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Wilson's disease is a very rare autosomal-recessive hereditary disorder characterised by copper accumulation and subsequent copper poisoning. It is still little researched in the medical world and often remains undiagnosed due to lack of knowledge. It is named after the American neurologist Alexander Kinnear Wilson, who was particularly struck at the beginning of the 19th century by the fact that both the brain and the liver of the same patient showed life-threatening damage. |
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In a patient with Wilson's disease, a mutation of the ATP7B gene causes impaired copper excretion from the liver (blood picture: the ceruloplasmin level is usually very low). The liver can store additional copper, but at some point the storage capacity is exhausted and the liver is gradually damaged by the excess copper. The tissue suffers so-called oxidative damage. In most Wilson patients the liver damage begins in the third or fourth year of life and presents with elevated liver values. Liver diseases typically present in adolescence or early adulthood as hepatitis with fatigue, jaundice and/or ascites, as liver cirrhosis or even as liver failure. The excess copper is then released into the blood and begins to accumulate in other organs. After the liver, the brain is the most sensitive organ. Movement disorders resulting from brain damage do not manifest as muscle weakness but as difficulties in controlling muscle actions and movements. Speech problems or slurred speech are often the first noticed changes. Another nervous system symptom is tremor (a shaking or trembling often of the hands, but also of the upper and lower limbs and the head). Another conspicuous feature is dystonia, a type of cramping or stiffening of the muscles. Because of tremor and/or dystonia, Wilson patients are often mistakenly diagnosed as Parkinson's patients. The final important nervous system symptom is deteriorating coordination, for example when trying to write legibly, eat or button clothing. The patient trips and falls unusually often. Many Wilson patients also show behavioural abnormalities resulting from brain damage. These include poor control of emotions, which can lead to outbursts of anger, bouts of crying, depression and sometimes bizarre behaviour. Patients often have difficulty concentrating on tasks; in children school grades can deteriorate. Short-term memory loss and insomnia are also common problems. After diagnosis, Wilson's disease is treated with decoppering medications such as penicillamine or trientine. The side-effect-free zinc acetate (trade name: Wilzin) is in Germany not used as initial therapy but only as maintenance therapy. Penicillamine was the first available medication but is very toxic and associated with many side effects (the skin of a 30-year-old patient, for example, then looked like that of a 60-year-old). In the initial treatment of neurological Wilson's disease it led to a permanent worsening of neurological symptoms in 25% of patients. The newer drug trientine is less toxic, but it can, among other things, cause kidney damage, anaemia and autoimmune diseases (such as systemic lupus erythematosus). Now to my story. In March 2009 Wilson's disease was diagnosed in my 11-year-old daughter by chance after a syncope and frequent dizziness with weakness. She had a fatty liver and markedly elevated liver values as well as high cholesterol. Since this is a copper storage disease, I acted according to Hahnemann's motto: "Similia similibus curentur" and from the end of March began to treat my daughter with Cuprum metallicum C200. Some of her main symptoms included mind – fear – of failure, need for constant reassurance, mind – colour – bluish – around the mouth, stomach – pain – cramping, extremities – cramps – feet. After extensive research I unfortunately found that until then no one had successfully treated this life-threatening disease with homeopathy. Because of the severe side effects we decided against the two drugs penicillamine and trientine. We wanted to continue to treat our daughter with Cuprum metallicum and the side-effect-free zinc acetate (Wilzin). After only 4 months of treatment with Cuprum metallicum, my daughter no longer had a fatty liver and was doing brilliantly; her cholesterol levels were normal and her liver values were slowly recovering. Despite the positive development with Cuprum metallicum, the additional decoppering therapy with zinc acetate was declared insufficient and vehemently rejected by all German professors, even though extensive studies by Prof. Brewer from the USA and Italy and Prof. Ferenci of the AKH Vienna confirm the effectiveness of zinc acetate. With massive threats (the youth welfare office was even mentioned!) three professors from the university hospitals of Regensburg, the Hauner Children's Clinic in Munich and Starnberg tried to force us to take these medications and were not willing to study, let alone use, the new side-effect-free therapy with zinc acetate. Thus, in January 2010 we began the additional decoppering therapy (Wilzin 3 x 25 mg/day) in Austria with Prof. Ferenci from the AKH Vienna and our paediatrician. It was incredible: after only 1 month of treatment with Wilzin all liver values were normal. The liver values from 29.12.2008 were GPT: 243, GOT: 115 and γ-GT: 27; on 22.1.2010 they were only GPT: 54, GOT: 42 and γ-GT: 17. Normally zinc takes 6 to 12 months to reduce copper toxicity and years to return liver values to normal. Neither Prof. Brewer nor Prof. Ferenci had ever seen such an astonishing and rapid course under pure zinc therapy. It is now suspected that thanks to the 9-month treatment with Cuprum metallicum the body was already largely decoppered and zinc cleared up the rest. Further evidence for this suspicion is the penicillamine test performed on my daughter in October 2009 at the Regensburg University Hospital. When administering a daily dose of 4 x 250 mg penicillamine, the 24-hour collected urine should show a copper increase of > factor 10 or in children > 1600 µg/day. This test is also used for the diagnosis of Wilson's disease. In my daughter's case the copper excretion rose only by a factor of 5, i.e. from 150 µg/day to 753 µg/day. Had we not diagnosed Wilson's disease genetically beforehand, this result would actually have been proof that she could not have Wilson's disease. During the one-day treatment with penicillamine my daughter collapsed twice without reason and showed an opisthotonus. This known side effect of exacerbating neurological symptoms strengthened our decision not to use penicillamine. One month after starting zinc treatment we immediately reduced the daily dose from 3 x 25 mg to 2 x 25 mg Wilzin because the first tablet caused severe nausea on an empty stomach. Although the zinc dose was reduced after 1 year to about 1 tablet/day, the liver values remained stable. This low zinc dose alone cannot be sufficient and suggests that Cuprum metallicum addressed the genetic defect. Course of treatment of Wilson's disease with Cuprum metallicum End of March 2009: Cuprum met. C200 3 times daily for 3 days
10.4.2009: Repeat Cuprum met. C200 3 times daily for 3 days
After 1.5 weeks Cuprum LM6 weekly
Cuprum met. LM12 every 4–5 days (from July 2009)
Treatment with Wilzin Start: 14.1.2010, daily 3 x 25 mg
In my clinical experience, Cuprum metallicum is not only the remedy for hepatic copper storage disorder, but should also be considered in disabled patients, patients with Parkinson-like symptoms, in autism, spasms, cramps of all kinds and ADHD. ************************************************************************** |
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Sources Brewer, George J. 2006. Wilson's Disease – A Guide for Patients and Their Relatives on Wilson's Disease and Copper Issues. Berlin. (Available free from Ophan Europe (Germany) GmbH, D-63128 Dietzenbach, Tel. 0049-(0)6074/812160) ************************************************************************** |
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