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The Oral Histopathological and Immunological Characteristics of a Xenogeneic Mouse Chronic Graft‐versus‐host Disease Model

The Oral Histopathological and Immunological Characteristics of a Xenogeneic Mouse Chronic Graft‐versus‐host Disease Model

Source : https://onlinelibrary.wiley.com/doi/10.1111/jop.13258

Qiaozhi Jiang , Xiangzhi Yong , Zhenmin Liu , Yuxi Zhou , Guocheng Mei , Qianming Chen , Tiantian Wu , Renchuan Tao , Corresponding Author Department of Periodontal and...


Inflammation in oral mucosa epithelium and salivary glands, and CD4 and CD8 T cells dominating infiltration are the main oral features in the xenogeneic cGVHD mouse model. The severity of oral histopathological lesions shows a dose and time correlation. These may be helpful to oral cGVHD research.

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Letermovir Prophylaxis and Cytomegalovirus Reactivation in Adult Hematopoietic Cell Transplant Recipients with and without Acute Graft Versus Host Disease - PubMed

Letermovir Prophylaxis and Cytomegalovirus Reactivation in Adult Hematopoietic Cell Transplant Recipients with and without Acute Graft Versus Host Disease - PubMed

Source : https://pubmed.ncbi.nlm.nih.gov/34771734/

1 Comprehensive Cancer Center, James Cancer Hospital Solove Research Institute, The Ohio State University, 460 West 10th St., Columbus, OH 43210, USA. 2 Franciscan Health Indianapolis, 8111 South Emerson Avenue,...


This data suggests that letermovir prophylaxis improves outcomes by preventing CS-CMVi in patients with aGVHD.

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Treating Acute Graft vs Host Disease

Graft-versus-host disease (GVHD) is a major complication of allogeneic hematopoietic stem cell transplantation (HSCT)caused by donor T cellsthat respond to the host polymorphic histocompatibility antigens as foreign, leading to inflammation and immune-mediated injury of host tissues. Acute GVHD (aGVHD) usually manifests within 100 days following HSCT, while chronic GVHD (cGVHD) generally occurs after 100 days and, has some features of autoimmune diseases. Clinical manifestations of aGVHD include skin rash or erythema, gastrointestinal symptoms (diarrhea, nausea, cramping, bleeding) and liver symptoms (hyperbilirubinemia and elevated serum levels of liver enzymes). Similar symptoms may occur in cGVHD, as well as nail, scalp, buccal mucosa, eye, and internal organ damage.





First line treatment for GVHD is topical and systemic corticosteroids. However, ~50% of aGVHD patients become steroid refractory, and broad spectrum immunosuppressants are commonly added ‘off label’ to a steroid regimen, leading to long-term side effects. Other options for steroid-refractory aGVHD include ruxolitib, a protein kinase inhibitor specific for JAK1 and JAK2, extracorporeal photopheresis, and various off-label treatments.





Given the choices, data, and potential risks - how do you treat steroid-refractory aGVHD ?





References



• Abedin, S. and Hamadani, M., 2020. Experimental Pharmaceuticals for Steroid-Refractory Acute Graft-versus-Host Disease. J. Exp. Pharmacology, 12, pp. 549-557. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7705269/



 



 


  • 4yr
    ruxolitinib, ibrutinib, rituximab, ECP, among others are all options for steroid refractory GvHD
  • 4yr
    Is there a way to risk stratify patients with steroid refractory GVHD? Do certain respond more favorably to ruxolitinib vs rituximab vs imbruvica ?

Show More Comments

  • Saved
Treating Acute Graft vs Host Disease

Graft-versus-host disease (GVHD) is a major complication of allogeneic hematopoietic stem cell transplantation (HSCT)caused by donor T cellsthat respond to the host polymorphic histocompatibility antigens as foreign, leading to inflammation and immune-mediated injury of host tissues. Acute GVHD (aGVHD) usually manifests within 100 days following HSCT, while chronic GVHD (cGVHD) generally occurs after 100 days and, has some features of autoimmune diseases. Clinical manifestations of aGVHD include skin rash or erythema, gastrointestinal symptoms (diarrhea, nausea, cramping, bleeding) and liver symptoms (hyperbilirubinemia and elevated serum levels of liver enzymes). Similar symptoms may occur in cGVHD, as well as nail, scalp, buccal mucosa, eye, and internal organ damage.


First line treatment for GVHD is topical and systemic corticosteroids. However, ~50% of aGVHD patients become steroid refractory, and broad spectrum immunosuppressants are commonly added ‘off label’ to a steroid regimen, leading to long-term side effects. Other options for steroid-refractory aGVHD include ruxolitib, a protein kinase inhibitor specific for JAK1 and JAK2, extracorporeal photopheresis, and various off-label treatments.


Given the choices, data, and potential risks - how do you treat steroid-refractory aGVHD ?


References

• Abedin, S. and Hamadani, M., 2020. Experimental Pharmaceuticals for Steroid-Refractory Acute Graft-versus-Host Disease. J. Exp. Pharmacology, 12, pp. 549-557. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7705269/

 

 

  • 4yr
    ruxolitinib, ibrutinib, rituximab, ECP, among others are all options for steroid refractory GvHD
  • 4yr
    Is there a way to risk stratify patients with steroid refractory GVHD? Do certain respond more favorably to ruxolitinib vs rituximab vs imbruvica ?

Show More Comments

  • Saved
Treating Acute Graft vs Host Disease

Graft-versus-host disease (GVHD) is a major complication of allogeneic hematopoietic stem cell transplantation (HSCT)caused by donor T cellsthat respond to the host polymorphic histocompatibility antigens as foreign, leading to inflammation and immune-mediated injury of host tissues. Acute GVHD (aGVHD) usually manifests within 100 days following HSCT, while chronic GVHD (cGVHD) generally occurs after 100 days and, has some features of autoimmune diseases. Clinical manifestations of aGVHD include skin rash or erythema, gastrointestinal symptoms (diarrhea, nausea, cramping, bleeding) and liver symptoms (hyperbilirubinemia and elevated serum levels of liver enzymes). Similar symptoms may occur in cGVHD, as well as nail, scalp, buccal mucosa, eye, and internal organ damage.





First line treatment for GVHD is topical and systemic corticosteroids. However, ~50% of aGVHD patients become steroid refractory, and broad spectrum immunosuppressants are commonly added ‘off label’ to a steroid regimen, leading to long-term side effects. Other options for steroid-refractory aGVHD include ruxolitib, a protein kinase inhibitor specific for JAK1 and JAK2, extracorporeal photopheresis, and various off-label treatments.





Given the choices, data, and potential risks - how do you treat steroid-refractory aGVHD ?





References



• Abedin, S. and Hamadani, M., 2020. Experimental Pharmaceuticals for Steroid-Refractory Acute Graft-versus-Host Disease. J. Exp. Pharmacology, 12, pp. 549-557. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7705269/



 



 


  • 4yr
    ruxolitinib, ibrutinib, rituximab, ECP, among others are all options for steroid refractory GvHD
  • 4yr
    Is there a way to risk stratify patients with steroid refractory GVHD? Do certain respond more favorably to ruxolitinib vs rituximab vs imbruvica ?

Show More Comments