kidney stones. Ongoing research indicates antagonism with oil soluble menatetrenone, MK-4, an internally transported natural form of vitamin K2, which is associated with bone formation and calcium retention in the bones.

Note: Hypervitaminosis D symptoms appear several months after excessive doses of vitamin D are administered. In almost every case, a low calcium diet combined with corticosteroid drugs will allow for a full recovery within a month.

Contraindicated medications

Vitamin D toxicity is considered an absolute contraindication to the use of the following medications:

Comparative safety statistics

Deaths by vitamin poisoning appear to be quite rare in the US, typically none in a given year. However before 1998, several deaths per year were typically associated with pharmaceutical iron-containing supplements, especially brightly-colored, sugar-coated, high-potency iron supplements, and most deaths were children[1]. Unit packaging restrictions on supplements with more than 30 mg iron have since reduced deaths to 0 or 1 per year[2]. These statistics compare with 59 deaths due to aspirin poisoning in [3], 147 deaths associated with acetaminophen-containing products in [4], and an average of 54 deaths per year due to lightning for [5].

Hypervitaminosis Dmust be differentiated from other causes of hypercalcaemia

Differential diagnosis of hyperparathyroidism on the basis of hypercalcemia
Disorder Mechanism of hypercalcemia Clinical features Laboratory findings Imaging & diagnostic modalities
PTH Calcium Phosphate Other findings
Hyperparathyroidism Primary hyperparathyroidism Increase in secretion of parathyroid hormone (PTH) from a primary process in parathyroid gland. Parathyroid hormone causes increase in serum calcium.
  • Usually asymptomatic
  • Hypercalcemia detected on routine biochemical panel
↓/Normal Normal/↑ calcitriol Findings of bone resorption:

Preoperative localization of hyperfunctioning parathyroid gland:

Predicting post-operative success:

Secondary hyperparathyroidism Increase in secretion of parathyroid hormone (PTH) from a secondary process. Parathyroid hormone causes increase in serum calcium after long periods. ↓/Normal --
Tertiary hyperparathyroidism Continuous elevation of parathyroid hormone (PTH) even after successful treatment of the secondary cause of elevated parathyroid hormone. Parathyroid hormone causes increase in serum calcium. --
Familial hypocalciuric hypercalcemia This is a genetic disorder caused my mutation in calcium-sensing receptor gene.
  • A benign condition
  • Does not require treatment
Normal/↑ Normal/↑ -- --
  • Urinary calcium/creatinine clearance ratio
Malignancy[6] Humoral hypercalcemia of malignancy[7][8][9] Tumor cells secretes parathyroid hormone-related protein (PTHrP) which has similar action as parathyroid hormone. -- ↓/Normal PTHrP

Normal/↑ calcitriol

Osteolytic tumors Multiple myeloma produces osteolysis of bones causing hypercalcemia. Osteolytic metasteses can cause bone resorption causing hypercalcemia. -- --
Production of calcitirol Some tumors has ectopic activity of 1-alpha-hydroxylase leading to increased production of calcitriol. Calcitriol is active form of vitamin D and causes hypercalcemia. -- -- Calcitriol
Ectopic parathyroid hormone[10] Some tumors leads to ectopic production of parathyroid hormone. ↓/Normal Normal/↑ calcitriol
Medication induced Lithium[11] Lithium lowers urinary calcium and causes hypercalcemia. Lithium has been reported to cause an increase in parathyroid hormone and enlargement if parathyroid gland after weeks to months of therapy. -- --
Thiazide diuretics Thiazide diuretics lowers urinary calcium excretion and causes hypercalcemia. -- -- -- --
Nutritional Milk-alkali syndrome Hypercalcemia is be caused by high intake of calcium carbonate. -- -- --
Vitamin D toxicity Excess vitamin D causes increased absorption of calcium from intestine causing hypercalcemia. -- -- Vitamin D (calcidiol and/or calcitriol) --
Granulomatous disease Sarcoidosis[14] Hypercalcemia is causes by endogeous production of calcitriol by disease-activated macrophages. -- -- Calcitriol

ACE levels

See also

External links


  1. [1]
  2. [2]
  3. 2003
  4. 2003
  5. 1990-2003
  6. Mirrakhimov AE (2015). "Hypercalcemia of Malignancy: An Update on Pathogenesis and Management". N Am J Med Sci. 7 (11): 483–93. doi:10.4103/1947-2714.170600. PMC 4683803. PMID 26713296.
  7. Ratcliffe WA, Hutchesson AC, Bundred NJ, Ratcliffe JG (1992). "Role of assays for parathyroid-hormone-related protein in investigation of hypercalcaemia". Lancet. 339 (8786): 164–7. doi:10.1016/0140-6736(92)90220-W. PMID 1346019.
  8. Ikeda K, Ohno H, Hane M, Yokoi H, Okada M, Honma T, Yamada A, Tatsumi Y, Tanaka T, Saitoh T (1994). "Development of a sensitive two-site immunoradiometric assay for parathyroid hormone-related peptide: evidence for elevated levels in plasma from patients with adult T-cell leukemia/lymphoma and B-cell lymphoma". J. Clin. Endocrinol. Metab. 79 (5): 1322–7. doi:10.1210/jcem.79.5.7962324. PMID 7962324.
  9. Horwitz MJ, Tedesco MB, Sereika SM, Hollis BW, Garcia-Ocaña A, Stewart AF (2003). "Direct comparison of sustained infusion of human parathyroid hormone-related protein-(1-36) [hPTHrP-(1-36)] versus hPTH-(1-34) on serum calcium, plasma 1,25-dihydroxyvitamin D concentrations, and fractional calcium excretion in healthy human volunteers". J. Clin. Endocrinol. Metab. 88 (4): 1603–9. doi:10.1210/jc.2002-020773. PMID 12679445.
  10. VanHouten JN, Yu N, Rimm D, Dotto J, Arnold A, Wysolmerski JJ, Udelsman R (2006). "Hypercalcemia of malignancy due to ectopic transactivation of the parathyroid hormone gene". J. Clin. Endocrinol. Metab. 91 (2): 580–3. doi:10.1210/jc.2005-2095. PMID 16263810.
  11. Mallette LE, Khouri K, Zengotita H, Hollis BW, Malini S (1989). "Lithium treatment increases intact and midregion parathyroid hormone and parathyroid volume". J. Clin. Endocrinol. Metab. 68 (3): 654–60. doi:10.1210/jcem-68-3-654. PMID 2918061.
  12. Jacobus CH, Holick MF, Shao Q, Chen TC, Holm IA, Kolodny JM, Fuleihan GE, Seely EW (1992). "Hypervitaminosis D associated with drinking milk". N. Engl. J. Med. 326 (18): 1173–7. doi:10.1056/NEJM199204303261801. PMID 1313547.
  13. Hoeck HC, Laurberg G, Laurberg P (1994). "Hypercalcaemic crisis after excessive topical use of a vitamin D derivative". J. Intern. Med. 235 (3): 281–2. PMID 8120527.
  14. Dusso AS, Kamimura S, Gallieni M, Zhong M, Negrea L, Shapiro S, Slatopolsky E (1997). "gamma-Interferon-induced resistance to 1,25-(OH)2 D3 in human monocytes and macrophages: a mechanism for the hypercalcemia of various granulomatoses". J. Clin. Endocrinol. Metab. 82 (7): 2222–32. doi:10.1210/jcem.82.7.4074. PMID 9215298.

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