Wilson’s disease

A disturbance of copper metabolism causes hepatolenticular degeneration (Wilson’s disease), an autosomal recessive disorder whose genetic locus lies on the long arm of chromosome 13. The concentration of the copper transport protein ceruloplasmin is abnormally low and, as a result, the serum free co...
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Autor*in:	A. Hancu [verfasserIn] C. Mihai [verfasserIn] D. Zguma [verfasserIn] A. Docu Axelerad [verfasserIn] E. Dumitru [verfasserIn] M. Kaivanifard [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2011

Schlagwörter:	wilson’s disease (wd) treatment global assessment scale for wd (gas for wd)

Übergeordnetes Werk:	In: Romanian Journal of Neurology - Amaltea Medical Publishing House, 2019, 10(2011), 3, Seite 148-153
Übergeordnetes Werk:	volume:10 ; year:2011 ; number:3 ; pages:148-153

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.37897/RJN.2011.3.8

Katalog-ID:	DOAJ021377103

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520			\|a A disturbance of copper metabolism causes hepatolenticular degeneration (Wilson’s disease), an autosomal recessive disorder whose genetic locus lies on the long arm of chromosome 13. The concentration of the copper transport protein ceruloplasmin is abnormally low and, as a result, the serum free copper concentration is high and an abnormally large amount of copper is eliminated in the urine. Free copper is deposited in the liver, the edge of the cornea, the brain. We present a case who debuted by tremors and thrombocytopenia. Continuous therapy with Trientine hydrochloride and Mega zinc, and elimination of copper rich foods were improved cognitive, behavioral and motor dysfunctions.
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title_auth	Wilson’s disease
abstract	A disturbance of copper metabolism causes hepatolenticular degeneration (Wilson’s disease), an autosomal recessive disorder whose genetic locus lies on the long arm of chromosome 13. The concentration of the copper transport protein ceruloplasmin is abnormally low and, as a result, the serum free copper concentration is high and an abnormally large amount of copper is eliminated in the urine. Free copper is deposited in the liver, the edge of the cornea, the brain. We present a case who debuted by tremors and thrombocytopenia. Continuous therapy with Trientine hydrochloride and Mega zinc, and elimination of copper rich foods were improved cognitive, behavioral and motor dysfunctions.
abstractGer	A disturbance of copper metabolism causes hepatolenticular degeneration (Wilson’s disease), an autosomal recessive disorder whose genetic locus lies on the long arm of chromosome 13. The concentration of the copper transport protein ceruloplasmin is abnormally low and, as a result, the serum free copper concentration is high and an abnormally large amount of copper is eliminated in the urine. Free copper is deposited in the liver, the edge of the cornea, the brain. We present a case who debuted by tremors and thrombocytopenia. Continuous therapy with Trientine hydrochloride and Mega zinc, and elimination of copper rich foods were improved cognitive, behavioral and motor dysfunctions.
abstract_unstemmed	A disturbance of copper metabolism causes hepatolenticular degeneration (Wilson’s disease), an autosomal recessive disorder whose genetic locus lies on the long arm of chromosome 13. The concentration of the copper transport protein ceruloplasmin is abnormally low and, as a result, the serum free copper concentration is high and an abnormally large amount of copper is eliminated in the urine. Free copper is deposited in the liver, the edge of the cornea, the brain. We present a case who debuted by tremors and thrombocytopenia. Continuous therapy with Trientine hydrochloride and Mega zinc, and elimination of copper rich foods were improved cognitive, behavioral and motor dysfunctions.
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container_issue	3
title_short	Wilson’s disease
url	https://doi.org/10.37897/RJN.2011.3.8 https://doaj.org/article/525e057db8314472a474c6c0b54f0ab4 https://rjn.com.ro/articles/2011.3/RJN_2011_3_Art-08.pdf https://doaj.org/toc/1843-8148 https://doaj.org/toc/2069-6094
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author2	C. Mihai D. Zguma A. Docu Axelerad E. Dumitru M. Kaivanifard
author2Str	C. Mihai D. Zguma A. Docu Axelerad E. Dumitru M. Kaivanifard
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doi_str	10.37897/RJN.2011.3.8
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up_date	2024-07-03T20:31:19.078Z
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