Secondary amyloidosis medical therapy
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Secondary amyloidosis Microchapters |
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Secondary amyloidosis medical therapy On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Roukoz A. Karam, M.D.[2]
Overview
Medical or surgical treatment of the underlying chronic infection or inflammatory disease is recommended among all patients who develop AA amyloidosis.
Medical Therapy
- Medical or surgical treatment of the underlying chronic infection or inflammatory disease is recommended among all patients who develop AA amyloidosis.[1]
- Aggressively treating the disease that is causing the excess amyloid protein can improve symptoms and slow down or halt the progression of the disease.
- Complications such as heart failure, renal failure, and other problems can sometimes be treated, when needed.
- Although the choice of therapy depends on the underlying cause of chronic inflammation, the aim is always to suppress production of SAA to within the normal range.
- Examples of treatments for the commonest disorders underlying AA amyloidosis, adapted from Rheumatic Diseases Clinics of North America:[2]
| Underlying Condition | Treatment Options | Examples |
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| Inflammatory arthritis | Conventional disease-modifying agents | |
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Other immunosuppressant agents |
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Biologic agents |
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| Periodic fevers | On-demand agents | |
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Colchicine (for familial mediterranean fever) |
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Biologic agents |
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| Inflammatory bowel disease | Conventional disease-modifying agents | |
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Biologic agents |
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Antibiotics |
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Biologic agents |
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Surgery |
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| Immunodeficiency | Immunoglobulins |
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Antibiotics |
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| Chronic infections | Antibiotics and surgery |
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Physiotherapy (in case of bronchiectasis) |
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| Immunodeficiency | Immunoglobulins |
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Antibiotics |
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| Neoplasia | Chemotherapy and surgery |
Varies according to type of cancer |
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Biologic agents (in Castleman disease) |
- Long-term inflammatory control can be accompanied by gradual regression of amyloid deposits and improvement in renal function.
- Currently a second clinical trial is in progress in order to evaluate a targeted inhibitor molecule, Kiacta, in the management of secondary amyloidosis.[3]
- Novel therapies aimed at promoting clearance of existing amyloid deposits soon may be an effective treatment approach.
References
- ↑ Desport E, Bridoux F, Sirac C, Delbes S, Bender S, Fernandez B; et al. (2012). "Al amyloidosis". Orphanet J Rare Dis. 7: 54. doi:10.1186/1750-1172-7-54. PMC 3495844. PMID 22909024.
- ↑ Papa R, Lachmann HJ (2018). "Secondary, AA, Amyloidosis". Rheum Dis Clin North Am. 44 (4): 585–603. doi:10.1016/j.rdc.2018.06.004. PMID 30274625.
- ↑ Hazenberg BP, Bijzet J, Limburg PC, Skinner M, Hawkins PN, Butrimiene I; et al. (2007). "Diagnostic performance of amyloid A protein quantification in fat tissue of patients with clinical AA amyloidosis". Amyloid. 14 (2): 133–40. doi:10.1080/13506120701260224. PMID 17577686.