On day 30 after allo-HSCT, the patient experienced steroid-refractory grade III acute GVHD of the skin and liver, which were treated with methylprednisolone, tacrolimus, ruxolitinib, and MMF. Cytomegalovirus polymerase chain reaction (CMV PCR) was detected on day 31 (937 copies/mL), with a peak level on day 40, measuring 57190 copies/mL. Intravenous immunoglobulin (IV IG) and oral valganciclovir were started since day 31 for CMV infection. It was difficult to differentiate liver GVHD from CMV hepatitis as liver biopsy was not performed due to thrombocytopenia. However, liver function improved while on IS, IV IG, and antiviral. Anti-hepatitis C virus, hepatitis B surface antigen, and total core antibody were not detected. Ultrasound of the hepatobiliary system showed no gallbladder obstruction or focal lesions in the liver. Skin biopsy confirmed cutaneous GVHD. He was discharged home after two months of stay in the ward. CMV infection resolved while ruxolitinib was discontinued during outpatient follow-up. Bone marrow smears, IP, trephine biopsy, and PET-CT scan on day 100 revealed the disease was in complete remission. Nevertheless, there was no repeat cytogenetic or FISH study due to an insufficient sample. There was difficulty in tapering tacrolimus, steroid, and MMF due to persistent lichenoid lesions at the buccal mucosa, hyperkeratotic plaques at the soft palate, recurrent oral ulcers, limited oral aperture due to sclerosis, poikilo-derma, palms and feet desquamation, lichen planus like skin eruption, and persistent liver transaminitis. The device for ECP was not available at that time.
Author(s) Details:
Ching Soon Teoh
Haematology Unit, Department of Internal Medicine, Hospital Pulau Pinang, Jalan Residensi, 10990
Georgetown, Penang, Malaysia.
Ai Sim Goh
Haematology Unit, Department of Internal Medicine, Hospital Pulau Pinang, Jalan Residensi, 10990
Georgetown, Penang, Malaysia.
Recent Global Research Developments in Stem Cell Transplantation and Graft-Versus-Host Disease
Chronic GVHD Advances:
- Chronic GVHD is a significant cause of morbidity and mortality after allogeneic hematopoietic cell transplantation.
- Symptoms and manifestations of chronic GVHD vary widely, and standard treatments mainly involve corticosteroids.
- Over the last two decades, advances have been made in defining the diagnosis, severity, and response criteria for clinical trials.
- Novel immunomodulatory and targeted therapies are being investigated, with several promising agents on the horizon for chronic GVHD treatment [1] .
Alternative Model for GVHD:
- New research challenges the prevailing hypothesis for how donor stem cell grafts cause GVHD.
- An alternative model could guide the development of novel therapies to manage GVHD [2] .
Acute GVHD Treatment Options:
- Acute GVHD occurs in approximately 50% of patients and remains a primary driver of non-relapse and transplant-related mortality.
- Researchers continue to explore new treatment options for acute GVHD[3] .
Standard for GVHD Prevention:
- A phase III study has set a new standard for GVHD prevention after allogeneic hematopoietic stem cell transplantation.
- Clinicians now have evidence-based guidelines to improve patient outcomes [4].
References
- Hamilton, B. K. (2021). Updates in chronic graft-versus-host disease. Hematology, 2021(1), 648-654.
- Study reframes understanding of graft-versus-host disease
https://www.sciencedaily.com/releases/2023/01/230130112356.htm - Patel, D.A., Crain, M., Pusic, I. et al. Acute Graft-versus-Host Disease: An Update on New Treatment Options. Drugs 83, 893–907 (2023). https://doi.org/10.1007/s40265-023-01889-2
- Penack, O., Marchetti, M., Ruutu, T., Aljurf, M., Bacigalupo, A., Bonifazi, F., … & Basak, G. W. (2020). Prophylaxis and management of graft versus host disease after stem-cell transplantation for haematological malignancies: updated consensus recommendations of the European Society for Blood and Marrow Transplantation. The Lancet Haematology, 7(2), e157-e167.