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• W2023285882 abstract "acute myeloid leukemia fluorescent in situ hybridization myelodysplastic syndrome neutrophilic dermatosis TO THE EDITOR Neutrophilic dermatoses (NDs) are characterized by dense infiltrates of mature neutrophils typically located in the upper dermis. Despite having dissimilar clinical presentations, Sweet’s syndrome, pyoderma gangrenosum, neutrophilic eccrine hidradenitis, and other related disorders are recognized as part of the spectrum of NDs because of their overlapping clinical and histopathological findings (Vignon-Pennamen and Wallach, 1991Vignon-Pennamen M.D. Wallach D. Cutaneous manifestations of neutrophilic disease. A study of seven cases.Dermatologica. 1991; 183: 255-264Crossref PubMed Google Scholar). Although most instances of ND have a benign course, some extracutaneous localizations of the neutrophilic infiltrates can be potentially life-threatening (Vignon-Pennamen, 2000Vignon-Pennamen M.D. The extracutaneous involvement in the neutrophilic dermatoses.Clin Dermatol. 2000; 18: 339-347Abstract Full Text Full Text PDF PubMed Scopus (62) Google Scholar). Little is known about the pathophysiology of ND. The findings of high CD3, IL-1, IL-8, and tumor necrosis factor-α expressions by immunohistochemical staining in the dermis of ND patients (Marzano et al., 2010Marzano A.V. Cugno M. Trevisan V. et al.Role of inflammatory cells, cytokines and matrix metalloproteinases in neutrophil-mediated skin diseases.Clin Exp Immunol. 2010; 162: 100-107Crossref PubMed Scopus (146) Google Scholar) and the impressive effects of corticosteroids in alleviating these diseases have underlined a role for activated T lymphocytes in the recruitment of mature neutrophils to the dermis. Moreover, targeted immunosuppressive agents such as tumor necrosis factor-α inhibitors and the IL-1R inhibitor anakinra have been successfully used in the treatment of Sweet’s syndrome, which has further emphasized the importance of these cytokines in the pathophysiology of ND (Yamauchi et al., 2006Yamauchi P.S. Turner L. Lowe N.J. et al.Treatment of recurrent Sweet’s syndrome with coexisting rheumatoid arthritis with the tumor necrosis factor antagonist etanercept.J Am Acad Dermatol. 2006; 54: S122-s126Abstract Full Text Full Text PDF PubMed Scopus (49) Google Scholar; Delluc et al., 2008Delluc A. Limal N. Puéchal X. et al.Efficacy of anakinra, an IL1 receptor antagonist, in refractory Sweet syndrome.Ann Rheum Dis. 2008; 67: 278-279Crossref PubMed Scopus (52) Google Scholar; Lipsker et al., 2010Lipsker D. Perrigouard C. Foubert A. et al.Anakinra for difficult-to-treat neutrophilic panniculitis: IL-1 blockade as a promising treatment option for neutrophil-mediated inflammatory skin disease.Dermatology (Basel). 2010; 220: 264-267Crossref PubMed Scopus (29) Google Scholar). Around 20% of patients with Sweet’s syndrome have an underlying hematological malignancy, which is predominantly a myeloid neoplasm (Cohen et al., 1988Cohen P.R. Talpaz M. Kurzrock R. Malignancy-associated Sweet’s syndrome: review of the world literature.J Clin Oncol. 1988; 6: 1887-1897PubMed Google Scholar). In these cases, one could hypothesize that neutrophils have differentiated from the malignant clone, showing an aberrant phenotype, which promotes dermal invasion. In this model, neutrophils in the dermal infiltrate should be clonally related to the underlying myeloid malignancy, which has never been formally demonstrated to date. We thus conducted a multicentric retrospective study, which included 14 ND patients (8 men and 6 women) with (1) a histopathological diagnosis of Sweet’s syndrome (n=12), pyoderma gangrenosum (n=1), or neutrophilic eccrine hidradenitis (n=1), and (2) a diagnosis of myelodysplastic syndrome (MDS, n=2) or acute myeloid leukemia (AML, n=12), and with a medullar cytogenetic abnormality that would be informative in a fluorescent in situ hybridization (FISH) study. In two patients, the ND was present at the initial presentation of AML. This condition was chemotherapy-induced in seven patients and occurred without any identifiable trigger in four patients. All patients but one were febrile when the ND diagnosis was established, and four patients had an extracutaneous involvement (lung (n=1), muscle (n=1), mouth (n=2)), which is a much higher frequency than what is reported in idiopathic ND (Vignon-Pennamen, 2000Vignon-Pennamen M.D. The extracutaneous involvement in the neutrophilic dermatoses.Clin Dermatol. 2000; 18: 339-347Abstract Full Text Full Text PDF PubMed Scopus (62) Google Scholar). No patient had concomitant neutrophil leukocytosis. Three patients were profoundly neutropenic at the time of ND occurrence. This observation confirms that hyperleukocytosis is irrelevant as a diagnostic criterion for ND associated with myeloid malignancies. To test the hypothesis of a clonal relationship between the skin-infiltrating neutrophils and the bone marrow blasts, the FISH study was conducted on 3μm skin tissue sections processed using the Histology FISH Accessory Kit (Dako, Glostrup, Denmark). After hybridization with specific probes (Table 1), scoring of the hybridization signals was performed on 200 consecutive morphologically intact nuclei, with a normal cutoff value evaluated at 10% (Haralambieva et al., 2002Haralambieva E. Kleiverda K. Mason D.Y. et al.Detection of three common translocation breakpoints in non-Hodgkin’s lymphomas by fluorescence in situ hybridization on routine paraffin-embedded tissue sections.J Pathol. 2002; 198: 163-170Crossref PubMed Scopus (73) Google Scholar). This approach was noninformative in three patients because of an insufficient number of analyzable nuclei. Among the other 11 patients analyzed, 8 showed the same cytogenetic anomaly in the neutrophils infiltrating the skin and in the bone marrow (Figure 1), whereas there were no evidence of any clonal cytogenetic abnormality in the neutrophils of the remaining three patients.Table 1Clinical and cytogenetic characteristics of the patients and results of the FISH studyPatientSex/age (years)Hematological malignancyBone marrow cytogeneticDermatologic diagnosisBlastic cells on skin biopsyAbsolute neutrophil count (G/l) at the time of skin biopsyProbeClonality of the skin-infiltrating neutrophils 1F, 74AML44-47,X,add(X)(q27),del(5)(q14q34),del(7)(q21q35),8,dic(12;22)(p11;p11), +13,[10],t(15;15)(p10;p10),+r(?)[23],+del(12)(p11)[3], +r(?)[7],+mar ou r(?)[3][cp23]/46,XX[2]Sweet syndromeNo5.4del 5q deletion probe (EGR1) (Amplitech, Compiegne, France)Yes 2M,31AML46,XY,t(11;19)(q23;p13)[22]/ 46,XY[2]Sweet syndromeNo2.5MLL Breakapart probe (Vysis Abbott, Chicago, IL)Yes 3M,39AML45,X,-Y,t(8;21)(q22;q22)[19] 46,XY[1]Sweet syndromeYes1.3AML1 Breakapart probe (Vysis Abbott)Not interpretable 4M,74MDS47,XY,+8[7]Sweet syndromeNo3.2Cep 8 SpectrumOrange (Vysis Abbott)Yes 5F,53APLNo karyotype, PML–RARA RT–PCR positiveSweet syndromeYes1.7LSI PML–RAR dual color dual fusion (Vysis Abbott)Not interpretable 6M, 66AML46,XY,del(11)(q13qter)[18]/46,XY[2]Sweet syndromeNo<0.1MLL Breakapart probe (Vysis Abbott)Yes 7M, 72AML46,XY,der(2)r(2;11)(p21q37;q23q25),der(11)t(2;11)(p21;q23)[20]Sweet syndromeNo2.1MLL Breakapart probe (Vysis Abbott)No 8F, 76AML49,XX,del(7)(q11),+8,+13, inv(16)(p13;q23),+21[23]Neutrophilic eccrine hydradenitisNo0.4Cep 8 SpectrumOrange (Vysis Abbott)Not interpretable 9F, 71AML46,XX,del(5)(q14q3?2)[13]/46,idem,?del(20)(q12)[2]/46,XX[1]Pyoderma gangrenosumNo4.6del 5q deletion probe(EGR1) (Amplitech)Yes10M, 69CMML46,XY,del(20)(q1?2q1?3)[20]Sweet syndromeNo5Del(20q) (PTPRT20q12/20q11)(Kreatech, Durham, North Carolina)Yes11M, 69AML45,X,-Y[14]/46,XY[6]Sweet syndromeNo<0.1Dual labeled X&Y probe (Cytocell, Cambridge, UK)Yes12F, 75AML47,XX,+8[7]/46,XX[20]Sweet syndromeYes0.9Cep 8 SpectrumOrange (Vysis Abbott)No13F,52APL46,XX,t(15;17)(q22;q21)[8]/ 46,XX[8]Sweet syndromeNo1LSI PML–RAR dual color dual fusion (Vysis Abbott)No14M, 65AML47,XY,+add(8)(q23),del(9) (q2?1q33),der(15)t(1;15)(q2?4;p1?1) [9]/ 46,XY[11]Sweet syndromeYesN.D.Cep 8 SpectrumOrange (Vysis Abbott)YesAbbreviations: AML, acute myeloid leukemia; APL, acute promyelocytic leukemia; CMML, chronic myelomonocytic leukemia; FISH, fluorescent in situ hybridization; MDS, myelodysplastic syndrome; N.D., not determined; RT–PCR, reverse transcriptase–PCR.FISH results were defined as positive if the same medullar cytogenetic anomaly was found in the neutrophils infiltrating the skin. Open table in a new tab Abbreviations: AML, acute myeloid leukemia; APL, acute promyelocytic leukemia; CMML, chronic myelomonocytic leukemia; FISH, fluorescent in situ hybridization; MDS, myelodysplastic syndrome; N.D., not determined; RT–PCR, reverse transcriptase–PCR. FISH results were defined as positive if the same medullar cytogenetic anomaly was found in the neutrophils infiltrating the skin. A previous study using a HUMARA assay has found evidence of clonality in the skin neutrophils of 80% of women (median age 60 years) with ND, regardless of whether they had an underlying hematological malignancy (Magro et al., 2007Magro C.M. Kiani B. Li J. et al.Clonality in the setting of Sweet’s syndrome and pyoderma gangrenosum is not limited to underlying myeloproliferative disease.J Cutan Pathol. 2007; 34: 526-534Crossref PubMed Scopus (36) Google Scholar). However, the HUMARA assay is no longer considered to be a reliable test for clonality, especially in elderly women (Busque et al., 1996Busque L. Mio R. Mattioli J. et al.Nonrandom X-inactivation patterns in normal females: lyonization ratios vary with age.Blood. 1996; 88: 59-65PubMed Google Scholar; Swierczek et al., 2012Swierczek S.I. Piterkova L. Jelinek J. et al.Methylation of AR locus does not always reflect X chromosome inactivation state.Blood. 2012; 119: e100-e109Crossref PubMed Scopus (41) Google Scholar). To avoid this potential bias, we utilized the FISH technique to unambiguously reveal that skin-infiltrating neutrophils arise from the differentiation of the myeloid clone. Nevertheless, FISH analysis of skin specimens is very technically challenging, partly because of the collagen fibers that exhibit autofluorescence. This may explain the failure of this technique in three of our patients. FISH analysis was previously used in two case reports. van Kamp et al., 1994van Kamp H. van den Berg E. Timens W. et al.Sweet’s syndrome in myeloid malignancy: a report of two cases.Br J Haematol. 1994; 86: 415-417Crossref PubMed Scopus (47) Google Scholar reported the presence of 5q- nuclei in some cells of the cutaneous biopsy of a patient with 5q- AML and ND. Nevertheless, the histological description of the lesion in this case was not detailed enough to exclude the possibility that the detected 5q- nuclei did not correspond to blastic cells infiltrating the dermis. In most of our current patients, our histological analysis revealed typical ND without any detectable blastic cells by standard colorations or by CD34 immunohistochemical staining. In our only FISH-positive patient who had a few blastic cells in the infiltrate, we considered that these cells were too few in number to explain the large majority of nuclei that were positive for the FISH abnormality. More recently, Loon et al., 2012Loon K.V. Gill R.M. McMahon P. et al.20q– clonality in a case of oral sweet syndrome and myelodysplasia.AJCP. 2012; 137: 310-315Google Scholar demonstrated with a FISH study a clonally restricted neutrophilic infiltrate in a single case of unusual neutrophilic dermatosis of the mouth associated with 20q- MDS, a result confirmed and generalized by our present study. Our present data show that in most cases of ND, the skin-infiltrating neutrophils that arise in the context of myeloid malignancies have differentiated from the malignant clone. For patient 11, the Y loss could have been an aging phenomenon (Wiktor et al., 2000Wiktor A. Rybicki B.A. Piao Z.S. et al.Clinical significance of Y chromosome loss in hematologic disease.Genes Chromosomes Cancer. 2000; 27: 11-16Crossref PubMed Scopus (135) Google Scholar), but the high proportion of mitosis with this anomaly and the normalization of the karyotype when the patient achieved complete remission with induction chemotherapy argues for an AML-related cytogenetic abnormality. In the three remaining patients, ND could be sustained by neutrophils that have differentiated from residual normal hematopoietic cells or from subclones of the myeloid malignancy that were below the threshold of detection, using our experimental approach. This pathophysiological explanation is consistent with the striking clinical similarities between Sweet’s syndrome and the differentiation syndrome observed in patients with acute promyelocytic leukemia treated with retinoic acid, i.e., the association with fever, multiorgan infiltration by neutrophils, and the marked response to corticosteroids. The occurrence of ND in three profoundly neutropenic patients in our study suggests that the differentiation event occurs in the dermis. More studies will be necessary to confirm this possibility and to identify the local factors involved in the MDS/AML differentiation in the dermis, which might be of therapeutic value. For example, it would be of great interest to evaluate whether local vitamin D production is involved in the dermal differentiation of blastic cells, as this hormone has been proven to be a differentiating agent for AML cells (Callens et al., 2010Callens C. Coulon S. Naudin J. et al.Targeting iron homeostasis induces cellular differentiation and synergizes with differentiating agents in acute myeloid leukemia.J Exp Med. 2010; 207: 731-750Crossref PubMed Scopus (149) Google Scholar). Hôpital Saint Louis approved this study. Written, informed consent was given by all the patients still alive when we started this retrospective study (2011). This study adheres to the declaration of Helsinki principles." @default.
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• W2023285882 date "2013-04-01" @default.
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• W2023285882 title "Evidence of Differentiation in Myeloid Malignancies Associated Neutrophilic Dermatosis: A Fluorescent In Situ Hybridization Study of 14 Patients" @default.
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• W2023285882 doi "https://doi.org/10.1038/jid.2012.408" @default.
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