Hypervitaminosis A syndrome

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 ... 

Silverman AK, EUis CN, Voorhees JJ. Hypervitaminosis A syndrome a paradigm of retinoid side effects. J Am Acad Dermatol 1987 16(5 Pt l) 1027-39. 

Vitamin A deficiency is characterized by squamous metaplasia of a variety of epithelia with increased cell proliferation and hyperkeratosis. These changes are also features of some benign dermatoses, for example, psoriasis. Once beneficial effects of oral vitamin A were observed, its use spread to the treatment of other diseases of the epidermis and epidermal appendages, including acne, psoriasis, and basal cell carcinoma. Since the hypervitaminosis A syndrome (see Chapter 13) interfered with long-term therapy with vitamin A, the need arose for synthetic derivatives that could be at least as efficacious as vitamin A and yet be less toxic. The use of isotretinoin and etretinate, as described above, represents the first development of this concept in clinical practice. 

Macapinlac MP, Olson JA (1981) A lethal hypervitaminosis A syndrome in young monkeys following a single intramuscular dose of a water-miscible preparation containing vitamins A, D2 and E. Int J Warn Nutr Res 51 331-341... 

The answer is e. (Hardman, p 1533.) Enthusiastic overmedication with vitamin D may lead to a toxic syndrome called hypervitaminosis D. The initial symptoms can include weakness, nausea, weight loss, anemia, and mild acidosis. As the excessive doses are continued, signs of nephrotoxicity are manifested, such as polyuria, polydipsia, azotemia, and eventually nephrocalcinosis. In adults, osteoporosis can occur. Also, there is CNS impairment, which can result in mental retardation and convulsions. 

Hypercalcemia causes central nervous system depression, including coma, and is potentially lethal. Its major causes (other than thiazide therapy) are hyperparathyroidism and cancer with or without bone metastases. Less common causes are hypervitaminosis D, sarcoidosis, thyrotoxicosis, milk-alkali syndrome, adrenal insufficiency, and immobilization. With the possible exception of hypervitaminosis D, these latter disorders seldom require emergency lowering of serum calcium. A number of approaches are used to manage the hypercalcemic crisis. 

Little is known about the biochemical mechanism of vitamin D action. It promotes the absorption of Ca++-ions in the gastro-intestinal tract and influences the metabolism of bone tissue. Deficiency of vitamin D results in the clinical syndrome rachitis (also in animal experiments), characterized by a softenii (inadequate calcification) of the bones. Excessive administration of vitamin D produces a hyper-vitaminosis, during which calcium is again mobilized out of the bone structure this hypervitaminosis resembles the action of the parathyroid hormone. 

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