Cases reported "Vitamin A Deficiency"

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1/5. The vitamin A spectrum: from deficiency to toxicity.

    dark adaptation has been used as a tool for identifying patients with subclinical vitamin a deficiency. With this functional test it was shown that tissue vitamin A deficiency occurs over a wide range of serum vitamin A concentrations. However, serum vitamin A concentrations >1.4 micromol/L predict normal dark adaptation 95% of the time. Other causes of abnormal dark adaptation include zinc and protein deficiencies. Stable isotopes of vitamin A and isotope-dilution techniques were used recently to evaluate body stores of vitamin A and the efficacy of vitamin A intervention programs in field settings and are being used to determine the vitamin A equivalences of dietary carotenoids. Vitamin A toxicity was described in patients taking large doses of vitamin A and in patients with type I hyperlipidemias and alcoholic liver disease. Conversely, tissue retinoic acid deficiency was described in alcoholic rats as a result of hepatic vitamin A mobilization, impaired oxidation of retinaldehyde, and increased destruction of retinoic acid by P450 enzymes. Abnormal oxidation products of carotenoids can cause toxicity in animal models and may have caused the increased incidence of lung cancer seen in 2 epidemiologic studies of the effects of high-dose beta-carotene supplementation. Major issues that remain to be studied include the efficiency of conversion of carotenoids in whole foods to vitamin A by using a variety of foods in various field settings and whether intraluminal factors (eg, parasitism) and vitamin A status affect this conversion. In addition, the biological activity of carotenoid metabolites should be better understood, particularly their effects on retinoid signaling.
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2/5. fluorescein angiography and vitamin A and oxalate levels in fundus albipunctatus.

    Two patients had fundus albipunctatus, one of the variants of congenital stationary night blindness. Neither the white dots in the retinas of these patients nor the retarded course of dark adaptation characteristically associated with the disease could be attributed to vitamin a deficiency or raised oxalate levels since both substances were present in normal amounts. Fluorescin angiography showed multiple discrete lesions in the pigment epithelium not coincident with the ophthalmoscopically visible changes. Since the pigment epithelium is the storage site for bleached visual pigment, these findings suggest abnormalities that underlie the major functional deficit in this disease, that is, the slow recovery of retinal sensitivity.
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3/5. Phrynoderma: a manifestation of vitamin a deficiency?...The rest of the story.

    Phrynoderma is a distinctive form of follicular hyperkeratosis associated with nutritional deficiency. Although originally thought to represent vitamin a deficiency, several studies have demonstrated multiple etiologies. Characteristic skin lesions are hyperkeratotic papules that first appear on the extensor surfaces of the extremities, shoulders, and buttocks. We report a 14-month-old boy with malnourishment and hyperkeratotic papules and plaques with histologic changes typical of phrynoderma. Despite an extensive evaluation, a specific nutritional deficiency was not identified. Phrynoderma is believed to be a manifestation of severe malnutrition, not necessarily accompanying low vitamin A levels. While the literature supports a link between phrynoderma and vitamins E, B, A, and essential fatty acids general malnutrition seems to be the strongest association. The clinical picture typically improves with enhanced nutritional status. Phrynoderma must be considered in the differential diagnosis in patients with extensor surface hyperkeratotic papules and plaques in the setting of malnourishment and should prompt the clinician to evaluate cell markers of nutritional status, not just vitamin A. We believe this patient exemplifies the conundrum that faces clinicians in evaluating patients with extensor surface predominant hyperkeratotic papules and plaques in the setting of malnourishment.
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4/5. night blindness after jejunoileal bypass surgery.

    A 53-year-old woman developed night blindness 9 years after jejunoileal bypass surgery. Abnormal rod function was confirmed by dark-adapted electroretinography, and vitamin a deficiency was confirmed by low serum levels of vitamin A and carotene. Administration of oral vitamin A supplementation resulted in complete resolution of the patient's symptom and return of the electroretinogram to normal. Based on this case and the four previously reported cases, we suggest that jejunoileal bypass patients be routinely questioned about decreased night vision. patients with this complaint should undergo thorough ophthalmic evaluation. Dark-adapted electroretinography or dark adaptation testing should be done to establish the presence of abnormal rod function, and serum levels of vitamin A or carotene should be obtained to identify the cause. It is important to identify vitamin A-deficient patients because of their potential to develop permanent impairment of night vision.
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5/5. night blindness secondary to vitamin a deficiency in a patient with bile duct strictures after liver transplantation.

    vitamin a deficiency and resulting night blindness have previously been reported in patients with chronic liver disease before undergoing liver transplantation. Because early identification of patients with vitamin a deficiency can lead to the relief of symptoms and the prevention of irreversible retinal degeneration, vitamin a deficiency should always be considered in the differential diagnosis of visual disturbances in patients with liver disease. We describe a case of night blindness due to vitamin a deficiency resulting from bile duct strictures in a post-orthotopic liver transplant patient and its successful resolution with vitamin A supplementation.
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