# Vitiligo and Alopecia Areata After Donor Lymphocyte Infusions in a Child With Relapsed Acute Myeloid Leukemia

## TL;DR

A child with relapsed AML achieved long-term remission after donor lymphocyte infusions, but developed vitiligo and alopecia areata linked to autoimmune reactions from cGVHD.

## Contribution

Demonstrates DLI effectiveness in eradicating AML relapse and links vitiligo/alopecia areata to cGVHD-induced autoimmune reactions.

## Key findings

- DLI successfully eliminated molecular leukemia in a child with relapsed AML after HCT.
- Vitiligo and alopecia areata occurred due to autoimmune reactions from cGVHD following DLI.
- The patient remained in clinical and molecular remission for five years post-DLI.

## Abstract

Rarely do patients with chronic graft-versus-host disease (cGVHD) experience vitiligo and alopecia areata. Nevertheless, the exact cause of vitiligo and alopecia areata is still not fully understood. The patient experienced a relapse of acute myeloid leukemia (AML) following a second complete remission after undergoing HLA-6/8 mismatched unrelated donor hematopoietic cell transplantation (HCT). Achieving full donor chimerism was successful during the initial stages of the transplant. Nevertheless, the molecular evidence of measurable residual disease remained, prompting the administration of donor lymphocyte infusions (DLI) following a dose-escalation protocol. After three cycles of DLI given at two-month intervals, the circulating blasts eventually vanished. After the third DLI dose, vitiligo developed despite achieving molecular remission. The dermatologist confirmed the presence of vitiligo and alopecia areata, along with cutaneous cGVHD. The outcome was the complete elimination of the molecular presence, and the patient experienced both clinical and molecular remission for a period of five years following DLI. Based on our observations, it was found that DLI could effectively eradicate molecular leukemia in cases of AML relapse after HCT. The development of vitiligo and alopecia areata was influenced by the destruction of melanocytes due to autoimmune reactions caused by cGVHD.