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עמוד בית
Tue, 21.05.24

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March 2023
Dorit Shitenberg MD, Barak Pertzov MD, Moshe Heching MD, Yael Shostak MD, Osnat Shtraichman MD, Dror Rosengarten MD, Moshe Yeshurun MD, Yury Peysakhovich MD, Yaron Barac MD, Mordechai R. Kramer MD

Background: Late-onset pulmonary complications can occur following hematological stem cell transplantation (HSCT). In allogeneic HSCT these complications are often associated with chronic graft-versus-host disease (GVHD). Lung transplantation (LTx) often remains the only viable therapeutic option in these patients.

Objectives: To describe our experience with LTx due to GVHD after HSCT and to compare the long-term survival of this group of patients to the overall survival of our cohort of LTx recipients for other indications.

Methods: We retrospectively retrieved all data on patients who had undergone LTx for end-stage lung disease as a sequela of allogeneic HSCT, between 1997 and 2021, at Rabin Medical Center in Israel.

Results: A total of 15 of 850 patients (1.7%) from our cohort of LTx recipients fulfilled the criteria of LTx as a sequela of late pulmonary complication after allogeneic HSCT. The median age at the time of HSCT was 33 years (median 15–53, range 3–60). The median time between HSCT and first signs of chronic pulmonary GVHD was 24 months (interquartile range [IQR] 12–80). The median time from HSCT to LTx was 96 months (IQR 63–120). Multivariate analysis showed that patients transplanted due to GVHD had similar survival compared to patients who were transplanted for other indications.

Conclusions: LTx for GVHD after allogeneic HSCT constitutes an important treatment strategy. The overall survival appears to be comparable to patients after LTx for other indications.

January 2013
M. Michael, A. Shimoni and A. Nagler
 Acute graft-versus-host disease (GVHD) is a major source of morbidity and mortality after allogeneic stem cell transplantation. Therapy of established acute GVHD depends heavily on corticosteroids, which have limited efficacy and are considerably toxic. It is still a matter of debate whether there is an alternative therapy to corticosteroids. Second-line treatment for acute GVHD after failure of steroids is not well substantiated due to the lack of controlled studies. This review examines the current treatment for acute GVHD, as well as novel therapeutics, such as cellular approaches (e.g., adoptive transfer of mesenchymal stem cells) and enhancement of regulatory T cells (e.g., photopheresis). These approaches avoid the toxicity of generalized immunosuppression and are likely to play a prominent future role in acute GVHD therapy.

March 2004
R.M. Nagler and A. Nagler

Patients with graft-versus-host disease suffer from xerostomia, oral infections and mucosal pathologies. The continuous increase in the number of patients treated worldwide with bone marrow transplants, combined with improved survival statistics result in a concomitant increase in the number of GVHD[1] patients. the pathogenesis of GVHD is based on donor graft T lymphocytes that recognize antigenic disparities between donor and recipient, and on the disregulation of a broad panel of cytokines. Consequently, various tissues and organs, including the mucosa of the oral and gastrointestinal tract, are damaged via cytotoxicity caused by infiltrating T cells. Since the salivary glands are a known major target of GVHD and their secretions significantly contribute to preserving mucosal integrity, this mucosal insult is further enhanced by the reduced quantity and altered quality of saliva. GVHD occurs in 40–70% of patients treated by bone marrow and peripheral blood stem cell transplantation. limited studies suggest that a large percentage of GVHD patients are affected and that the induced salivary dysfunction occurs rapidly following transplantation, affecting both major and minor salivary glands and reflecting the severity of the disease. Moreover, profound sialochemical alterations may be diagnostic of GVHD. an additional reason for the vast amount of research is that GVHD, as an autoimmune-like disease, seems to be an appropriate model for studying a much more prevalent, well-known and studied autoimmune disease involving salivary glands, namely, sjögren’s syndrome. The present review describes the GVHD-related sialometric and sialochemical data available in the literature for both major and minor salivary glands in both human and rodent models, and discusses a possible mechanism.






[1] GVHD = Graft-Versus-Host Disease


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