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Systemic Diseases and the Skin
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Jana Kazandjieva, Razvigor Darlenski, Nikolai Tsankov
The skin manifestations of acute and chronic graft versus host disease may occur in recipients of allogeneic hematopoietic stem cell transplants induced by immune-competent donor cells attacking host tissues. GVHD signs and symptoms appearing within the first 100 days after transplantation are considered acute, whereas those occurring beyond 100 days are categorized as chronic. Acute GVHD presents with erythematous maculopapular eruptions starting on the face, ears, palms, and soles. Follicular erythema is a frequent acute GVHD early manifestation
Immunotoxin-Mediated Depletion of CD5+ T Cells from Bone Marrow for Graft-vs.-Host Disease Prophylaxis
Published in Adrian P. Gee, BONE MARROW PROCESSING and PURGING, 2020
Joseph H. Antin, Howard J. Weinstein, Cyril Bouloux, Barbara E. Bierer
In contrast, acute GvHD was more prevalent in patients receiving marrow from MHC-mismatched donors. Grade 2 to 4 acute GvHD was observed in 7/17 (41%) evaluable patients (Figure 6), and three patients died of grade 4 acute GvHD. There were no new cases after 5 weeks. Chronic GvHD was observed in 0/9 evaluable patients.
Infections in Haematopoietic Stem Cell Transplants
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
In addition to infective complications, GvHD is a serious complication that can occur either in the early post-transplant period or as a longer-term chronic complication. The importance of GvHD for infection teams is that it can mimic infection (diarrhoea, rash and fever being common manifestations of both) but also that chronic GvHD is a significant risk factor for developing infective complications, both from the condition itself and the increased intensity immunosuppression used to treat it. During flares of GvHD it may be appropriate to re-commence prophylaxis against mould infections and possibly also viral disease as well.
Intensified conditioning regimen with fludarabine combined with post-transplantation cyclophosphamide for haploidentical allogeneic hematopoietic stem cell transplantation in children with high-risk acute leukemia
Published in Hematology, 2023
Junjie Cao, Xiaodong Xu, Ying Lu, Tiantian Wang, Dong Chen, Shuangyue Li, Xuhui Liu, Peipei Ye, Zhong-zheng Zheng, Renzhi Pei
ATG-based and PTCy-based T cell removal in vivo were commonly used after haplo-HSCT for GVHD prevention. Wang et al. [6] added GVHD prevention program based on G-CSF/ATG, low-dose CTX (14.5 mg/kg/d on day +3, +4) after transplantation. One hundred fourteen patients who used ATG + PTCy and 125 patients who used ATG alone as GVHD prevention were compared, results showed that III–IV aGVHD and NRM in ATG + PTCy group were significantly lower than those in ATG group (5% vs 18%, P = 0.003 and 6% vs 15%, P = 0.045, respectively). There was no significant difference between the two-year cumulative recurrence rate (13% vs 14%, P = 0.62) and OS (83% vs 77%, P = 0.18). GRFS in ATG PTCy group was significantly better than that in ATG group (63% vs 48%, P = 0.039). Law et al. [27] reported that the addition of ATG (total 4.5 mg/kg, −3 to −1 day) on the basis of PTCy prevention program also achieved good results. The cumulative incidence of total and III–IV aGVHD 100 days after transplantation was 38.3% and 5.2%, respectively, the incidence of chronic GVHD was 15.5%.
Budget impact analysis of belumosudil for chronic graft-versus-host disease treatment in the United States
Published in Journal of Medical Economics, 2022
Carlos R. Bachier, Jeffrey R. Skaar, Sumudu Dehipawala, Benjamin Miao, Jonathan Ieyoub, Haya Taitel
cGVHD is a multi-system, immune-mediated, inflammatory, and fibrotic disease in which immune cells from an HCT attack the recipient, resulting in significant morbidity and mortality. Five-year survival rates of patients with chronic GVHD range from 58–82%3. Quality-of-life (QoL) is also negatively impacted by cGVHD. The National Institutes of Health (NIH) Consensus Criteria state that the severity of cGVHD is significantly related to impairment in QoL independent of other comorbidities, donor sources for transplantation, and socio-demographic variables. The condition can be characterized by a combination of tissue inflammation and fibrosis manifesting across multiple organ systems and frequently involves, but is not limited to, the skin, mucosa, and lungs. cGVHD-induced fibrosis leads to chronic disability, especially when affecting joints or extensive areas of the skin. Widespread sclerotic skin manifestations caused by inflammation and fibrosis are associated with poor survival4. In post-HCT patients, cGVHD is the leading cause of non-relapse mortality more than 2 years after allogeneic transplantation.
Lacrimal Gland Insufficiency in Aqueous Deficiency Dry Eye Disease: Recent Advances in Pathogenesis, Diagnosis, and Treatment
Published in Seminars in Ophthalmology, 2022
Acquired causes of non-Sjögren’s-type ADDE include immune-mediated conditions such as Stevens–Johnson syndrome (SJS), mucous membrane pemphigoid (MMP) and graft versus host disease (GVHD).3,17,18 Stevens-Johnson syndrome is a chronic mucocutaneous blistering disease, which is triggered by drugs or viral infections.19–22 It is said to occur as a result of dysregulated immune response, mainly pertaining to innate immunity.23,24 It is a cytokine-mediated response, which leads to the deposition of neutrophils in the conjunctiva of these patients.25 In both SJS and MMP, there is chronic inflammation of the ocular surface, which if not treated in time, leads to cicatrising conjunctivitis, ultimately causing ADDE. Graft versus host disease (GVHD) is an adverse immunological event following allogeneic hematopoietic stem cell transplantation. It includes a T cell-mediated immune response which causes infiltration and inflammation of ocular structures such as the lacrimal glands and conjunctiva, leading to ADDE.26,27 Other acquired causes of non-Sjögren’s-type ADDE include ocular chemical burns, iatrogenic causes such as kerato-refractive surgeries, long-term use of topical and systemic medications and radiation therapy for head and neck cancers. Some of these conditions, like radiation therapy, cause direct damage to the lacrimal gland and the ocular surface, while others, like topical anti-glaucoma medications, cause chronic inflammation and fibrosis of the ocular surface leading to cicatrising changes.