Secondary amyloidosis medical therapy: Difference between revisions
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==Medical Therapy== | ==Medical Therapy== | ||
* Medical or surgical treatment of the underlying chronic infection or inflammatory disease is recommended among all patients who develop AA amyloidosis. | * 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. | * 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. | * 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. | *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:<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> | *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> | ||
{| | {| | ||
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| style="padding: 5px 5px; background: #F5F5F5;" | Conventional disease-modifying agents | | style="padding: 5px 5px; background: #F5F5F5;" | Conventional disease-modifying agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Gold | *[[Gold]] | ||
*Hydroxychloroquine sulfasalazine | *[[Hydroxychloroquine]] [[sulfasalazine]] | ||
*Azathioprine | *[[Azathioprine]] | ||
*Methotrexate | *[[Methotrexate]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Other immunosuppressant agents | Other immunosuppressant agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Cyclosporine | *[[Cyclosporine]] | ||
*Cyclophosphamide | *[[Cyclophosphamide]] | ||
*Mycophenolate | *[[Mycophenolate]] | ||
*Leflunomide | *[[Leflunomide]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Biologic agents | Biologic agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Infliximab | *[[Infliximab]] | ||
*Etanercept | *[[Etanercept]] | ||
*Adalimumab | *[[Adalimumab]] | ||
*Tocilizumab | *[[Tocilizumab]] | ||
*Rituximab | *[[Rituximab]] | ||
|- | |- | ||
| rowspan="3" style="padding: 5px 5px; background: #DCDCDC;" |Periodic fevers | | 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;" | On-demand agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Nonsteroidal anti-inflammatory drugs | *[[Nonsteroidal anti-inflammatory drugs]] | ||
*Prednisone | *[[Prednisone]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Colchicine (for familial mediterranean fever) | Colchicine (for familial mediterranean fever) | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Colchicine | * [[Colchicine]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Biologic agents | Biologic agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Anakinra | *[[Anakinra]] | ||
*Canakinumab | *[[Canakinumab]] | ||
|- | |- | ||
| rowspan="5" style="padding: 5px 5px; background: #DCDCDC;" |Inflammatory bowel disease | | 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;" | Conventional disease-modifying agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Sulfasalazine | *[[Sulfasalazine]] | ||
*Mesalazine | *[[Mesalazine]] | ||
*Azathioprine | *[[Azathioprine]] | ||
*Methotrexate | *[[Methotrexate toxicity|Methotrexate]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Biologic agents | Biologic agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Infliximab | *[[Infliximab]] | ||
*Adalimumab | *[[Adalimumab]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Antibiotics | Antibiotics | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Metronidazole | *[[Metronidazole]] | ||
*Ciprofloxacin | *[[Ciprofloxacin]] | ||
*Azithromycin | *[[Azithromycin]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Biologic agents | Biologic agents | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Infliximab | *[[Infliximab]] | ||
*Adalimumab | *[[Adalimumab]] | ||
|- | |- | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
Surgery | Surgery | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
ileo-cecal resection and primary reconstruction | * ileo-cecal resection and primary reconstruction | ||
|- | |- | ||
| rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Immunodeficiency | | rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Immunodeficiency | ||
| Line 103: | Line 103: | ||
Antibiotics | Antibiotics | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Cotrimoxazole | *[[Cotrimoxazole]] | ||
*Miconazole | *[[Miconazole]] | ||
|- | |- | ||
| rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Chronic infections | | rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Chronic infections | ||
| Line 124: | Line 124: | ||
Antibiotics | Antibiotics | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
*Cotrimoxazole | *[[Cotrimoxazole]] | ||
*Miconazole | *[[Miconazole]] | ||
|- | |- | ||
| rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Neoplasia | | rowspan="2" style="padding: 5px 5px; background: #DCDCDC;" | Neoplasia | ||
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Biologic agents (in Castleman disease) | Biologic agents (in Castleman disease) | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
* Tocilizumab | *[[Tocilizumab]] | ||
|- | |- | ||
|} | |} | ||
* Long-term inflammatory control can be accompanied by gradual regression of amyloid deposits and improvement in renal function. | * 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. | *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. | *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
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Secondary amyloidosis Microchapters |
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Secondary amyloidosis medical therapy On the Web |
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American Roentgen Ray Society Images of Secondary amyloidosis medical therapy |
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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.