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violBiol, 2003,[link widoczny dla zalogowanych],212: lll-28. [10] KochMelbyeM, SorensenP, Acuteresph ~ orytractinfee-lionsandmannose-bindingleelininsufficiencyduringearlychild-hood [J]. JAMA, 2001,285 (1o) :1316-21. [11] CrosdaleDJ, PouRonKV, OilierWE, of. Mannose-bindingleclingenepolymorphismsasasusceptibilityfllL ~ torforchronicnecrotiz-ingpulmonaryaspergiHosis [J]. JInfectDis, 2001,[link widoczny dla zalogowanych],184 (5) :653-6. (Editor: Wong Kai-Yan ) (Continued from 1160 ) to discuss the cases of 2 patients with significant family history. Check the support of clinical and experimental edge of hepatolenticular degeneration complicated with acute hemolysis and acute liver failure. The patient was admitted to hospital suffering from respiratory tract infection the previous week . Possible pathogenesis of acute upper respiratory tract infection to promote the body produces too much li2 () 2,[link widoczny dla zalogowanych], oxidation and inactivation of red blood cell surface membrane proteins with SH -based and enzyme protein. Make 6. Glucose phosphate dehydrogenase deficiency or cause the enzyme with thiol metabolism . Red blood cells induced by acute hemolysis , infection was induced degeneration Wilson edge of acute intravascular hemolysis of the important reasons. In addition, when blood can not be synthesized ceruloplasmin copper from time to time deposited in the liver cytoplasm . Liver cells are destroyed, a large number of intracellular copper released into the blood. Blood copper and copper , with an increasing red blood cell , red blood cell peroxidation enhanced. Denaturation of hemoglobin to red cell membrane stiffness, easily damaged ,[link widoczny dla zalogowanych], causing hemolysis , accompanied by significantly increased urinary copper 】【 l . In addition . Because ceruloplasmin synthesis of obstacles , and excretion decreased. Copper combined with the organization and deposition of protein in the body organs, especially the liver, brain mass of lenticular copper edge , resulting in tissue and organ dysfunction, organ failure and end up dead - ~-t2]. Hepatolenticular degeneration complicated edge in patients with fulminant liver failure associated with more alkaline phosphatase activity decreased. With further reduction in exacerbations , the reason for the blood of competitive binding of copper and zinc serum alkaline phosphatase and its inactivation caused by 【 3t, alkaline phosphatase activity can help combat the low variability of Wilson 's clinical diagnosis of eucalyptus . Although this line of artificial liver support treatment of patients . But the end result of liver failure and death.
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