Secondary amyloidosis medical therapy: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{ | {{Secondary amyloidosis}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}} {{RAK}} | ||
==Overview== | ==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.<ref name="pmid22909024">{{cite journal| author=Desport E, Bridoux F, Sirac C, Delbes S, Bender S, Fernandez B et al.| title=Al amyloidosis. | journal=Orphanet J Rare Dis | year= 2012 | volume= 7 | issue= | pages= 54 | pmid=22909024 | doi=10.1186/1750-1172-7-54 | pmc=3495844 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22909024 }}</ref> | |||
* 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:<ref name="pmid30274625">{{cite journal| author=Papa R, Lachmann HJ| title=Secondary, AA, Amyloidosis. | journal=Rheum Dis Clin North Am | year= 2018 | volume= 44 | issue= 4 | pages= 585-603 | pmid=30274625 | doi=10.1016/j.rdc.2018.06.004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30274625 }} </ref> | |||
{| | |||
| valign="top" | | |||
|+ | |||
! style="background: #4479BA;" |{{fontcolor|#FFF|Underlying Condition}} | |||
! style="background: #4479BA;" |{{fontcolor|#FFF|Treatment Options}} | |||
! style="background: #4479BA;" |{{fontcolor|#FFF|Examples}} | |||
|- | |||
| rowspan="3" style="padding: 5px 5px; background: #DCDCDC;" |Inflammatory arthritis | |||
| style="padding: 5px 5px; background: #F5F5F5;" | Conventional disease-modifying agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Gold]] | |||
*[[Hydroxychloroquine]] [[sulfasalazine]] | |||
*[[Azathioprine]] | |||
*[[Methotrexate]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Other immunosuppressant agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Cyclosporine]] | |||
*[[Cyclophosphamide]] | |||
*[[Mycophenolate]] | |||
*[[Leflunomide]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Biologic agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Infliximab]] | |||
*[[Etanercept]] | |||
*[[Adalimumab]] | |||
*[[Tocilizumab]] | |||
*[[Rituximab]] | |||
|- | |||
| rowspan="3" style="padding: 5px 5px; background: #DCDCDC;" |Periodic fevers | |||
| style="padding: 5px 5px; background: #F5F5F5;" | On-demand agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Nonsteroidal anti-inflammatory drugs]] | |||
*[[Prednisone]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Colchicine (for familial mediterranean fever) | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
* [[Colchicine]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Biologic agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Anakinra]] | |||
*[[Canakinumab]] | |||
|- | |||
| rowspan="5" style="padding: 5px 5px; background: #DCDCDC;" |Inflammatory bowel disease | |||
| style="padding: 5px 5px; background: #F5F5F5;" | Conventional disease-modifying agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Sulfasalazine]] | |||
*[[Mesalazine]] | |||
*[[Azathioprine]] | |||
*[[Methotrexate toxicity|Methotrexate]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Biologic agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Infliximab]] | |||
*[[Adalimumab]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Antibiotics | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Metronidazole]] | |||
*[[Ciprofloxacin]] | |||
*[[Azithromycin]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Biologic agents | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Infliximab]] | |||
*[[Adalimumab]] | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Surgery | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
* ileo-cecal resection and primary reconstruction | |||
|- | |||
| rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Immunodeficiency | |||
| style="padding: 5px 5px; background: #F5F5F5;" | Immunoglobulins | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
* | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Antibiotics | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Cotrimoxazole]] | |||
*[[Miconazole]] | |||
|- | |||
| rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Chronic infections | |||
| style="padding: 5px 5px; background: #F5F5F5;" | Antibiotics and surgery | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
* | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Physiotherapy (in case of bronchiectasis) | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
* | |||
|- | |||
| rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Immunodeficiency | |||
| style="padding: 5px 5px; background: #F5F5F5;" | Immunoglobulins | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
* | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Antibiotics | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Cotrimoxazole]] | |||
*[[Miconazole]] | |||
|- | |||
| rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Neoplasia | |||
| style="padding: 5px 5px; background: #F5F5F5;" | Chemotherapy and surgery | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Varies according to type of cancer | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
Biologic agents (in Castleman disease) | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*[[Tocilizumab]] | |||
|- | |||
|} | |||
* 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.<ref name="pmid17577686">{{cite journal| author=Hazenberg BP, Bijzet J, Limburg PC, Skinner M, Hawkins PN, Butrimiene I et al.| title=Diagnostic performance of amyloid A protein quantification in fat tissue of patients with clinical AA amyloidosis. | journal=Amyloid | year= 2007 | volume= 14 | issue= 2 | pages= 133-40 | pmid=17577686 | doi=10.1080/13506120701260224 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17577686 }}</ref> | |||
*Novel therapies aimed at promoting clearance of existing amyloid deposits soon may be an effective treatment approach. | |||
Latest revision as of 20:18, 1 November 2019
Secondary amyloidosis Microchapters |
Diagnosis |
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Treatment |
Case Studies |
Secondary amyloidosis medical therapy On the Web |
American Roentgen Ray Society Images of Secondary amyloidosis medical therapy |
Risk calculators and risk factors for Secondary amyloidosis medical therapy |
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 |
---|---|---|
Inflammatory arthritis | Conventional disease-modifying agents | |
Other immunosuppressant agents |
||
Biologic agents |
||
Periodic fevers | On-demand agents | |
Colchicine (for familial mediterranean fever) |
||
Biologic agents |
||
Inflammatory bowel disease | Conventional disease-modifying agents | |
Biologic agents |
||
Antibiotics |
||
Biologic agents |
||
Surgery |
| |
Immunodeficiency | Immunoglobulins |
|
Antibiotics |
||
Chronic infections | Antibiotics and surgery |
|
Physiotherapy (in case of bronchiectasis) |
| |
Immunodeficiency | Immunoglobulins |
|
Antibiotics |
||
Neoplasia | Chemotherapy and surgery |
Varies according to type of cancer |
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.