Cases reported "Vitamin E Deficiency"

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11/85. Hemolytic anemia and edema as the initial signs in infants with cystic fibrosis. Consider this diagnosis even in absence of pulmonary symptoms.

    This is a report of five infants eventually proven to have cystic fibrosis of the pancreas, who presented with hemolytic anemia and edema. Since the sweat test is often unreliable in edematous states, the possibility of cystic fibrosis should be considered. Use of either a protein hydrolysate or addition of pancreatic enzymes will improve nutritional status, and when edema disappears, a definite sweat test can be performed. Evidence of vitamin e deficiency in some of the cases is presented, and the possibility of this as a cause of anemia is raised.
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keywords = deficiency
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12/85. Ataxia with vitamin e deficiency and severe dystonia: report of a case.

    mutation of the gene for alpha-tocopherol transfer protein causes ataxia with isolated vitamin e deficiency, a disorder usually stabilized or improved after vitamin E supplementation. dystonia has rarely been described in ataxia with isolated vitamin e deficiency (AVED) patients. We present the case of a young boy with AVED, whose neurological and extra-neurological cardinal symptoms of the disease improved after vitamin E supplementation but who progressively developed generalized dystonia.
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keywords = deficiency
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13/85. vitamin e deficiency induced neurological disease in common variable immunodeficiency: two cases and a review of the literature of vitamin e deficiency.

    vitamin e deficiency causes a neurological disorder characterised by sensory loss, ataxia and retinitis pigmentosa due to free radical mediated neuronal damage. Symptomatic vitamin e deficiency has been reported in genetic defects of the vitamin E transport protein and in malabsorption complicating cholestasis, abetalipoproteinaemia, celiac disease, cystic fibrosis and small bowel resection. There are no reports to date of vitamin e deficiency in patients with primary immunodeficiencies. We describe two CVID patients with the associated enteropathy who developed neurological disease because of vitamin e deficiency, suggesting a possible predisposition to developing this complication. We recommend that all CVID patients with evidence of an enteropathy be screened for vitamin e deficiency, as early detection and consequent treatment may prevent, halt or reverse the neurological sequelae.
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ranking = 17.009875294471
keywords = deficiency, lipoprotein
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14/85. Reversible inflammatory and vacuolar myopathy with vitamin e deficiency in celiac disease.

    We report a patient with late-onset celiac disease and neurological manifestations including myopathy, polyneuropathy, and ataxia. Laboratory investigations showed anti-gliadin antibodies and severe vitamin e deficiency. Muscle biopsy revealed inflammatory infiltrates and rimmed vacuoles, similar to those found in inclusion-body myositis. A gluten-free diet and vitamin E supplementation reversed both the clinical neurological manifestations and the abnormalities in the muscle biopsy. Anti-gliadin antibodies were no longer present. This case illustrates the spectrum of neurological complications of celiac disease and documents the occurrence of reversible pathology resembling inclusion-body myopathy in the muscle.
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ranking = 5
keywords = deficiency
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15/85. Delayed onset of ataxia in a patient with short bowel syndrome: a case of vitamin e deficiency.

    Chronic gastrointestinal disease can result in nutritional deficiencies that can have a direct effect on the neurologic system. Although acute abnormalities can be corrected, symptoms are rarely reversible. Recognizing the appropriate abnormality is a crucial part of long-term treatment strategies in this population. Because motor and cerebellar symptoms can contribute to poor feeding, aggressive supplementation should begin as soon as symptoms are recognized. We present a patient with delayed onset and progressive hypovitaminosis E and briefly review diagnostic and therapeutic options.
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ranking = 4
keywords = deficiency
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16/85. cerebellar ataxia due to isolated vitamin e deficiency.

    Ataxia is a common and important neurological finding in medical practice. Severe deficiency of Vitamin E can profoundly affect the central nervous system and can cause ataxia and peripheral neuropathy resembling Friedreich's ataxia. Vitamin E deficiency can occur with abetalipoproteinemia, cholestatic liver disease or fat malabsorption. Ataxia with isolated Vit E deficiency (AVED) is an Autosomal Recessive genetic disorder with a mutation in the alpha tocopherol transfer protein gene (TTPA). This condition responds to high dose of Vit E and is one of the important causes of treatable ataxia. We report a young patient with Ataxia with isolated Vit E deficiency (AVED) who responded partially to replacement of Vitamin E.
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ranking = 8.0098752944713
keywords = deficiency, lipoprotein
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17/85. Isolated vitamin e deficiency with demyelinating neuropathy.

    A 22-year-old man, with a past history of generalized tonic-clonic seizures treated with phenobarbital, presented with spinocerebellar ataxia. The electrophysiological studies revealed a demyelinating motor-sensory neuropathy. The serum vitamin E level was low. sural nerve biopsy revealed loss of large myelinated fibers with evidence of remyelination. Vitamin E supplementation led to clinical and electrophysiological recovery of sensory conduction and evoked potentials. Motor nerve conduction, however, showed only partial recovery. vitamin e deficiency leading to a demyelinating neuropathy, as in the present case, suggests that the full spectrum of the disease entity is not fully defined.
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ranking = 5
keywords = deficiency
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18/85. vitamin e deficiency and impaired cellular immunity related to intestinal fat malabsorption.

    This report describes a patient in whom a severe vitamin e deficiency developed secondary to an intestinal malabsorptive disorder. In vivo and in vitro impairment of T-cell function, as well as a polyneuropathy, were observed in conjunction with this vitamin deficiency. Repletion of the vitamin deficiency was associated with marked improvement in the T-cell functions and modest improvement in the neuropathy. Observations in this patient suggest that severe vitamin e deficiency in humans may impair T-cell activity and that correction of the deficient state may reverse these T-cell abnormalities. Further studies will need to be performed to confirm these findings.
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ranking = 8
keywords = deficiency
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19/85. Brown bowel syndrome: case report and review.

    Brown bowel syndrome is characterized by deposits of lipofuscin in the tunica muscularis of the small intestine. Its etiology is associated with chronic malabsorption resulting in a deficiency of vitamin E. This hypovitaminosis is believed to cause a mitochondrial myopathy secondary to loss of the antioxidant properties of vitamin E, which further worsens the malabsorption and leads to atonic, dilated segments of bowel. Current treatment options involve nutritional supplementation, surgical resection of the affected segments, and intestinal transplantation.
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ranking = 1
keywords = deficiency
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20/85. vitamin e deficiency secondary to chronic intestinal malabsorption and effect of vitamin supplement: a case report.

    We report the clinical, neurophysiological (comprehending electromyography, nerve conduction velocities, and multimodal evoked potentials), histological study of the nerve and muscle and the effect of vitamin E supplement in a 32-year-old case with chronic vitamin e deficiency subsequent to acquired intestinal malabsorption. An early diagnosis for an early treatment is essential in preventing severe neurological deterioration.
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ranking = 5
keywords = deficiency
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