Vitamin Toxicity Medication

Updated: Dec 21, 2016
  • Author: Mark Rosenbloom, MD, MBA; Chief Editor: Asim Tarabar, MD  more...
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Medication

Medication Summary

Care for vitamin toxicity is generally symptomatic and supportive. Gastrointestinal decontamination may be helpful to minimize amount of vitamin absorbed systemically. Administer charcoal for acute overdoses. Antiemetics or antidiarrheals are helpful if needed.

As previously stated, patients with increased intracranial pressure from vitamin A toxicity may need treatment with medications such as diuretics and mannitol.

In cases of vitamin D toxicity, patients with severe hypercalcemia may require hydration, diuretics, steroids (hydrocortisone 100 mg IV q6h), calcitonin (4-8 IU/kg q6-12h), and/or mithramycin (25 mcg/kg IV over 4-6 h, once daily for 1-4 days).

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Vitamins, Fat-soluble

Class Summary

In cases of vitamin E toxicity, vitamin K replacement through the oral or subcutaneous route should reduce an elevated prothrombin time (PT) and decrease the risk of bleeding in patients who are taking anticoagulants or who have vitamin K deficiency.

Vitamin K, phytonadione (MEPHYTON, K100)

Vitamin K is a fat-soluble vitamin absorbed by the gut and stored in the liver. It is necessary for the function of clotting factors in the coagulation cascade and is used to replace an essential vitamin not obtained in sufficient quantities in the diet or to further supplement levels.

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Antidotes, Other

Class Summary

Activated charcoal is used empirically to minimize systemic absorption of a toxin. It may be of benefit only if administered within 1 hour of ingestion.

Activated charcoal (Actidose-Aqua, EZ-Char, Kerr Insta-Char)

Activated charcoal binds vitamin within the gastrointestinal tract. Multiple doses can be administered to help enhance elimination (although little evidence supports multiple doses of activated charcoal in vitamin overdose). The initial dose may be administered with a cathartic (eg, sorbitol). Subsequent doses should be half of the original dose, without a cathartic, administered as often as every 2-6 hours. Do not administer subsequent doses in the presence of ileus.

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Diuretics, Loop

Class Summary

Diuretics induce calciuresis. In patients with severe hypercalcemia, the individual typically is volume depleted, which means that volume should be replaced with saline prior to institution of diuretic therapy.

Furosemide (Lasix)

Furosemide inhibits the resorption of sodium and chloride in the loop of Henle and the proximal and distal tubules of the kidney. Its onset of action is rapid after an intravenous dose.

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Corticosteroids

Class Summary

Patients with severe hypercalcemia may require corticosteroids. Corticosteroids have profound and varied metabolic effects.

Hydrocortisone (Cortef, Solu-Cortef)

Glucocorticoids increase urinary calcium excretion. In addition, vitamin D–mediated gastrointestinal calcium absorption is inhibited. However, 1-2 weeks may elapse before serum calcium concentrations decrease. A dosage of 100 mg IV q6h may be administered.

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Calcium Metabolism Modifiers

Class Summary

Calcitonin analogues may be used if the patient is severely hypercalcemic following the diuretic therapy. These agents directly inhibit osteoclastic bone resorption and have significant analgesic effects on bone.

Salmon calcitonin (Miacalcin, Fortical)

This agent is a peptide hormone that binds to calcitonin receptors on osteoclasts and rapidly inhibits bone resorption. Osteoclasts do not induce cytotoxic effects in bone cells.

Salmon calcitonin induces reductions in urinary hydroxyproline and serum alkaline phosphatase levels. Serum alkaline phosphatase begins to decline 4 weeks after initiation of treatment. Levels of urinary hydroxyproline may decrease quickly, indicating inhibition of bone resorption. These laboratory markers slowly increase back to pretreatment levels if treatment is stopped.

Restoration of more normal bone can be seen radiographically, especially after long-term calcitonin treatment. Bone biopsy samples also reflect reduced disease activity because decreased bone cells, marrow fibrosis, and woven bone are present. Improvement of neurologic deficits and stabilization of hearing have been noted. A dosage of 4-8 IU/kg IM/SC q6-12h may be administered.

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