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Introduction Free copper accumulation in many tissues (liver, brain, cornea, joints) also known as hepatolenticular degeneration mutation in ATP7B results in inadequate copper excretion by liver into bile failure of copper to enter circulation bound to ceruloplasmin free copper generates free radicals that damage tissues see Metabolism of copper topic AR inheritance Presentation Symptoms Parkinson-like symptoms secondary to copper desposits in putamen hemiballismus secondary to copper desposits in subthalamic nucleus dementia secondary to copper desposits in cerebral cortex Physical exam cirrhosis corneal deposits on slit lamp examination Evaluation total serum copper due to ceruloplasmin serum non-ceruloplasmin bound copper urine/serum free copper hemolytic anemia Liver Biopsy If performed will show increased hepatic copper Treatment Medical ammonium tetrathiomolybdate facilitates urinary excretion of copper copper chelating agent trientine copper chelating agent zinc competes with copper for absorbtion in the gut via the same transporter Surgical Consider liver transplantation as clinical condition deteriorates Prognosis, Prevention, and Complications At risk for liver disease hepatitis cirrhosis carcinoma (hepatocellular) Also at risk for Fanconi's disease of the proximal tubules

It is recommended to start with a low dose of the peptide combination and gradually increase it over time in order to minimize the risk of side effects

The choice often depends on whether the primary concern is local GI healing versus systemic chronic inflammation affecting multiple systems

A Graph to show the half life of a drug On this graph we can see that it takes one hour for the drug concentration in the plasma to decrease by half