Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with multiple enterocutaneous fistulae who developed the skin manifestations of acrodermatitis enteropathica while on total parenteral nutrition is described. The value of monitoring the serum alkaline phosphatase to demonstrate zinc deficiency is shown. The skin manifestations responded rapidly to the re-introduction of zinc to the diet.
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PMID:Zinc deficiency in total parenteral nutrition. 10 10

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 (7 and 13 years old) had a low absorption, 3.3 and 1.8% respectively, corroborating their high need for additional elemental zinc (about 2 mg/kg/day). Three adult AE patients, all in their twenties, had a considerably lower need for extra zinc (about 0.2 mg/kg/day). Their zinc absorption ranged from 28 to 36% (mean 34%). In the controls the range was 27 - 65% (mean 43%). Turnover of retained 65Zn from day 8 - 30 was about 0.7% in the patient as well as in the control groups. Oral zinc therapy was withdrawn prior to the study. During the zinc-free period (3-7) a marked decrease in serum zinc and serum alkaline phosphatase values was noted in the two children with AE and they showed clinical evidence of zinc deficiency (angular stomatitis, scaling around finger nails, and irritability). None of the adult patients showed such evidence of impending zinc deficiency. One complained of exacerbation of facial acne, and another of pain in her feet. All symptoms disappeared promptly when oral zinc therapy was resumed.
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PMID:65Zinc absorption in patients suffering from acrodermatitis enteropathica and in normal adults assessed by whole-body counting technique. 11 22

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 microscopy of the Paneth cells initially revealed abnormal inclusion bodies which disappeared during therapy, suggesting that the abnormality is secondary to zinc deficiency, and not a primary defect. These abnormal inclusions may represent altered secretory granules and a proliferation of lysosomes. We were unable to define the heterozygous state biochemically or histologically.
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PMID:Acrodermatitis enteropathica, zinc, and the Paneth cell. A case report with family studies. 19 72

The skin lesions seen in 10 patients who received parenteral nutrition during treatment of chronic enteropathy are described. All of these patients had a lowered serum zinc concentration. The skin lesions were similar to those seen in acrodermatitis enteropathica. After supplementation with zinc sulphate, the skin lesions disappeared completely. A decrease in the serum alkaline phosphatase level can be regarded as a sign of an impending zinc deficiency. Parenteral nutrition formulae should contain a sufficient amount of zinc.
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PMID:Skin lesions in acquired zinc deficiency due to parenteral nutrition. 41 40

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 tryptophane load. In addition, histopathological and histochemical studies for lactase, succinic dehydrogenase, alkaline phosphatase, acid phosphatase, and alpha-non-specific esterases activities were done for the intestinal mucosal biopsies. All the previous investigations were then repeated after two months treatment with 500 mg/day diiodohydroxyquinoline. The tryptophan metabolites were significantly low in the diseased infants, both basal and after tryptophan load. Moreover, the intestinal enzymes activities were altered. After 2 months treatment with diiodohydroxyquinoline the diseased infants became clinically improved, tryphtophan metabolites became normal, but the activities of the intestinal enzymes were not altered. The biochemical and histochemical findings were discussed, giving the possibility of competitive inhibition of the diiodohydroxyquinolines and the by-product 8 OH Quinololic acid resulting in more degradation of Kneurine and 3 OH Kneurenine to nicotinamide adenine dinucleotide.
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PMID:Clinical, biochemical and histochemical studies on infants with Acrodermatitis enteropathica chronica. 82 55

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 well as alkaline phosphatase, which were very low before treatment, returned to normal after therapy. This brief report confirms the efficacy of oral zinc in the treatment of Acrodermatitis enteropathica.
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PMID:Treatment of acrodermatitis enteropathica with zinc sulphate. Rerport of 3 cases. 95 34

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 per 24 hours) were extremely low. Di-iodohydroxyquin therapy was accompanied by a modest increase in plasma zinc concentrations. Oral zinc sulfate (220 mg three times a day or 50 mg twice a day) resulted in rapid and complete clinical remission, and in a return of plasma zinc, serum alkaline phosphatase and urinary zinc excretion to normal. These data are compatible with a severe zinc deficiency state and indicate that the inherited defect in this disease is either in or closely related to zinc metabolism. The beneficial effects of zinc therapy in this patient provide further confirmation of the efficacy of oral zinc in the treatment of acrodermatitis enteropathica.
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PMID:Zinc therapy of acrodermatitis enteropathica. 109 Aug 26

Thirty-three patients with alcoholic cirrhosis (AC), selected on widely recognized criteria (16, 57), were investigated prospectively for cutaneous manifestations of zinc deficiency. The patients were divided into 3 groups: group A (n = 12): AC without skin lesions; group B (n = 12): AC with skin lesions responsive to a zinc-free topical treatment or resistant to enteral zinc sulfate intake; group C (n = 9): AC with skin lesions cured by oral zinc replacement therapy alone. The lesions observed in group C were studied microscopically. Data concerning zinc metabolism (Zn concentrations in plasma, red cells, urine and hair; alkaline phosphatase values), biochemical criteria of AC (plasma serum-albumin concentration, IgA/transferrin ratio) and a malabsorption test (xylosemia 120 min after oral absorption of D-xylose 25 g) were compared by the variance analysis method. A control group (D, n = 12) was used as reference. Few cases of cutaneous manifestations of zinc deficiency in AC patients have been published. In more than one half of the 15 or so we found in the literature, an aggravating factor (total parenteral nutrition, digestive tract surgery) had to be taken into account. In this prospective study 9 new cases in which AC was the only cause of zinc deficiency are reported. A clinical picture similar to acrodermatitis enteropathica with peribuccal bullous lesions was observed in only one patient. In all other cases the patients presented with a cracked and reticulated eczema on the extensor aspect of the limbs and (often erosive) in the perianal and genital regions. The eczema was associated with cheilitis, glossitis, stomatitis, alopecia and, seldom, ungual Beau's lines. Disorders of behaviour, diarrhoea and bouts of lever regressing under zinc replacement therapy were frequent. Histology was not very specific, except for the presence of necrotic areas in the stratum germinativum, sometimes associated with small subcorneal pustules containing altered polymorphonuclears. In every case, it was the rapid regression of symptoms under zinc sulfate treatment that confirmed the diagnosis. Plasma zinc concentrations were most significantly decreased in all AC groups as compared to controls (61.2 +/- 19.4 vs 97.8 +/- 10.4 micrograms/100 ml) and also in AC patients with skin manifestations of zinc deficiency as compared to the other AC patients (44.4 +/- 9.2 vs 66.5 +/- 18.8 micrograms/100 ml) table V). Changes in serum-albumin levels and in hepatocellular function were parallel to changes in plasma zinc concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cutaneous manifestations of zinc deficiency in ethylic cirrhosis]. 357 31

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 neutrophilia, consistently low activities of serum alkaline phosphatase and alanine transaminase, and frequently, hypercholesterolemia. Lymphocyte blastogenic responses were decreased and there was dysgammaglobulinemia in pups in which quantitative studies of immunoglobulins were made. The mean of plasma zinc concentrations in 5 affected pups was significantly lower than the mean of age- and breed-matched controls. Pathologic findings included parakeratosis, hyperkeratosis, and superficial bacterial infections of the skin. There was severe reduction of lymphocytes in T-lymphocyte areas of lymphoid tissue. Bronchopneumonia and dilatation of the cerebral ventricles were found in most affected pups. Family studies indicated that the syndrome is inherited as an autosomal recessive trait. In spite of its similarities to lethal trait A46 in Black Pied Danish cattle and acrodermatitis enteropathica in man, oral or parenteral treatment with zinc failed to ameliorate the clinical signs of the syndrome.
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PMID:Lethal acrodermatitis in bull terriers. 371 Aug 72

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 younger patients without Zn deficiency. In (A) serum Zn and serum AP values were low, but following parenteral Zn the parameters rose to normal levels (r = +0.79, p less than 0.001). In (B) serum Zn and serum AP levels decreased when oral Zn was stopped, but shortly returned to normal upon reinitiation of Zn. In (C) Zn therapy caused a rise in the serum Zn concentration whereas the serum AP activity decreased (r = -0.01, p greater than 0.1). The results suggest that serial determinations of serum Zn and serum AP during Zn supplementation may be a valid tool in the diagnosis of severe and mild Zn deficiency as well as in the exclusion of the diagnosis.
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PMID:Serum alkaline phosphatase and serum zinc levels in the diagnosis and exclusion of zinc deficiency in man. 400 29


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