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We are analyzing https://link.springer.com/article/10.1007/bf00412489.

Title:
Hereditary uroporphyrinogen-decarboxylase deficiency predisposing porphyria cutanea tarda (chronic hepatic porphyria) in females after oral contraceptive medication | Archives of Dermatological Research
Description:
Porphyria cutanea tarda (PCT) was diagnosed in 27 women aged 23–48 years (mean, 35 years) who had been under oral-hormonal-contraceptive medication for 1–18 years, in 3 women under substitutional estrogen treatment in the menopause, and in 2 men aged 65 and 76 years after estrogen treatment of prostatic carcinoma. In all patients, total urinary porphyrin excretion was elevated, with an average uro-and heptacarboxyporphyrin predominance of 88%, thus proving PCT. On the patients, 84% showed a significant decrease of erythrocyte uroporphyrinogen-decarboxylase (UD; EC 4.1.1.37) activity to β‰ˆ50% of control levels suggesting a hereditary predisposition for the development of a chronic hepatic porphyria. Estrogens and alcohol are capable of reducing hepatic UD activity. Women with hereditary red cell UD deficiency may be regarded as predisposed to PCT when under estrogen intake, especially in combination with the potentiating influence of alcohol and chronic liver disease. Normal erythrocyte UD values in patients with additive alcohol consumption may implicate a stronger inhibitory effect for alcohol on UD, suggesting a merely toxic form of chronic hepatic porphyria.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

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Custom-built

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Traffic Estimate {πŸ“ˆ}

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 8,170,536 visitors per month in the current month.

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We're unsure if the website is profiting.

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Keywords {πŸ”}

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Topics {βœ’οΈ}

oral-hormonal-contraceptive medication hereditary predisposition month download article/chapter uroporphyrinogen decarboxylase deficiency oral contraceptive medication uroporphyrinogen decarboxylase defect dermatological research aims porphyria cutanea tarda chronic hepatic porphyria hepatic uroporphyrinogen decarboxylase chronic liver disease genetic defect sporadic porphyria cutanea erythrocyte uroporphyrinogen-decarboxylase erythrocyte uroporphyrinogen decarboxylase porphyria cutanea tarba uroporphyrinogen decarboxylase activity immunoreactive uroporphyrinogen decarboxylase inherited enzymatic defect privacy choices/manage cookies full article pdf acute intermittent porphyria leber und erythrozyten hepatoerythropoietic porphyria misdiagnosed steroid hormones roenigk hh jr liver cirrhosis uroporphyrinogen decarboxylase check access instant access article sixel-dietrich substitutional estrogen treatment porphyria induced european economic area scope submit manuscript stronger inhibitory effect related subjects aminolevulinic acid synthase poh-fitzpatrick mb acute ethanol ingestion conditions privacy policy alcohol-induced decrease article archives accepting optional cookies control levels suggesting 5Ξ±-reductive metabolism oestrogenic drugs diethylstilboestrol von tiepermann additive alcohol consumption main content log

Schema {πŸ—ΊοΈ}

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         headline:Hereditary uroporphyrinogen-decarboxylase deficiency predisposing porphyria cutanea tarda (chronic hepatic porphyria) in females after oral contraceptive medication
         description:Porphyria cutanea tarda (PCT) was diagnosed in 27 women aged 23–48 years (mean, 35 years) who had been under oral-hormonal-contraceptive medication for 1–18 years, in 3 women under substitutional estrogen treatment in the menopause, and in 2 men aged 65 and 76 years after estrogen treatment of prostatic carcinoma. In all patients, total urinary porphyrin excretion was elevated, with an average uro-and heptacarboxyporphyrin predominance of 88%, thus proving PCT. On the patients, 84% showed a significant decrease of erythrocyte uroporphyrinogen-decarboxylase (UD; EC 4.1.1.37) activity to β‰ˆ50% of control levels suggesting a hereditary predisposition for the development of a chronic hepatic porphyria. Estrogens and alcohol are capable of reducing hepatic UD activity. Women with hereditary red cell UD deficiency may be regarded as predisposed to PCT when under estrogen intake, especially in combination with the potentiating influence of alcohol and chronic liver disease. Normal erythrocyte UD values in patients with additive alcohol consumption may implicate a stronger inhibitory effect for alcohol on UD, suggesting a merely toxic form of chronic hepatic porphyria.
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      headline:Hereditary uroporphyrinogen-decarboxylase deficiency predisposing porphyria cutanea tarda (chronic hepatic porphyria) in females after oral contraceptive medication
      description:Porphyria cutanea tarda (PCT) was diagnosed in 27 women aged 23–48 years (mean, 35 years) who had been under oral-hormonal-contraceptive medication for 1–18 years, in 3 women under substitutional estrogen treatment in the menopause, and in 2 men aged 65 and 76 years after estrogen treatment of prostatic carcinoma. In all patients, total urinary porphyrin excretion was elevated, with an average uro-and heptacarboxyporphyrin predominance of 88%, thus proving PCT. On the patients, 84% showed a significant decrease of erythrocyte uroporphyrinogen-decarboxylase (UD; EC 4.1.1.37) activity to β‰ˆ50% of control levels suggesting a hereditary predisposition for the development of a chronic hepatic porphyria. Estrogens and alcohol are capable of reducing hepatic UD activity. Women with hereditary red cell UD deficiency may be regarded as predisposed to PCT when under estrogen intake, especially in combination with the potentiating influence of alcohol and chronic liver disease. Normal erythrocyte UD values in patients with additive alcohol consumption may implicate a stronger inhibitory effect for alcohol on UD, suggesting a merely toxic form of chronic hepatic porphyria.
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