AA Amyloidosis is caused by the accumulation of Serum Amyloid A protein into amyloid fibrils causing organ dysfunction. It is usually a complication of patients who have states of chronic inflammation as the inflammation causes a heightened production of this particular protein. Clinically, patients with AA amyloidosis present with kidney disease such as proteinuria or renal failure. Patients who have chronic rheumatological conditions such as SLE, rheumatoid arthritis, or chronic infections such as bronchiectasis, osteomyelitis or tuberculosis that are not controlled are at risk. The treatment is focused upon controlling the causative condition. By controlling the infection or rheumatological condition, the Amyloid A protein concentration within the blood stream will reduce and the amyloid process will slow. There is a new drug in development that has shown promise to treat people with this condition. A clinical trial is currently open here at Cedars-Sinai for such patients. Finally, patients with a diagnosis of FMF (Familial Mediterranean Fever) can also develop this amyloid complication. Drug treatment, typically with colchicine, to control this inherited condition will also slow the development of amyloidosis in these patients.
In secondary amyloidosis, the goal is to treat the underlying inflammatory condition. In cases where this is not possible, other agents are being developed to help slow the deposition of the Amyloid A protein in the body. We currently have a clinical trial using a drug that has shown promise in one research trial for patients with AA Amyloidosis and kidney disease. Interested individuals can contact our research office.