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Útgefiđ gćđaskjal: Leiđbeiningar
Skjalnúmer: Rklín-275
Útg.dags.: 01/25/2019
Útgáfa: 5.0
Áb.mađur: Ísleifur Ólafsson

2.02.03.02.01 Kopar, S-


Samheiti: Cu, S-Kopar, S-Kupfers, Copper, Koppar
Hide details for Sýnataka, geymsla og sýnasending Sýnataka, geymsla og sýnasending
Gerđ sýnis : Sermi, (heparín-plasma). Sýni tekiđ í serum glas međ rauđum tappa međ geli (gul miđja).
Má líka taka í lithium heparin glös. Sýni tekiđ í glas međ grćnum tappa .
Litakóđi samkvćmt Greiner

Magn: 2 mL en má vera allt niđur í 0,5 mL af mjög ungum börnum (verđur ţá ekki tvítekiđ).
Geymsla sýnis: Kćlir, stofuhiti.
Sýnasending: Hrađsending til útlanda.
Hide details for Heiti tilvísunarannsóknastofu og heimilisfangHeiti tilvísunarannsóknastofu og heimilisfang
MVZ Labor PD Dr. Volkmann und Kollegen GbR
Kriegsstrasse 99
76133 Karlsruhe

Tel:  0721 85000-0
Fax: 0721 85000-199

www.laborvolkmann.de
E-Mail:
 labor@laborvolkmann
Hide details for HeimildirHeimildir
kupfer.pdfkupfer.pdf

http://www.laborvolkmann.de/analysenspektrum/HTML/index.html




Fróđleikur:
 Suggests clinical disorders or settings where the test may be helpful

Diagnosis of: 1. -Wilson disease 2. -Primary biliary cirrhosis 3. -Primary sclerosing cholangitis

 Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

In serum from normal, healthy humans, more than 95% of the copper is incorporated into ceruloplasmin; the remaining copper is loosely bound to albumin.

 Low serum copper, most often due to excess iron or zinc ingestion and infrequently due to dietary copper deficit, results in severe derangement in growth and impaired erythropoiesis. Low serum copper is also observed in hepatolenticular degeneration (Wilson disease) due to a decrease in the synthesis of ceruloplasmin and allelic variances in cellular metal ion transporters. In Wilson disease, the albumin-bound copper may actually be increased, but ceruloplasmin copper is low, resulting in low serum copper. However, during the acute phase of Wilson disease (fulminant hepatic failure), ceruloplasmin and copper may be normal; in this circumstance, hepatic inflammation causes increased release of ceruloplasmin. It is useful to relate the degree of liver inflammation to the ceruloplasmin and copper-see discussion on hypercupremia below. Significant hepatic inflammation with normal ceruloplasmin and copper suggest acute Wilson disease.

 Other disorders associated with decreased serum copper concentrations include malnutrition, hypoproteinemia, malabsorption, nephrotic syndrome, Menkes disease, copper toxicity, and megadosing of zinc-containing vitamins (zinc interferes with normal copper absorption from the gastrointestinal tract).

 Hypercupremia is found in primary biliary cirrhosis, primary sclerosing cholangitis, hemochromatosis, malignant diseases (including leukemia), thyrotoxicosis, and various infections. Serum copper concentrations are also elevated in patients taking contraceptives or estrogens and during pregnancy.

 Since the gastrointestinal (GI) tract effectively excludes excess copper, it is the GI tract that is most affected by copper ingestion. Increased serum concentration does not, by itself, indicate copper toxicity.



Ritstjórn

Ingibjörg Loftsdóttir
Sigrún H Pétursdóttir
Guđmundur Sigţórsson
Kristín Sigurgeirsdóttir

Samţykkjendur

Ábyrgđarmađur

Ísleifur Ólafsson

Útgefandi

Sigrún H Pétursdóttir

Upp »


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