Chronic Graft-Versus-Host Disease Mimicking Psoriasis in a Patient with Hemophagocytic Lymphohistiocytosis

Abstract

Graft-versus-host disease (GVHD) is a common complication of bone marrow transplantation (BMT) that can be classified as acute or chronic. Chronic GVHD, which usually occurs more than 3 months after BMT, includes typical lichenoid or sclerodermatous lesions. Psoriasiform eruption is a rare clinical manifestation of chronic GVHD, and there have been no reports of psoriasiform chronic GVHD associated with hemophagocytic lymphohistiocytosis. A 33-year-old woman who was diagnosed with hemophagocytic lymphohistiocytosis 10 years ago visited our outpatient clinic with psoriasiform eruption over her entire body. She underwent allogeneic BMT 7 months previously from her sibling. Skin biopsy was performed on the lesion, and the histological features suggested GVHD. The psoriasiform lesions improved with narrow-band ultraviolet B phototherapy, with secondary vitiligo remaining on the corresponding locations.

Psoriasiform graft‐versus‐host disease distributed along Blaschko's lines

“…His past medical history was significant for aplastic ane- initially unresponsive to triamcinolone 0.1% cream, but was later controlled and improved with clobetasol 0.05% gel and ruxolitinib 10 mg. lesions as well as in the affected skin of patients with GVHD. 2,9 The latter suggestion extrapolates its hypothesis from evidence of psoriatic exacerbations in patients with acquired immunodeficiency syndrome, who were also shown to have decreased LC, 10 along with evidence of inflammatory reactions when LC are actively depleted from the skin. 11 The pathogenesis of psoriasis is heavily dependent on the roles of T-helper cells (Th) and multiple cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-2, IL-6, IL-12, IL-15, IL-23 and interferon-γ (IFN-γ).…”

“…While the etiology of a psoriasiform type of cGVHD is lacking elucidation, 1 hypothesis postulates that a donor lymphocytic interaction induces recipient keratinocyte hyperproliferation, resulting in an eruption clinically similar to psoriasis. Another proposal suggests a correlation with a decreased number of antigen‐presenting Langerhans cells (LC) in the epidermis, as this has been reported in psoriatic lesions as well as in the affected skin of patients with GVHD .…”

“…While the etiology of a psoriasiform type of cGVHD is lacking elucidation, 1 hypothesis postulates that a donor lymphocytic interaction induces recipient keratinocyte hyperproliferation, resulting in an eruption clinically similar to psoriasis. Another proposal suggests a correlation with a decreased number of antigen‐presenting Langerhans cells (LC) in the epidermis, as this has been reported in psoriatic lesions as well as in the affected skin of patients with GVHD . The latter suggestion extrapolates its hypothesis from evidence of psoriatic exacerbations in patients with acquired immunodeficiency syndrome, who were also shown to have decreased LC, along with evidence of inflammatory reactions when LC are actively depleted from the skin .…”

“…Cutaneous involvement of cGVHD presents varied features from lichenoid to sclerodermoid changes that some clinicians may find difficult to accurately diagnose, particularly when the cGVHD mimics other disease processes. Psoriatic eruptions of this disease are particularly rare, with fewer than 6 cases presented in the literature . There have also been reports of both the development and the remission of psoriasis itself following stem cell transplant, further obfuscating delineation and the clinical diagnosis .…”

“…Psoriatic eruptions of this disease are particularly rare, with fewer than 6 cases presented in the literature. [2][3][4][5][6] There have also been reports of both the development and the remission of psoriasis itself following stem cell transplant, further obfuscating delineation and the clinical diagnosis. [5][6][7][8] One such case demonstrated the acquisition of psoriasis from a donor who already carried the diagnosis, emphasizing the concept of adoptive autoimmunity.…”