Acute toxicity is unlikely after ingestion of vitamin products that do not contain iron (for situations in which iron is present, see iron). Vitamins A and D may cause toxicity, but only after chronic use. Serious toxicity has been reported in individuals attempting to mask urine drug screens by ingesting large quantities of niacin.

1. Vitamin A. The mechanism by which excessive amounts of vitamin A produce increased intracranial pressure is not known.
2. Vitamin C. Chronic excessive use and large IV doses can produce increased levels of the metabolite oxalic acid. Urinary acidification promotes calcium oxalate crystal formation, which can result in nephropathy or acute renal failure.
3. Vitamin D. Chronic ingestion of excessive amounts of vitamin D enhances calcium absorption and produces hypercalcemia.
4. Niacin. The most common adverse effects of niacin are cutaneous flushing and pruritus mediated by prostaglandin release.
5. Pyridoxine. Chronic overdose may alter neuronal conduction, resulting in paresthesias and muscular incoordination.

1. Vitamin A. Acute ingestion of more than 12,000 IU/kg is considered toxic. Chronic ingestion of more than 25,000 IU/d for 2-3 weeks may produce toxicity.
2. Vitamin C. Acute intravenous doses of more than 1.5 g and chronic ingestion of more than 4 g/d have produced nephropathy.
3. Vitamin D. Acute ingestion is highly unlikely to produce toxicity. In children, chronic ingestion of more than 5,000 IU/d for several weeks may result in toxicity (adults >25,000 IU/d).
4. Niacin. Acute ingestion of more than 100 mg may cause a dermal flushing reaction. Immediate-release products are more likely to cause flushing than are the timed-release preparations. Ingestion of 2.5 g produced nausea, vomiting, dizziness, hypoglycemia followed by hyperglycemia, and coagulopathy.
5. Pyridoxine. Chronic ingestion of 2-5 g/d for several months has resulted in neuropathy.

Most acute overdoses of multivitamins are associated with nausea, vomiting, and diarrhea.

1. Chronic vitamin A toxicity is characterized by dry, peeling skin; alopecia; and signs of increased intracranial pressure (headache, altered mental status, and blurred vision [idiopathic intracranial hypertension]). Bulging fontanelles have been described in infants. Liver injury may cause jaundice and ascites.
2. Vitamin C. Calcium oxalate crystals may cause acute renal failure or chronic nephropathy. Hemolysis can occur in patients with G6PD deficiency and iron overload in patients with history of hemochromatosis.
3. Chronic excessive use of vitamin D resulting in levels greater than 940 ng/mL has been associated with hypercalcemia, leading to weakness, altered mental status, nausea, vomiting, constipation, polyuria, polydipsia, renal tubular injury, musculoskeletal pains, weight loss, occasionally cardiac arrhythmias, and tumoral calcinosis around joints and in the vasculature. However, a level as low as 106 ng/mL was associated with hypercalcemia, hypertension, vomiting, constipation, and lethargy in a 2-year-old child who received 2,400,000 IU vitamin D over 4 days.
4. Chronic excessive use of vitamin E can cause nausea, headaches, and weakness. Vitamin E acetate has been linked to e-cigarette or vaping product-associated lung injury (EVALI).
5. Vitamin K can cause hemolysis in newborns (particularly if they are G6PD deficient).
6. Acute ingestion of niacin, but not niacinamide (nicotinamide), may produce unpleasant, dramatic cutaneous flushing and pruritus that may last for a few hours. Intentional ingestion of large amounts in an attempt to produce a negative urine drug screen has caused nausea, vomiting, abdominal pain, palpitations, dizziness, and hypoglycemia, followed by persistent hyperglycemia, anion gap metabolic acidosis, hypotension, and coagulopathy. Chronic excessive use (particularly of the sustained-release form) has been associated with hepatitis.
7. Chronic excessive pyridoxine use may result in peripheral neuropathy.
8. Large doses of B vitamins may intensify the yellow color of urine, and riboflavin may produce yellow perspiration.

Of vitamin overdose usually is based on a history of ingestion. Cutaneous flushing and pruritus suggest a niacin reaction but may be caused by other histaminergic agents.

1. Specific levels. Serum vitamin A (retinol) or carotenoid assays may assist in the diagnosis of hypervitaminosis A. Levels of 25-hydroxy vitamins D₂ and D₃ are useful in assessing excessive intake and the form of the supplement taken, and are increasingly available through clinical laboratories.
2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, calcium, (total and ionized), serum iron, creatinine, liver aminotransferases, and urinalysis including microscopy for oxalate crystals.

1. Emergency and supportive measures
   1. Treat fluid losses caused by gastroenteritis with IV crystalloid solutions.
   2. Treat vitamin A-induced elevated intracranial pressure and vitamin D-induced hypercalcemia if they occur.
   3. Nonsteroidal anti-inflammatory agents may prevent or alleviate prostaglandin-mediated niacin flushing or pruritus.
2. Specific drugs and antidotes. There is no specific antidote.
3. Decontamination . Usually, gut decontamination is unnecessary unless a toxic dose of vitamin A or D has been ingested or the product contains a toxic amount of iron.
4. Enhanced elimination. Forced diuresis, dialysis, and hemoperfusion are of no clinical benefit.