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  • Presentation

Morbilliform Eruptions After Stem Cell Transplant: Differential Diagnosis and Management

Description

This talk reviews morbilliform eruptions after stem cell transplant, focusing on how to distinguish common causes in allogeneic versus autologous recipients. In allogeneic transplant patients, the key differential includes drug eruption, viral exanthem, acute graft-versus-host disease (GVHD), engraftment syndrome, and cutaneous eruption of lymphocyte recovery. Acute GVHD is primarily a clinical diagnosis because biopsy is often nonspecific; clues include a folliculocentric rash, involvement of the face, ears, palms/soles, dorsal hands and feet, and associated systemic findings such as diarrhea, nausea, weight loss, elevated liver enzymes, or hyperbilirubinemia. Risk factors include HLA mismatch, donor lymphocyte infusion, and tapering immunosuppression. Treatment depends on severity, with topical steroids for limited skin disease and systemic steroids as first-line for more extensive disease; ruxolitinib and extracorporeal photopheresis are options for refractory cases. In autologous transplant patients, acute GVHD is uncommon, so engraftment syndrome is more likely when fever, rash, edema/weight gain, and pulmonary findings appear around neutrophil recovery. Cutaneous eruption of lymphocyte recovery is another self-limited rash seen after chemotherapy-associated lymphocyte rebound, usually without major systemic involvement.

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Conclusions

  • After stem cell transplant, morbilliform eruptions require careful clinical correlation because drug eruption, viral exanthem, acute GVHD, engraftment syndrome, and lymphocyte recovery eruptions can look very similar.
  • In allogeneic transplant recipients, acute cutaneous GVHD is a leading concern and is suggested by folliculocentric rash, acral involvement such as palms, soles, ears, and scalp, and concurrent GI or liver abnormalities.
  • Time since transplant alone is not sufficient to diagnose GVHD, because modern classification relies more on morphology and systemic context than on a strict day-100 cutoff.
  • Skin biopsy has limited value for distinguishing acute GVHD from drug eruption because histology is often nonspecific, so treatment should not be delayed when clinical suspicion is high.
  • Facial involvement, especially with palms and soles, plus diarrhea and hyperbilirubinemia, strongly favors acute GVHD over morbilliform drug eruption.
  • General GVHD risk is increased by HLA mismatch, unrelated donors, older donor or recipient age, female donor to male recipient, total body irradiation, donor lymphocyte infusion, and tapering immunosuppression.
  • Newer conditioning regimens may reduce the overall incidence of acute GVHD.
  • Acute GVHD is treated first with systemic steroids when extensive or systemic, while skin-limited disease may be managed with topical steroids, calcineurin inhibitors, phototherapy, or topical ruxolitinib.
  • For steroid-refractory acute GVHD, ruxolitinib and other institution-dependent systemic therapies or extracorporeal photopheresis may be used.
  • In autologous transplant recipients, acute GVHD is uncommon, and engraftment syndrome is often a more likely explanation for fever, rash, edema, and pulmonary infiltrates around neutrophil recovery.
  • Engraftment syndrome is characterized by noninfectious fever, morbilliform rash, and edema or pulmonary edema during ANC recovery, and it is usually responsive to systemic steroids.
  • Cutaneous eruption of lymphocyte recovery is a self-limited morbilliform eruption that occurs 1 to 3 weeks after chemotherapy during lymphocyte recovery and usually lacks significant systemic involvement.
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