porphyrias/phosphatase

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Absence of close linkage between acute intermittent porphyria and the ABO, Rh, P, acid phosphatase, Pr, orosmucoid and pepsinogen loci.

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A first report of porphyria cutanea tarda successfully treated with glycyrrhizin.

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Porphyria cutanea tarda (PCT) is a condition that affects liver and skin by reduction of hepatic uroporphyrinogen decarboxylase activity. It is characterized by blistering lesions, erosions and crusts on sun-exposed areas. We report a 51-year-old male presenting with recurrent episodes of bullae,

The osteodystrophy of congenital erythropoietic porphyria.

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Congenital erythropoietic porphyria (CEP) is a rare disorder of heme biosynthesis that results in the production of large quantities of photoactive porphyrins. The clinical syndrome is dominated by extreme photosensitivity with mutilation of light exposed extremities and hemolytic anemia. Bone

Hexachlorobenzene impairs glucose metabolism in a rat model of porphyria cutanea tarda: a mechanistic approach.

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Hexachlobenzene (HCB), one of the most persistent environmental pollutants, induces porphyria cutanea tarda (PCT). The aim of this work was to analyze the effect of HCB on some aspects of glucose metabolism, particularly those related to its neosynthesis in vivo. For this purpose, a time-course

Effect of ursodeoxycholic acid on experimental hepatic porphyria induced by griseofulvin.

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Griseofulvin(GF) has become the drug of choice as an antifungal agent for patients who suffer from many kinds of fungal infection. In order to clarify hepatic injury by griseofulvin(GF) overload and the effect of UDCA on GF-induced hepatic injury, the authors carried out biochemical, histologic, and

Alpha-1-fetoprotein and the heat stable alkaline phosphatase in some liver diseases.

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The presence of alpha-1-fetoprotein, the heat stable alkaline phosphatase and Australia antigen was examined in 103 patients with porphyria cutanea tarda, 300 patients with cirrhosis and 18 patients with primary liver carcinoma. The heat stable alkaline phosphatase was determined in 46 percent of

Immunohistochemical studies on vitronectin in elastic tissue disorders, cutaneous amyloidosis, lichen ruber planus and porphyria.

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Vitronectin, identical with serum-spreading factor and S-protein of complement, is a glycoprotein present in both plasma and tissue. It stimulates cell adhesion and spreading and affects the complement and coagulation pathways. Vitronectin immunoreactivity was recently found in conjunction with

Porphyria cutanea tarda and sarcoidosis.

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A 38-year-old black woman presented with a multisystem disease characterized by malaise, fever, sweats, and diffuse hyperpigmentation. Laboratory examinations showed anemia, elevated alkaline phosphatase, granulomas in the liver and bone marrow, and elevated porphyrins in the urine and feces,

Congenital erythropoietic porphyria: a case report.

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Congenital erythropoietic porphyria is a rare autosomal recessive disorder of heme synthesis resulting from deficiency of uroporphyrinogen III synthase (UROIIIS). It is the most severe porphyria. The clinical manifestations are markedly variable due to the different mutation in the UROIIIS gene. We

Congenital erythropoietic porphyria: skeletal manifestations and effect of pamidronate treatment.

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Congenital erythropoietic porphyria (CEP) is a rare disorder of heme biosynthesis. Skeletal abnormalities have been described in patients with this disease. We report a 25-year-old woman with osteodystrophy from CEP. On examination, mild hepatosplenomegaly, multiple hyperpigmented scars,

Porphyria cutanea tarda, hepatitis C virus and selected symptoms of cholestasis.

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BACKGROUND The influence of hepatitis C virus (HCV) infection on the development of porphyria cutanea tarda (PCT) was recently detected, but the status of trace elements in etiology of the diseases is relatively poorly recognized. Individually observed symptoms of cholestasis do not seem to be

Hepatic pathology in porphyria cutanea tarda.

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We examined clinical and laboratory data and the liver pathology of 48 patients in whom porphyria cutanea tarda was related to alcohol ingestion, estrogen use and pregnancy, or was idiopathic. Biochemical test results, when abnormal, tended to be mild in most cases, with less than two-fold

[Morphological changes in liver tissue in experimental porphyria].

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Miscroscopic changes in the liver tissue of mice became detectable 42 hours after the administration of gricine through the appearance of porphyrins in the plasma of hepatocytes marked by the enlargement of their volume, nuclei, and nucleoli. 72 hours after gricine, porphyrins were also found in the

Loss of Wnt Secretion by Macrophages Promotes Hepatobiliary Injury after Administration of 3,5-Diethoxycarbonyl-1, 4-Dihydrocollidine Diet.

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Exposure of mice to a diet containing 3,5-diethoxycarbonyl-1, 4-dihydrocollidine (DDC) induces porphyrin accumulation, cholestasis, immune response, and hepatobiliary damage mimicking hepatic porphyria and sclerosing cholangitis. Although β-catenin signaling promotes hepatocyte proliferation, and

Drug-induced protoporphyria in beagle dogs.

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As part of regulatory safety testing program, a 13-week oral toxicity study with a new antipsychotic drug candidate was performed in beagle dogs. During this study, dark red/brown feces were recorded in treated dogs and increases in liver parameters (alanine aminotransferase, alkaline phosphatase,

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