Linked Life Data

712342

Source:http://linkedlifedata.com/resource/pubmed/id/712342

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1979-1-15
pubmed:abstractText
In chronic hepatic porphyria, including the clinical phase, porphyria cutanea tarda, the activity of uroporphyrinogen decarboxylase is decreased not only in the liver, but also in the erythrocytes. The synonomous decrease in the enzymic activity in liver and erythrocytes in both familial and sporadic hepatic porphyria shows that the disturbance of this enzyme is the primary genetic defect of this condition; inheritance of the defect is probably autosomal and dominant. The clinical manifestation of disturbances of porphyrin metabolism are precipitated, however, by additional factors, such as liver damage, alcohol, oestrogens and neoplastic growths. In the absence of these other pathogenic influences, the enzyme defect is compensated and does not result in disturbances of haem or haemoglobin synthesis, either in the liver or the bone marrow.
pubmed:language
ger
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0340-076X
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
513-7
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed:year
1978
pubmed:articleTitle
[Uroporphyrinogen decarboxylase in erythrocytes: studies on the primary genetic enzyme defect in chronic hepatic porphyria (author's transl)].
pubmed:publicationType
Journal Article, English Abstract