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I cured my own GVHD

Outline. CaseOverview of GVHClinicalPathophysiologyOverview of current aGVH managementPotential of autologous stem cell infusion as treatment. Case. A 29 year old male was diagnosed with acute promyelocytic leukemia in March 2005. He was successfully induced and consolidated with standard ther

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I cured my own GVHD

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    1. I cured my own GVHD Jeevan Sekhar Hem/Onc Grand Rounds March 20, 2009

    2. Outline Case Overview of GVH Clinical Pathophysiology Overview of current aGVH management Potential of autologous stem cell infusion as treatment

    3. Case A 29 year old male was diagnosed with acute promyelocytic leukemia in March 2005. He was successfully induced and consolidated with standard therapy including ATRA. Autologous stem cells collected in 8/06 3/07 he relapsed and dz persisted despite 2 cycles of arsenic. Gemtuzumab (Mylotarg) worked. Concern that dz was too refractory so got allo transplant w/ bu/cy conditioning

    4. Case cont’d D+ 30, he developed grade IV GI acute GVH Treated w/ methylpred, pentostatin, tacrolimus, budesonide, beclomethasone. Nothing worked. Then idea to ablate the graft. Reconditioned with fludarabine, cytarabine, and 200 cGy TBI and reinfused with autologous stem cells in 12/07. In 4-6 weeks, GVH improved In 11/07, chimerism studies revealed full donor engraftment. In 12/07 chimerism studies after autologous SCT showed only recipient cells. At the end of 12/07, biopsy revealed grade II GVH.

    5. Acute GVH Mainstay of treatment is high dose steroids However, only about 50% respond, the rest are steroid refractory. Mortality with steroid refractory GVH is about 50% Thus, intense area to be addressed to improve post-transplant survival

    6. Overview of acute GVH Risk up to 50-60% in matched related donors despite immunosuppresant prophylaxis Risk factors: Increased age Degree of mismatch Doses of prophylactic immunosuppresants Source of cells Conditioning regimen – more intense, the greater the risk

    7. Clinical Manifestations of Acute GVH Skin First manifestation Most common Si/Sx Maculopapular rash usually at the time of engraftment. Involves epidermal and dermal layers T cell infiltrate Severe disease includes bullae formation and desquamation

    8. Clinical Manifestations cont’d -Liver- Second most common Unlikely to have liver manifestation without skin. Manifested as abnormal liver tests Definitive diagnosis only by Bx

    9. Clinical Manifestations Cont’d - GI Tract- GI Tract Most commonly lower GI tract Non-specific symptoms: Diarrhea Abd Pain Diagnosis by rectal bx showing crypt necrosis and epithelial denudation similar to skin GVH

    10. Pictures

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