Background: Graft-versus-host disease (GVHD) is a systemic disease, and skin is often one of the target organs. An atopic dermatitis (AD)-like presentation has never to our knowledge been reported.
Objective: We sought to describe an AD-like presentation of cutaneous GVHD.
Methods: Data on 11 patients with an AD-like presentation of GVHD were collected. The clinical and laboratory findings were retrospectively studied.
Results: All 11 patients developed skin lesions after hematopoietic stem-cell transplantation. The skin lesions occurred between 2 to 12 months after transplantation. Eight patients received their transplant from a first-degree family member; 3 received their transplant from an unrelated donor. The skin lesions were pruritic and suggestive of AD, whereas the histology showed features of AD and GVHD. The lesions responded to topical and systemic anti-inflammatory and immunosuppressive therapy and phototherapy.
Limitations: The number of patients is small and the study is retrospective.
Conclusions: AD-like GVHD might represent a novel form of chronic cutaneous GVHD and responds well to treatment.
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http://dx.doi.org/10.1016/j.jaad.2012.12.970 | DOI Listing |
PLoS One
January 2025
Department of Surgical Pathology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Immunologic bile duct destruction is a pathogenic condition associated with vanishing bile duct syndrome (VBDS) after liver transplantation and hematopoietic stem-cell transplantation. As the bile acid receptor sphingosine 1-phosphate receptor 2 (S1PR2) plays a critical role in recruitment of bone marrow-derived monocytes/macrophages to sites of cholestatic liver injury, S1PR2 expression was examined using cultured macrophages and patient tissues. Bile canaliculi destruction precedes intrahepatic ductopenia; therefore, we focused on hepatocyte S1PR2 and the downstream RhoA/Rho kinase 1 (ROCK1) signaling pathway and bile canaliculi alterations using three-dimensional hepatocyte culture models that form obvious bile canaliculus-like networks.
View Article and Find Full Text PDFBlood Adv
January 2025
The Jackson Laboratory, United States.
Gut dysbiosis is linked to mortality and the development of graft-versus-host disease (GVHD) after hematopoietic stem cell transplantation (HSCT), but the impact of cutaneous dysbiosis remains unexplored. We performed a pilot observational study and obtained retroauricular and forearm skin swabs from 12 adult patients prior to conditioning chemotherapy/radiation, and at 1-week, 1-month and 3-months after allogeneic HSCT, and performed shotgun metagenomic sequencing. The cutaneous microbiome among HSCT patients was enriched for gram-negative bacteria such as E coli and Pseudomonas, fungi, and viruses.
View Article and Find Full Text PDFRev Med Chil
September 2024
Red UC Christus, Pontificia Universidad Católica de Chile, Santiago, Chile.
Unlabelled: Allogeneic transplantation (HSCT) is a curative option for several hematological diseases. Our center has privileged the use of identical family donors (IFD) or haploidentical (HD) donors. However, the chances of finding family donors may be challenging in small families or unsuitable donors.
View Article and Find Full Text PDFBioengineering (Basel)
January 2025
Department of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA 90095, USA.
Chimeric Antigen Receptor (CAR)-engineered T (CAR-T) cell therapy represents a highly promising modality within the domain of cancer treatment. CAR-T cell therapy has demonstrated notable efficacy in the treatment of hematological malignancies, solid tumors, and various infectious diseases. However, current CAR-T cell therapy is autologous, which presents challenges related to high costs, time-consuming manufacturing processes, and the necessity for careful patient selection.
View Article and Find Full Text PDFJ Am Acad Dermatol
January 2025
Division of Blood and Marrow Transplantation and Cellular Therapy, Department of Medicine, Stanford University, Stanford, CA; Department of Dermatology, Stanford University, Stanford, CA. Electronic address:
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