Acute vitamin A toxicity: a report of three paediatric cases.

The following report describes three paediatric cases of vitamin A toxicity secondary to carnivorous fish liver ingestion. Further discussion of vitamin A toxicity and management of toxicity is included.

Acute hypervitaminosis A in a young lady.

Acute vitamin A toxicity from a large dose has been reported to cause pseudotumour cerebri. Usually it is common in children. Herein we present the case of a young lady of 18 years old with the complaints of headache, vomiting, back pain and diplopia after ingestion of high dose (about 10 million international units) vitamin A capsule intentionally at a time due to some family problems. She gave no history of fever, convulsion, unconsciousness, pain in eyes, difficulties in walking and jaundice or any urinary problem during this illness. On query she gave no history of taking any other drugs including oral contraceptive and tetracycline & steroids. She also gave no history of sleep disorder. There was bilateral papilloedema, pupils were a bit dilated symmetrically but reacting to light, visual acuity 6/60 on left eye and 6/18 on right eye and bilateral 6th cranial nerve palsy more marked on left side. MRI of brain and orbits showed normal study. Patient improved after giving acetazolamide.

Vitamin A abuse: development of cirrhosis despite cessation of vitamin A. A six-year clinical and histopathologic follow-up.

We report the case of a 35-year-old man who contracted vitamin A-induced liver cirrhosis. Five years before, he had been investigated for vitamin A-induced non-cirrhotic portal hypertension. In this case, the clinical and histopathologic evolution from non-cirrhotic portal hypertension to cirrhosis was documented. In spite of the cessation of pharmaceutical vitamin A intake, the disease progressed. Therapy with colchicine and phenobarbital apparently did not influence evolution to cirrhosis. This suggests that vitamin A can trigger largely unknown mechanisms of liver fibrosis which seem to be self-perpetuating.

Hydroxypropylcyclodextrins in parenteral use. II: Effects on transport and disposition of lipids in rabbit and humans.

Hydroxypropyl ethers of cyclodextrins, after parenteral administration, come into contact with lipids in tissues and in circulation and form water-soluble inclusion complexes with these lipids. A single intravenous administration of hydroxypropyl-beta-cyclodextrin to a hereditary hyperlipidemic Watanabe rabbit slightly and temporarily decreased the level of total cholesterol in serum. Single injections of hydroxypropyl-alpha-cyclodextrin and of the corresponding gamma-homologue, both of which are less potent solubilizers of cholesterol, had lesser effects. Repeated administration of hydroxypropyl-beta-cyclodextrin to rabbits led to a gradual increase in total cholesterol in circulation and eventually to a slight relief of atherosclerotic lesions in the thoracic aorta. The only untoward effects of repeated treatments (total doses of up to 40 g/kg) were vacuoles in cells of proximal convoluted tubules in the kidneys. Repeated administration also strongly increased cholesterol in urine, probably because of excretion of the soluble cholesterol-hydroxypropyl-beta-cyclodextrin complex. Proteins in urine increased significantly, whereas triglycerides increased only moderately after repeated administrations. Intravenous infusion of hydroxypropyl-beta-cyclodextrin into a patient with hypervitaminosis A led to a release of liver-stored retinoids into serum in quantities much higher than those that could be directly solubilized by hydroxypropyl-beta-cyclodextrin. Levels of total cholesterol in the circulation of this patient decreased during the infusion. Thus, hydroxypropylcyclodextrins may serve as artificial lipid carriers in the circulation, and because the exchanges that involve inclusion complexation occur very quickly, the presence of hydroxypropylcyclodextrins in organisms may catalytically augment the establishment of equilibria in lipid distribution.

Vitamin A in cystic fibrosis: case report and review of the literature.

Much has been learned about vitamin A physiology in the last 50 years, yet few changes have been made in therapy. Unfamiliarity with vitamin A bioavailability and distribution may inadvertently result in toxicity. A literature search demonstrates that hypovitaminosis A has rarely been reported in patients with cystic fibrosis, and may manifest very differently in children of different ages. Furthermore, hypervitaminosis A may present with similar features, and can result from correction of deficiency. We report such a case in a 4.5-month-old infant, newly diagnosed with cystic fibrosis, who suffered first from vitamin A deficiency and then vitamin A toxicity. A brief review of vitamin A physiology, deficiency, and toxicity is presented.

Vitamin-A-induced hypercalcemia: response to corticosteroids.

Hypercalcemia caused by vitamin A toxicity and its prompt response to prednisone is described. Diagnosis was difficult in this 16-year-old patient because she denied recent ingestion of vitamin A and was thought to be bulimic. Intravenous fluids and loop diuretics lowered the serum calcium and ameliorated the symptoms of nausea and vomiting temporarily. During the 10 days of this therapy the serum calcium never fell below 11.5 mg/dl. Oral prednisone was then started and produced a prompt and lasting reduction of the serum calcium to normal. Physicians should be aware of this complication in teenagers who use vitamin A for cosmetic purposes and in patients who habitually overuse vitamin preparations.

Severe hypervitaminosis A in siblings: evidence of variable tolerance to retinol intake.

A 2-year-old boy had signs and symptoms of chronic hypervitaminosis A. A course of increasing severity led to eventual death. A younger brother later had similar clinical features. Chicken liver spread containing up to 420 IU/g vitamin A was the likely source of intoxication. Markedly elevated circulating retinyl ester levels have persisted in the surviving sibling for 3 subsequent years despite severe restriction of vitamin A intake. A therapeutic trial of the carbohydrate-derived complexing agent 2-hydroxypropyl-beta-cyclodextrin was initiated. Circulating retinyl esters transiently increased during the infusion (from 407 to 4791 micrograms/dL), and urinary total vitamin A excretion, undetectable before infusion, increased to 23 micrograms/dL after infusion. The frequency of hypervitaminotic episodes has decreased somewhat in the 2 years since the infusion, probably related to dietary vitamin A restriction. The occurrence of this syndrome in two brothers, while a sister ingesting the same diet remains completely healthy, suggests an inherited variance in tolerance to vitamin A intake.