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acrodermatitis/phosphatase

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Serum alkaline phosphatase activity in acrodermatitis enteropathica: an index of the serum zinc level.

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A significant positive correlation between serum zinc and serum alkaline phosphatase levels was demonstrated in four patients suffering from acrodermatitis enterophathica for which they received oral zinc sulphate therapy. In one of the male patients a significant inverse relation between serum zinc

Treatment of acrodermatitis enteropathica with zinc sulphate. Rerport of 3 cases.

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The therapeutic effect of orally administered zinc in 3 patients affected with Acrodermatitis enteropathica is reported. Single daily doses of zinc resulted in rapid improvement of the general condition of these patients and in clinical remission within a week. Serum, urine and hair zinc levels as

Zinc therapy of acrodermatitis enteropathica.

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The therapeutic effect of orally administered zinc was evaluated in an adult woman with acrodermatitis enteropathica. When she was off therapy and in clinical relapse the plasma zinc concentration (10 mug per 100 ml), serum alkaline phosphatase (3 1U per liter) and urine zinc excretion rate (39 mug

Clinical, biochemical and histochemical studies on infants with Acrodermatitis enteropathica chronica.

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7 infants diseased with Acrodermatitis enteropathica and 10 normal controls were included in this study. The values of anthranilic acid glucuronide, 6- aminohippuric, anthranilic acid, N-acetyl Kneurine, Kneurine and 30 H Kneurenine, were estimated in mg/24 hours urine, both basal and after

Acrodermatitis enteropathica Reversibility of cerebral atrophy with zinc therapy.

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A six-month-old Saudi boy with acrodermatitis enteropathica confirmed by low serum zinc and alkaline phosphatase levels is described. Both the patient and a sibling developed acrodermatitis enteropathica while entirely breastfed. The mother had low serum zinc levels. Cranial computed tomography

Acquired acrodermatitis enteropathica.

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Acrodermatitis enteropathica has an hereditary, infantile form and an acquired form which usually develops secondary to total parenteral nutrition. Both forms are caused by a zinc deficiency. The use of a reduced serum alkaline phosphatase level as a marker for acrodermatitis enteropathica is

65Zinc absorption in patients suffering from acrodermatitis enteropathica and in normal adults assessed by whole-body counting technique.

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65Zinc absorption was studied in five acrodermatitis enteropathica (AE) patients and in eight normal adults by means of a whole-body counting assay. The absorption was calculated from retention values recorded in the time interval 8-30 days after oral administration of the isotope. Two AE patients

Acrodermatitis enteropathica, zinc, and the Paneth cell. A case report with family studies.

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An infant with acrodermatitis enteropathica was studied before and after starting zinc therapy. Clinical recovery was rapid, and the plasma zinc, serum and mucosal alkaline phosphatase activities returned to normal. Light microscopy of small intestinal biopsies showed normal mucosa. Electron

Serum alkaline phosphatase and zinc undernutrition in infants with chronic diarrhea.

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III infants and children need zinc replacement in total parenteral nutrition solutions, but assessment of these needs and total body zinc status is difficult. Seven infants with severe diarrhea initially given 80 to 100 micrograms/kg/day of elemental zinc developed systemic zinc deficiency as

Serum alkaline phosphatase and serum zinc levels in the diagnosis and exclusion of zinc deficiency in man.

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In the present study we monitored serum zinc (Zn) and serum alkaline phosphatase (AP) levels during Zn supplementation in (A) a young zinc depletion syndrome (ZDS) patient with severe Zn deficiency, (B) three acrodermatitis enteropathica (AEP) patients with mild Zn deficiency and (C) 7 elderly and 3

Acquired zinc deficiency acrodermatitis associated with nephrotic syndrome.

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We present a child with new-onset nephrotic syndrome, acrodermatitis, low serum zinc levels and decreased serum alkaline phosphatase. A diagnosis of acquired zinc deficiency acrodermatitis was made. Oral zinc supplementation led to rapid clinical resolution. The etiology of zinc deficiency in

Lethal acrodermatitis in bull terriers.

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A lethal syndrome characterized clinically by growth retardation, progressive acrodermatitis, chronic pyoderma and paronychia, diarrhea, pneumonia, and abnormal behavior was observed in 17 related Bull Terrier pups. Median survival time was 7 months. Laboratory evaluation revealed non-degenerative
Acrodermatitis enteropathica (AE) is a rare autosomal recessive hereditary skin disease caused by mutations in the SLC39A4 gene and is characterized by periorificial dermatitis, alopecia and diarrhoea due to insufficient zinc absorption. Only one of the three known sets of twins with

[Zinc deficiency dermatoses. Etiology, clinical aspects and treatment].

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In zinc deficiency disorders the serum zinc concentration is low and the activity of alkaline phosphatase in serum is declining. The clinical picture includes a poor general condition and a characteristic dermatitis on hands, feet, in the face, and the anogenital region. In acute zinc deficiency,

Hair changes due to zinc deficiency in a case of sucrose malabsorption.

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A 7-year-old girl suffering from chronic diarrhoea due to sucrase deficiency was referred because of poor hair growth. Her scalp hair had a poor, colourless appearance and was much thinned in the occipital region. Her skin was dry, but otherwise normal. P-zinc was low (7.9 mumol/l), whereas
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