Elsevier

Leukemia Research

Volume 35, Issue 5, May 2011, Pages e35-e36
Leukemia Research

Letter to the Editor
Treating myelodysplastic syndrome improves an accompanying autoimmune disease along with a reduction in regulatory T-cells

https://doi.org/10.1016/j.leukres.2010.12.015Get rights and content

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Conflict of interest statement

The authors have no conflict of interest to report.

Acknowledgements

Supported partially by grants from the National Cancer Institute Grant CA16056 (OAU, JF, PKW, MW) and the Leonard S. LuVullo Endowment for Leukemia Research, Buffalo, NY (MW).

Contributions. OAU followed the case and reviewed the literature, JF assisted in the literature review, PKW oversaw the flow cytometry analysis, JA assisted in the autoimmune diagnosis of this patient and MW oversaw the conduct of the study, contributed to the care of the patient and to the manuscript preparation and all

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    Therefore not unexpectedly most of the T-cell abnormalities observed in MDS patients (Fozza et al., 2009; Fozza and Longinotti, 2012) tend to revert during therapy with Azacytidine, especially within the CD4+ subset (Fozza et al., 2015). When focusing on the potential beneficial effects on AD, the first reports described MDS patients showing a complete response of deep neutrophilic dermatosis (Raj et al., 2007) and an improvement of systemic lupus erythematosus (SLE) after treatment, which was interestingly paralleled by a reduction in the frequency of Treg (Al Ustwani et al., 2011). Also BD was shown to significantly improve with Azacytidine (Tanaka et al., 2013; Endo et al., 2015).

  • Biologics in myelodysplastic syndrome-related systemic inflammatory and autoimmune diseases: French multicenter retrospective study of 29 patients

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    Treatment of SIAD-related MDS is challenging, with usually a high steroid-dependence rate and risk of infections favored by cytopenia associated with MDS [10–14]. Although steroids usually achieve good response, the steroid-sparing strategy and the response rates of various immunosuppressive drugs are poorly reported [10–14]. Several previous studies showed insufficient response to TNF-α antagonists for MDSs alone but have a relatively acceptable safety profile [4,15].

  • Efficacy of Azacitidine in autoimmune and inflammatory disorders associated with myelodysplastic syndromes and chronic myelomonocytic leukemia

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    Azacitidine significantly improves survival in higher risk MDS [5] and in myelodysplastic type CMML [6,7] and is also approved outside Europe for the treatment of lower risk MDS. Eight patients with MDS/CMML and AID treated with Azacitidine have been reported to our knowledge [8–12]. We retrospectively analyzed the efficacy of Azacitidine in MDS/CMML patients with concomitant AID seen between 2007 and May 2014 in registries of the Société Nationale Française de Médecine Interne (SNFMI) and of the Groupe Francophone des Myélodysplasies.

  • The immune landscape of myelodysplastic syndromes

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    Noteworthy, after Azacytidine treatment a patient with concomitant MDS and systemic lupus erythematosus experienced not only a clear haematologic improvement but also the resolution of his autoimmune disorder. The potential ability of Azacytidine to modify the immunological milieu in these patients was further highlighted by a reduction in regulatory T-cells (Treg) (Al Ustwani et al., 2011). A complete resolution of intestinal Behçet's syndrome (Tanaka et al., 2013) and deep neutrophilic dermatosis (Raj et al., 2007) was demonstrated in two further patients treated with Azacitidine.

  • Myelodysplastic syndromes and autoimmune diseases-Case series and review of literature

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    In summary, though the exact mechanism(s) underlying MDS and AD are not well established, it is important to look for early signs of autoimmunity in MDS patients. Treatment options include treating MDS only as suggested by others [41] and our observation [42] of treating both diseases concomitantly with 5-azacitidine. None of the authors of this paper has a financial or personal relationship with other people or organisations that could inappropriately influence or bias the content of the paper.

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