Chronic inflammation does not appear to modify the homozygous hereditary hemochromatosis phenotype.
Blood Cells Mol Dis
; 35(3): 326-7, 2005.
Article
em En
| MEDLINE
| ID: mdl-16154780
ABSTRACT
The mechanism of excessive iron storage in patients with hereditary hemochromatosis caused by mutations of the HFE gene seems to be a failure to up-regulate hepcidin in the face of increased body iron. Since the cytokines IL-1 and IL-6 stimulate hepcidin transcription in the absence of HFE, chronic inflammatory states might counteract the effect of HFE mutations. We measured the pre-phlebotomy plasma levels of C reactive protein (CRP) and of interleukin 6 (IL-6) in homozygotes for the C282Y mutation of HFE. There was no difference in these levels in subjects with high iron stores than in those with low iron stores, suggesting that the phenotypic differences between such homozygotes is not appreciably affected by ongoing chronic inflammation.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Antígenos de Histocompatibilidade Classe I
/
Hemocromatose
/
Inflamação
/
Proteínas de Membrana
Limite:
Female
/
Humans
/
Male
Idioma:
En
Revista:
Blood Cells Mol Dis
Ano de publicação:
2005
Tipo de documento:
Article