IMS 2023 | Diagnosis and potential therapeutic options for AA amyloidosis
Nelson Leung, MD, Mayo Clinic, Rochester, MN, explains that AA amyloidosis is characterized by a rise in serum amyloid A (SAA) protein, usually occurring as a result of chronic infection, inflammatory disease or genetic predisposition. Dr Leung highlights that in order to treat AA amyloidosis, the underlying disease must be treated. For example, anti-cytokine therapies such as tocilizumab and anakinra have been effective at suppressing inflammation. This interview took place at the 20th International Myeloma Society (IMS) Annual Meeting, held in Athens, Greece.
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Transcript (edited for clarity)
The cause of AA amyloidosis is a rise in the serum SAA protein, and this is usually the result of one of three etiologies. The first one is infection: chronic infection such as osteomyelitis or chronic pulmonary infection, tuberculosis is another common cause of AA amyloidosis. The second category is inflammatory diseases. These are usually autoimmune diseases such as Crohn’s disease, rheumatoid arthritis, or ankylosing spondylitis...
The cause of AA amyloidosis is a rise in the serum SAA protein, and this is usually the result of one of three etiologies. The first one is infection: chronic infection such as osteomyelitis or chronic pulmonary infection, tuberculosis is another common cause of AA amyloidosis. The second category is inflammatory diseases. These are usually autoimmune diseases such as Crohn’s disease, rheumatoid arthritis, or ankylosing spondylitis. Finally, there is a genetic component. These are typically patients with familial periodic fever syndrome, such as familial Mediterranean fever, TRAP syndrome, Muckle-Wells syndrome (MWS), as well as hyper-IgD syndrome. In order to treat renal AA amyloidosis, you need to treat the underlying disease. For example, in patients with infection, eradication of the infection is essential for resolution of the AA amyloidosis. In terms of the inflammatory diseases, and the hereditary periodic fever syndrome, anti-cytokine therapies have been very effective. Anti-IL-6 such as tocilizumab, has been used quite frequently, and anti-IL-1 with anakinra. These have been found to be quite effective at suppressing the inflammation which then causes a decrease in SAA levels.
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