Hypervitaminosis acute

High doses of vitamin A can produce the toxic side effects of the acute or chronic hypervitaminosis A syndrome, which in humans is characterized by the following ... 

Acute hypervitaminosis A in humans requires doses of at least 600 mg in adults and 100 mg in children chronic hypervitaminosis A requires 20 to 50 mg daily for several years (Dawson, 2000). 

Adverse effects are most commonly manifest as acute pancreatitis. The strongest association is with alcohol abuse. High plasma calcium, including that caused by hypervitaminosis D, and parenteral nutrition also increase the risk. Corticosteroids, didanosine, azathoipurine, diuretics (including thiazides and frusemide), sodium valproate, mesalazine and paracetamol (in overdose) have also been causally related. 

There have been very occasional reports of mental disturbances, including depression (16), cerebellar ataxia, peripheral facial paresis, apathy, lack of interest, and (in cases of acute poisoning) even stupor (SEDA-8, 804) (17-19). Mental changes can occur before the appearance of any somatic symptoms. There may be a correlation between the serionsness of hypervitaminosis D and the extent of electroe-ncephalographic changes (20-22). 

HypervitamininosisA. In high doses, retinol can be toxic. Acute poisoning is rare and dependent on the dosage form. Nausea and vomiting are the most common symptoms. Most rapidly absorbed are the "clear" emulsions (usually formulated with a Tween or other surfactant). Next in order are the standard emulsions, usually produced from fish liver oils. The most slowly absorbed are the dry tablet formulations or an oil solution in a capsule. Chronic hypervitaminosis is... 

HYPERVITAMINOSIS D The acute or chronic administration of excessive amounts of vitamin D can cause hypervitaminosis D and hypercalcemia. The amount of vitamin D necessary to induce this condition varies widely. As an approximation, prolonged daily ingestion of 50,000 U or more can cause poisoning. The signs and symptoms are those associated with hypercalcemia. 

Toxicology Vitamin A hypervitaminosis can lead to clinical symptoms such as headache, nausea, in chronic cases disturbances of sleep, loss of appetite, loss of hair, bone swellings in the limbs however, all symptoms disappear when the consumption of vitamin A is reduced. Acute poisonings have been observed in, e.g., polar explorers after consumption of the extremely vitamin A,-rich polar bear liver. The metabolite of R., vitamin A acid (retinoic acid, tretinoin, C20H28O3, Mr 316.44, mp. 180-182 °C) can cause malformations and thus pregnant women should not consume more than 3.3 mg of vitamin A] per day Synthesis R. was obtained in the past from fish oils, which have contents of up to 17%, while it is now mostly produced synthetically . ... 

For centuries, Eskimos and arctic travelers who ingested polar bear or seal liver experienced acute and severe illness that was later found to be a result of acute hypervitaminosis A. Rodahl and Moore (1943) found that polar bear livers were frequently rich in retinol, often containing 5.4-8.1 mg retinol equiv-alents/g liver. 

Acute hypervitaminosis A is now rarely seen in adults but is still fairly common in infants due to accidental ingestion or to overdosing by misguided parents. Acute symptoms usually occur within a few hours following consumption the most prominent effects are on the central nervous system followed by effects on the gastrointestinal tract (Koemer and Voellm, 1975). 

Koemer and Voellm (1975) have described the toxic effects of acute hypervitaminosis A these are listed in decreasing order of occurrence in Table IV... 

Chronic hypervitaminosis A, recognized as a clinical entity in the mid-twentieth century, is more commonly observed and is a more subtle disease than the acute form. Many more cases of chronic hypervitaminosis A have been documented in children than in adults. 

Acute side effects of isotretinoin have mainly been limited to the skin and mucous membranes. The side effects described for hypervitaminosis A are, in general, greatly reduced in frequency and severity in patients treated with oral isotretinoin, except for cheilitis and conjunctivitis, which occur with greater frequency and/or severity. 

High doses of vitamin A and other retinoids also cause serious toxic manifestations namely, teratogenicity, chronic toxicity, and acute hypervitaminosis (13-15). Some individuals may also show a genetic sensitivity to vitamin A—... 

Chronic toxic symptoms (hypervitaminosis A) may occur in adults who receive doses of vitamin A in excess of 50,000 lU daily over a prolonged period. Lesser doses will produce symptoms in children infants who receive 18,500 lU daily may show signs of toxicity within 12 weeks. Acute toxicity occurs in adults who are given massive doses of 2 to 5 million lU daily, and in infants from doses as low as 75,000 to 300,000 lU daily. Vitamin C can help prevent the harmful effects of vitamin A toxicity. When excess intake of vitamin A is discontinued, recovery is usually rapid and complete in some cases, the toxicity symptoms disappear within 72 hours. 

In the case of a 43-year-old man, treated for 4 weeks with a total of 130 mg vitamin D3, a hypercalcaemic crisis developed following intensive exposure to the sun and he succumbed 5 weeks later from acute cardiac failure (44 -). This patient also showed other side effects of hypervitaminosis D, including anorexia, weight loss, polydipsia, polyuria, scaling and flush of the skin, exudative dermatitis, dryness of the mucous membranes, jaundice, constipation, tiredness and mental disorientation. At autopsy massive deposits of calcium salts were observed in the lungs and in the skin. 

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