Graft-versus-host disease medical therapy: Difference between revisions
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Intravenously administered [[corticosteroids]], such as [[prednisone]], are the standard of care in acute GVHD<ref>{{cite journal |author=Goker H, Haznedaroglu IC, Chao NJ |title=Acute graft-vs-host disease: pathobiology and management |journal=Exp. Hematol. |volume=29 |issue=3 |pages=259–77 |year=2001 |pmid=11274753 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0301-472X(00)00677-9}}</ref> and chronic GVHD. The use of these [[corticosteroids]] is designed to suppress the T-cell mediated immune onslaught on the host tissues; however in high doses this immune-suppression raises the risk of infections and cancer relapse. Therefore it is desirable to taper off the post-transplant high level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect. | Intravenously administered [[corticosteroids]], such as [[prednisone]], are the standard of care in acute GVHD<ref>{{cite journal |author=Goker H, Haznedaroglu IC, Chao NJ |title=Acute graft-vs-host disease: pathobiology and management |journal=Exp. Hematol. |volume=29 |issue=3 |pages=259–77 |year=2001 |pmid=11274753 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0301-472X(00)00677-9}}</ref> and chronic GVHD. The use of these [[corticosteroids]] is designed to suppress the T-cell mediated immune onslaught on the host tissues; however in high doses this immune-suppression raises the risk of infections and cancer relapse. Therefore it is desirable to taper off the post-transplant high level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect. | ||
For steroid-refractory GvHD, there are a few options available. Ruxolitinib | For steroid-refractory GvHD, there are a few options available, though the data is not robust. | ||
***Ruxolitinib: This is an inhibitor of Janus kinase 2 (JAK2), has been used.<ref name="pmid28444730">{{cite journal| author=Assouan D, Lebon D, Charbonnier A, Royer B, Marolleau JP, Gruson B| title=Ruxolitinib as a promising treatment for corticosteroid-refractory graft-versus-host disease. | journal=Br J Haematol | year= 2017 | volume= | issue= | pages= | pmid=28444730 | doi=10.1111/bjh.14679 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28444730 }} </ref> | |||
***Alemtuzumab: This is an antibody to CD52, which is found to lymphocytes. Alemtuzumab has been used in patients with [[chronic lymphocytic leukemia]] and [[T cell pro-lymphocytic leukemia]].<ref name="pmid28444730">{{cite journal| author=Assouan D, Lebon D, Charbonnier A, Royer B, Marolleau JP, Gruson B| title=Ruxolitinib as a promising treatment for corticosteroid-refractory graft-versus-host disease. | journal=Br J Haematol | year= 2017 | volume= | issue= | pages= | pmid=28444730 | doi=10.1111/bjh.14679 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28444730 }} </ref> | |||
***mTOR inhibitors: These agents inhibitor the mammalian target of rapamycin. Everolimus is an mTOR inhibitor.<ref name="pmid28444730">{{cite journal| author=Assouan D, Lebon D, Charbonnier A, Royer B, Marolleau JP, Gruson B| title=Ruxolitinib as a promising treatment for corticosteroid-refractory graft-versus-host disease. | journal=Br J Haematol | year= 2017 | volume= | issue= | pages= | pmid=28444730 | doi=10.1111/bjh.14679 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28444730 }} </ref> | |||
***Rituximab: This is a monoclonal antibody to CD20, which is found on B cells. Rituximab is known for its immunomodulatory effects and is currently FDA-approved for [[non-Hodgkin lymphoma]], [[chronic lymphocytic leukemia]], [[rheumatoid arthritis]], [[Wegener's granulomatosis]], [[microscopic polyangitis]], and [[immune thrombocytopenia purpura]].<ref name="pmid28444730">{{cite journal| author=Assouan D, Lebon D, Charbonnier A, Royer B, Marolleau JP, Gruson B| title=Ruxolitinib as a promising treatment for corticosteroid-refractory graft-versus-host disease. | journal=Br J Haematol | year= 2017 | volume= | issue= | pages= | pmid=28444730 | doi=10.1111/bjh.14679 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28444730 }} </ref> | |||
***Anti-TNF agents: Examples of anti-TNF agents include etanercept and adalilumab. TNF is involved in the inflammatory response, so TNF blockade results in immunosuppression.<ref name="pmid28444730">{{cite journal| author=Assouan D, Lebon D, Charbonnier A, Royer B, Marolleau JP, Gruson B| title=Ruxolitinib as a promising treatment for corticosteroid-refractory graft-versus-host disease. | journal=Br J Haematol | year= 2017 | volume= | issue= | pages= | pmid=28444730 | doi=10.1111/bjh.14679 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28444730 }} </ref> | |||
==References== | ==References== | ||
Revision as of 01:29, 26 May 2017
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Graft-versus-host disease |
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Differentiating Graft-versus-host disease from other Diseases |
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Graft-versus-host disease medical therapy On the Web |
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American Roentgen Ray Society Images of Graft-versus-host disease medical therapy |
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Risk calculators and risk factors for Graft-versus-host disease medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Medical Therapy
Intravenously administered corticosteroids, such as prednisone, are the standard of care in acute GVHD[1] and chronic GVHD. The use of these corticosteroids is designed to suppress the T-cell mediated immune onslaught on the host tissues; however in high doses this immune-suppression raises the risk of infections and cancer relapse. Therefore it is desirable to taper off the post-transplant high level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect.
For steroid-refractory GvHD, there are a few options available, though the data is not robust.
- Ruxolitinib: This is an inhibitor of Janus kinase 2 (JAK2), has been used.[2]
- Alemtuzumab: This is an antibody to CD52, which is found to lymphocytes. Alemtuzumab has been used in patients with chronic lymphocytic leukemia and T cell pro-lymphocytic leukemia.[2]
- mTOR inhibitors: These agents inhibitor the mammalian target of rapamycin. Everolimus is an mTOR inhibitor.[2]
- Rituximab: This is a monoclonal antibody to CD20, which is found on B cells. Rituximab is known for its immunomodulatory effects and is currently FDA-approved for non-Hodgkin lymphoma, chronic lymphocytic leukemia, rheumatoid arthritis, Wegener's granulomatosis, microscopic polyangitis, and immune thrombocytopenia purpura.[2]
- Anti-TNF agents: Examples of anti-TNF agents include etanercept and adalilumab. TNF is involved in the inflammatory response, so TNF blockade results in immunosuppression.[2]
References
- ↑ Goker H, Haznedaroglu IC, Chao NJ (2001). "Acute graft-vs-host disease: pathobiology and management". Exp. Hematol. 29 (3): 259–77. PMID 11274753.
- ↑ 2.0 2.1 2.2 2.3 2.4 Assouan D, Lebon D, Charbonnier A, Royer B, Marolleau JP, Gruson B (2017). "Ruxolitinib as a promising treatment for corticosteroid-refractory graft-versus-host disease". Br J Haematol. doi:10.1111/bjh.14679. PMID 28444730.