FAQ About Wilson Disease

You should first see your primary care physician, who will refer you to a gastroenterologist or hepatologist if necessary. 

Wilson’s disease causes copper to build up in the liver and brain. Although symptoms can be worse on one side of the body than the other, the brain is affected symmetrically. This could be due to asymmetric neurological development, such as being right- or left-handed. 

While 0.1 ppm isn’t harmful, it does imply that significant copper is coming from somewhere, and the level might be higher at times or under specific situations. 

 Is it possible for a patient with Wilson’s disease to get vaccinated against Hepatitis A or B? 

Yes. Because Wilson’s disease frequently affects the liver, many patients cannot afford further liver damage. The hepatitis A or B vaccine is just as safe for Wilson’s patients as it is for everyone else. 

Hepatic: Asymptomatic hepatomegaly; isolated splenomegaly; persistently increased AST, ALT; Fatty Liver; 

Acute hepatitis; autoimmune hepatitis-like cirrhosis; fulminant hepatic failure Drooling, dysarthria; rigid dystonia; pseudobulbar palsy; seizures; migraine headaches; 

 Neurological: Movement disorders (tremor, involuntary motions); drooling, dysarthria; rigid dystonia; pseudobulbar palsy; seizures; migraine headaches insomnia 

 Psychiatric Conditions: Depression, neuroses, personality abnormalities, and psychosis are all Other signs and symptoms include: Renal abnormalities include amino-aciduria and nephrolithiasis; skeletal abnormalities include early osteoporosis and arthritis; cardiomyopathy, dysrhythmias, pancreatitis, and hypoparathyroidism; and cardiomyopathy, dysrhythmias, pancreatitis, and hypoparathyroidism. Menstruation Irregularities: Infertility, miscarriages frequently 

 Wilson’s cirrhosis has a different trajectory than other types of cirrhosis for many patients. Wilson’s illness is caused by an excess of free copper in the liver. When excess copper is treated with zinc acetate maintenance medication, the liver condition usually stabilises or improves. 

Only approximately 5% of Wilson’s disease patients require a transplant. Liver failure is observed in two-thirds of the patients. The remaining patients have severe liver disease that does not respond well to medical treatment, those who discontinue treatment and deteriorate, or those who have severe cirrhosis complications like frequent GI bleeding from varices due to portal hypertension or low oxygenation to hepatopulmonary syndrome. 

Patients with Wilson disease have a life expectancy of 40 years if they are not treated, and they can live a normal life if they are treated properly. Patients who are diagnosed early on have a better chance of living longer.