Cases reported "vitamin a deficiency"

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1/72. Through a shade darkly.

    A 43-year-old man complained of difficulty seeing in dim light (nyctalopia). A prolonged photostress test and abnormal electroretinogram confirmed retinal rather than optic nerve dysfunction. vitamin a deficiency secondary to remote ileal-jejunal bypass was diagnosed, and his visual symptoms and signs reversed with oral vitamin A supplementation. ( info)

2/72. vitamin a deficiency phrynoderma: due to malabsorption and inadequate diet.

    We describe a patient with vitamin a deficiency phrynoderma caused by a combination of inadequate dietary intake of vitamin A and beta-carotene and malabsorption secondary to primary visceral myopathy and total colectomy. ( info)

3/72. A case of human vitamin a deficiency caused by an inherited defect in retinol-binding protein without clinical symptoms except night blindness.

    Two German siblings were found to suffer from night blindness and mild retinal dystrophy but no other clinical symptoms of vitamin a deficiency. Even though they had no detectable plasma retinal-binding protein (RBP) and their plasma retinol was exceedingly low, they showed normal physiologic functions and growth. Their RBP gene was found to harbor two point mutations. Their post-prandial plasma levels of retinyl esters were normal, and it is likely that they derived their tissue retinol from retinyl esters. ( info)

4/72. night blindness precipitated by isotretinoin in the setting of hypovitaminosis A.

    A 16-year-old male developed night blindness 2 weeks after starting isotretinoin at a dose of 20 mg per day for cystic acne. He also had cystic fibrosis, complicated by hepatic cirrhosis. Despite long-term oral vitamin A supplementation, serum vitamin A levels were found to be 0.3 mumol/L (normal range 0.9-2.5 mumol/L). Oral vitamin A replacement was instituted with resolution of his visual symptoms in 6 months. isotretinoin therapy was successfully continued with no deterioration in liver function. isotretinoin has been reported to cause deterioration in night vision. in vitro evidence suggests isotretinoin may interfere with the processing of endogenous vitamin A in the retina. This case highlights the need for careful monitoring of serum vitamin A status in patients with malabsorptive states on isotretinoin therapy. ( info)

5/72. 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. ( info)

6/72. Keratomalacia.

    xerophthalmia and keratomalacia are public health problems of great magnitude which are usually associated with multiple vitamin and protein deficiencies. The authors report the case of a 27-year-old commune member who subjected herself to a bizarre protein and vitamin deficient diet for many months. This ultimately produced nyctalopia, xerophthalmia and keratomalacia with bilateral corneal perforation. Despite therapy, she remained comatose and expired shortly after admission. Ocular pathological changes included bilateral corneal melting with prolapse of intraocular contents, conjunctival epidermidalization, goblet cell atrophy and thinning of the outer nuclear layer of the retina. It is noted that ocular findings in pure avitaminosis A produced experimentalyy include epithelial atrophy followed by keratinization. ( info)

7/72. 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. ( info)

8/72. Recurrent cleft lip and palate in siblings of a patient with malabsorption syndrome, probably caused by hypovitaminosis a associated with folic acid and vitamin B(2) deficiencies.

    We present a woman with metabolic disorders secondary to malabsorption and renal disease who gave birth to a stillborn male fetus with left unilateral cleft lip and palate and a live born infant with left unilateral cleft lip and palate. We discuss potential cofactors that could be implicated in the abnormal embryonic process. ( info)

9/72. Hypovitaminosis A in metropolitan Adelaide.

    Hypovitaminosis A is a well-recognized condition in many developing countries. However, in the developed world the diagnosis is frequently missed or delayed because of its rarity. A 67-year-old man from metropolitan Adelaide presented to us with gradual but severe bilateral visual loss. He had marked punctate epithelial keratopathy in both eyes. Hypovitaminosis was suspected because of his bizarre dietary habit, and this was confirmed by a combination of impression cytology of the ocular surface and biochemical testing of his venous blood. His vision responded dramatically to vitamin A supplementation. Hypovitaminosis A should be suspected in severe cases of 'dry-eye', especially in those patients with unusual dietary habit or malabsorption. ( info)

10/72. PAGOD syndrome: eighth case and comparison to animal models of congenital vitamin a deficiency.

    We observed a 46, XY infant with atrophy of the optic nerve, complex congenital heart disease including a double outlet right ventricle, hypoplasia of the right pulmonary artery and lung, eventration of the diaphragm, and ambiguous genitalia. The baby died of cardiac arrhythmias at 204 days. The pattern of malformations was compatible with pulmonary tract and pulmonary artery, agonadism, omphalocele, diaphragmatic defect, and dextrocardia (PAGOD) syndrome. The condition may resemble the malformation complex associated with developmental deficiency of vitamin A or retinoic acid, as described in animal models. ( info)
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