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The incorrect use of the terms vitamin overdosage and overload, hypervitaminosis and dysvitaminosis gives rise to errors in the classification and evaluation of their etiology and pathogenesis. Vitamin overdosage and overload are observed with every vitamin and produce high blood and tissue levels of the vitamin itself; however, the overdosage can be obtained only upon administration of high doses of a vitamin, while vitamin overload may originate from a variety of factors. Hypervitaminoses are known for vitamin A and D; they are accompanied by high blood levels, but are characterized by a specific symptomatology. The term dysvitaminosis comprises "every alteration of the physiological status of the vitamin, in terms of both its deficiency and its surplus". These considerations provide a unitary view of vitamin pathology and lead to the following proposal of an etiopathogenetic classification of dysvitaminoses: class A) dysvitaminoses due to overload, class B) dysvitaminoses due to deficiency. Each class in turn may be divided into congenital and acquired syndromes. In class A) the congenital syndromes are still not well known, the acquired syndromes comprise those with hypervitaminosis (hypervitaminosis A and D) and those without hypervitaminosis (for the other vitamins). In class B) the congenital syndromes comprise diseases produced by inborn enzymatic errors and by other etiologies, the acquired syndromes can be distinguished in physiological (age, pregnancy, etc.) and pathological (nutritional, iatrogenic, etc.) ones. On this basis hypervitaminoses A and D can be considered as non obligatory dysvitaminoses due to overload; their origin has a complex etiology, since the liposolubility of the vitamins and the prolonged use of high dosages are not the only factors responsible for the hypervitaminosis.
Chronic hypervitaminosis A can occur in many species after excessive dietary intake of Vitamin A (retinol). The most common presentation of chronic hypervitaminosis A is a polyarthropathy with hyperostosis and ankylosis of various joints. This case report describes a probable case of naturally occurring hypervitaminosis A-induced polyarthropathy in a rabbit after chronic ingestion of a diet made up almost exclusively of carrots. Carrots do not contain retinol, but are rich in provitamin A (or beta-carotene). Rabbits are unique in that they can convert 100% of dietary beta-carotene into retinol. A syndrome of naturally occurring hypervitaminosis A-induced polyarthropathy has not been described in a rabbit before.
OBJECTIVES: The purpose of the study was to identify cases of hypervitaminosis D caused by the inadvertent overfortification of milk from a home-delivery dairy and to identify risk factors for this illness. METHODS: Hospital discharge, laboratory, and state health department data were used to define, identify, and describe cases of hypervitaminosis D diagnosed in the exposed communities between January 1, 1985, and June 30, 1991. To identify disease risk factors, community-based sex- and age-matched controls were used in a case-control study. RESULTS: Of the 56 case patients identified, at least 41 were hospitalized; 2 died. The study included 33 case patients and 93 control subjects. Nineteen of the 33 case patients had been customers of the implicated dairy. Risk of illness rose with increasing consumption of the dairy's milk and was also associated with vitamin D supplement use, sunburn susceptibility, and cancer history. Accounting for these factors did not alter the association between drinking the dairy's milk and developing hypervitaminosis D. CONCLUSIONS: Overfortification of milk with vitamin D can lead to hypervitaminosis D, manifested by severe illness and death. The episode highlights the need for monitoring the fortification process and enforcing the upper limit for vitamin D addition to milk.
Effects of mild and severe hypervitaminosis A on retinol transport and clearance were studied in mature ewes. Excessive vitamin A intake was assoicated with high concentrations of vitamin A in plasma and liver, with elevated serum enzymes, with decreased feed consumption and packed cell volume, and with epithelial hyperplasia. Retinol transport in plasma increased 6- to 8-fold with excessive dietary vitamin A, was greater with mild hypervitaminosis A, and increased exponentially with vitamin A concentration in plasma. Clearance of retinol from plasma increased 2-fold with hypervitaminosis A, exhibited a greater response in the mild group, and increased linearly with vitamin A concentration in plasma. The relationship of clearance to vitamin A concentration in liver was described best by a power function. Retinol clearance represents a mechanism to maintain vitamin A concentration in plasma and may be most effective below vitamin A concentrations of 135 microgram/dl plasma. With severe hypervitaminosis A, massive vitamin A accumulates in liver leading to hepatic dysfunction and a resultant decrease in retinol clearance from plasma.
Hypervitaminosis D produces extensive vascular alterations which are similar to Monckeberg's calcinosis. The present study was undertaken to examine early changes in vascular ultrastructure of rats receiving tap water supplemented with either calcium chloride or a relatively low dosage of irradiated ergocalciferol ad libitum for 21 days. Untreated rats received normal tap water ad libitum. A significant increase in serum calcium levels was obtained in hypervitaminosis D treated rats. Calcium deposits were seen near the internal elastic lamina, within new elastic elements and around degenerating smooth muscle cell fragments in the extracellular organic matrix of hypervitaminosis D treated rats. Calcium deposits were not detected in vascular sections from untreated rats or those receiving calcium chloride. A complex pathogenesis of vascular lesions produced by hypervitaminosis is suggested. One possible pathogenic mechanism for calcification of elastic matrix may be via altered microfibrils. Our data support this hypothesis and indicate that much lower levels of vitamin D administration, compared to other reports, produce considerable vascular calcinosis in this experimental preparation. Several hypotheses regarding possible mechanisms of pathologic calcification are discussed.
Chronic hypervitaminosis A in adults is a clinical syndrome that can develop over varying periods of time depending on the average daily intake of vitamin A. Two adult cases of chronic hypervitaminosis A are described and illustrate this diverse dosage-duration relationship. Hepatic cirrhosis developed as a manifestation of vitamin A toxicity in one of the patients; this appears to be the first reported case of chronic hypervitaminosis A in an adult induced by the long-term frequent ingestion of beef liver.
The hysterical reaction among Eskimo peoples known as pibloktoq, one of a group of aberrant behaviors occurring among Arctic and Circumarctic societies termed 'arctic hysterias', has been explained by a variety of theories: ecological, nutritional, biological-physiological, psychological-psychoanalytic, social structural and cultural. This study hypothesizes the possible implication of vitamin intoxication, namely, hypervitaminosis A, in the etiology of some cases of pibloktoq. Its biocultural approach implicates elements of several explanatory classes, which are not mutually exclusive. Experimental and clinical studies of nonhumans and humans reveal somatic and behavioral effects of hypervitaminosis A which closely parallel many of the symptoms reported for Western patients diagnosed as hysterical and Inuit sufferers of pibloktoq. Eskimo nutrition provides abundant sources of vitamin A and lays the probable basis in some individuals for hypervitaminosis A through ingestion of livers, kidneys, and fat of arctic fish and mammals, where the vitamin often is stored in poisonous quantities. Possible connections between pibloktoq and hypervitamonosis A are explored. A multifactorial framework may yield a more compelling model of some cases of pibloktoq than those that are mainly unicausal, since, among other things, the disturbance has been reported for males and females, adults and children, and dogs.
Retinoids have and will continue to revolutionize dermatologic therapy in a manner analogous to the development of topical corticosteroids. Isotretinoin, for example, has made nodulocystic scarring acne an eminently treatable condition. The dermatologic armamentarium now includes a powerful new agent, etretinate, which will radically change the approach to psoriasis (and other keratinizing disorders). Although each new retinoid is developed with the aim of maximizing specific therapeutic effects and minimizing toxicity, the fact remains that the major side effects of retinoid treatment are those of hypervitaminosis A syndrome. Optimal clinical utilization of new retinoids is best accomplished by an assessment of what is currently known about retinol absorption, metabolism and organ-specific effects, as well as by a thorough understanding of hypervitaminosis A syndrome. In this paper, hypervitaminosis A syndrome is reviewed as a paradigm of retinoid side effects.
Portal hypertension consecutive to hypervitaminosis A has seldom been well documented. Two cases are reported here. The first case concerns a 39-year old woman who had taken meladinine (8-methoxypsoralen) for the purpose of tanning. In the second case, a 43-year old woman had absorbed Plethoryl (a combination of tiratricol, cyclovalone and retinol) in order to lose weight. Both patients had histological hepatic lesions, such as hypertrophic Ito cells, perisinusoidal cirrhosis and spontaneous autofluorescence, suggestive of vitamin A overload, associated with a hepatic vein pressure gradient of 10 mmHg or more and high liver concentrations of vitamin A. The responsibility of Plethoryl in case 2 is beyond any doubt, but the mechanism of hypervitaminosis in case 1 is controverted. A review of the literature has provided detailed information on the signs of vitamin A overload, the frequency of which is probably underestimated. Patients with portal hypertension of unknown origin should be investigated for hypervitaminosis A.
A 10-year-old cat that was kept on a diet consisting largely of raw liver was evaluated because of lethargy, partial anorexia, and weight loss of several months' duration. The cat's head and neck were rigidly extended, and a hard mass was palpable in the ventral cervical region. Cervical and thoracic radiography revealed proliferative bony lesions of the cervical and thoracic vertebrae as well as of the sternum and costal cartilages. Serum vitamin A concentration was 4 times normal. For reasons unrelated to hypervitaminosis A, euthanasia and necropsy were performed 6 months after evaluation. The skull and the cervical and first few thoracic vertebrae were rigidly fused, and the vertebral architecture was altered by deposition of new bone. The sternum and costal cartilages were similarly affected. The historical, physical, radiographic, laboratory, and postmortem findings were consistent with the diagnosis of hypervitaminosis A. On the basis of findings in this cat, hypervitaminosis A should be suspected in any sick cat fed a diet consisting partly or completely of raw liver.
A case of chronic hypervitaminosis A in a 51-year-old female is discussed. The patient was ingesting 27,500--35,000 international units of vitamin A daily for 30 years. The patient displayed the classic symptoms of the disease, including skin and hair changes, esophageal varices and extensive liver disease. Vitamin A products were discontinued and the patient's dietary intake of the vitamin was minimized. Previous reports and studies of hypervitaminosis A are reviewed. Social factors causing increased consumption of vitamin A and regulations governing the sale of vitamin A are discussed. By being aware of the factors influencing vitamin A consumption, hypervitaminosis A can be detected and prevented more readily.
A case of acute hypervitaminosis A complicating viral hepatitis is reported. Twenty days after presenting with hepatitis B, a 42-yr-old vegetarian developed acute hypervitaminosis A in the absence of recent, massive exposure to the vitamin. Findings included headache, confusion, skin desquamation, and hypercalcemia. Prior to developing hepatitis, he had ingested supplemental vitamin A without recognized ill effect. Liver and serum vitamin A without recognized ill effect. Liver and serum vitamin A levels were both elevated; the liver biopsy showed abundant, lipid-filled Ito cells and perisinusoidal fibrosis. This case demonstrates that patients with excessive hepatic stores of vitamin A may develop hypervitaminosis A during acute, intercurrent liver disease. Levels of retinol binding protein are reduced in hepatitis. This phenomenon may account for the findings in this case, since vitamin A is more toxic when not specifically bound to retinol binding protein. The size of the population at risk for this complication of hepatitis in unknown, but presumably it is growing with the widespread use of supplemental vitamin A.
Concentrations of intestinal 1,25-dihydroxyvitamin D receptor were measured in rats receiving pharmacological amounts (25,000 IU/rat daily for 6 days) of either vitamin D2 or vitamin D3. The data showed that both hypervitaminosis D2 and hypervitaminosis D3 resulted in significant up-regulation of intestinal 1,25-dihydroxyvitamin D receptor (fmol/mg protein) relative to controls (409 +/- 24, vitamin D2-treated; 525 +/- 41, vitamin D3-treated; and 249 +/- 19, control). The 1,25-dihydroxyvitamin D receptor enhancement also was accompanied by elevated plasma 25-hydroxyvitamin D and hypercalcemia. These data suggest that increased target-tissue 1,25-dihydroxyvitamin D receptor may play a role in enhancing target-tissue responsiveness and, thus, have a significant role in mediating the toxic effects of hypervitaminosis D.