Graft-versus-host disease medical therapy: Difference between revisions

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==Medical Therapy==
==Medical Therapy==
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, 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>


==References==
==References==

Revision as of 01:18, 26 May 2017

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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. Ruxolitinib, an inhibitor of Janus kinase 2 (JAK2), has been used.[2]

References

  1. Goker H, Haznedaroglu IC, Chao NJ (2001). "Acute graft-vs-host disease: pathobiology and management". Exp. Hematol. 29 (3): 259–77. PMID 11274753.
  2. 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.

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