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Namespaces Article Talk. Views Read Edit View history. Help Learn to edit Community portal Recent changes Upload file. Download as PDF Printable version. Once a mutation is confirmed, it is possible to screen family members for the disease as part of clinical genetics family counseling. Since mutations of the WD gene vary between populations, research and genetic testing done in countries like the USA or United Kingdom can pose problems as they tend to have more mixed populations.
In general, a diet low in copper-containing foods is recommended with the avoidance of mushrooms , nuts , chocolate , dried fruit , liver, sesame seeds and sesame oil, and shellfish. Medical treatments are available for Wilson's disease. Some increase the removal of copper from the body, while others prevent the absorption of copper from the diet. Generally, penicillamine is the first treatment used. This binds copper chelation and leads to excretion of copper in the urine.
Hence, monitoring of the amount of copper in the urine can be done to ensure a sufficiently high dose is taken. In those who presented with neurological symptoms, almost half experience a paradoxical worsening in their symptoms. While this phenomenon is observed in other treatments for Wilson's, it is usually taken as an indication for discontinuing penicillamine and commencing second-line treatment.
Some recommend trientine as first-line treatment, but experience with penicillamine is more extensive. This is regarded as experimental,  though some studies have shown a beneficial effect.
Once all results have returned to normal, zinc usually in the form of a zinc acetate prescription called Galzin may be used instead of chelators to maintain stable copper levels in the body. Zinc stimulates metallothionein , a protein in gut cells that binds copper and prevents their absorption and transport to the liver. Zinc therapy is continued unless symptoms recur or if the urinary excretion of copper increases. In rare cases where none of the oral treatments are effective, especially in severe neurological disease, dimercaprol British anti-Lewisite is occasionally necessary.
This treatment is injected intramuscularly into a muscle every few weeks and has unpleasant side effects such as pain. People who are asymptomatic for instance, those diagnosed through family screening or only as a result of abnormal test results are generally treated, as the copper accumulation may cause long-term damage in the future.
It is unclear whether these people are best treated with penicillamine or zinc acetate. Physiotherapy and occupational therapy are beneficial for patients with the neurologic form of the disease. The copper chelating treatment may take up to six months to start working, and these therapies can assist in coping with ataxia , dystonia , and tremors, as well as preventing the development of contractures that can result from dystonia.
Liver transplantation is an effective cure for Wilson's disease but is used only in particular scenarios because of the risks and complications associated with the procedure. It is used mainly in people with fulminant liver failure who fail to respond to medical treatment or in those with advanced chronic liver disease. Liver transplantation is avoided in severe neuropsychiatric illness, in which its benefit has not been demonstrated. Left untreated, Wilson's disease tends to become progressively worse and is eventually fatal.
With early detection and treatment, most of those affected can live relatively normal lives. Liver and neurologic damage that occurs prior to treatment may improve, but it is often permanent. The disease bears the name of the British physician Samuel Alexander Kinnier Wilson — , a neurologist who described the condition, including the pathological changes in the brain and liver, in In , Cumings, and New Zealand neurologist Derek Denny-Brown , working in the United States, simultaneously reported the first effective treatment, using metal chelator British anti-Lewisite.
The genetic basis of Wilson's disease, and its linkage to ATP7B mutations, was elucidated by several research groups in the s and s. Hereditary copper accumulation has been described in Bedlington Terriers ,  where it generally only affects the liver.
From Wikipedia, the free encyclopedia. Not to be confused with Wilson's temperature syndrome , an alternative medicine concept. Genetic multisystem copper-transport disease. Main article: ATP7B. July Archived from the original on Retrieved Joanne; Newton, Herbert B. The 5-minute Neurology Consult. Elsevier Health Sciences. Annals of the New York Academy of Sciences. Biller, J ed. Duker Edinburgh: Mosby. Scientific Reports. Bibcode : NatSR.. Wintrobe's clinical hematology. Nat Clin Pract Neurol.
Human Genetics. Journal of Hepatology. Archived from the original PDF on ICD - 10 : E Metal deficiency and toxicity disorders.
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