Cutaneous involvement of chronic graft-versus-host disease (cGVHD) has a wide range of manifestations including a lichenoid form with a currently assumed mixed Th1/Th17 signature and a sclerotic form with Th1 signature. Despite substantial heterogeneity of innate and adaptive immune cells recruited to the skin and of the different clinical manifestations, treatment depends mainly on the severity of the skin involvement and relies on systemic, high-dose glucocorticoids alone or in combination with a calcineurin inhibitor. We performed the first study using RNA sequencing to profile and compare the transcriptome of lichen planus cGVHD (n = 8), morphea cGVHD (n = 5), and healthy controls (n = 6). Our findings revealed shared and unique inflammatory pathways to each cGVHD subtype that are both pathogenic and targetable. In particular, the deregulation of IFN signaling pathway was strongly associated with cutaneous cGVHD, whereas the triggering receptor expressed on myeloid cells 1 pathway was found to be specific of lichen planus and likely contributes to its pathogenesis. The results were confirmed at a protein level by performing immunohistochemistry staining and at a transcriptomic level using real-time quantitative polymerase chain reaction.

Thibault Mahévas, Department of Dermatology, Saint-Louis Hospital, AP-HP, 1 avenue Claude Vellefaux, 75010, Paris, France

L’amylose papuleuse (AP) est une amylose cutanée primaire caractérisée par des papules prurigineuses, difficile à traiter et qui peut être associée à une dermatite atopique (DA). Nous rapportons l’efficacité du dupilumab chez deux patientes présentant une AP avec une DA. Une femme de 28 ans ayant une DA sévère (EASI = 24/72) présentait de multiples petites papules pigmentées monomorphes, fermes et très prurigineuses sur les avant-bras et la face antérieure des jambes. L’EVA prurit des lésions de l’AP était de 9/10. Une biopsie cutanée montrait des dépôts amyloïdes dans les papilles dermiques, confirmant l’AP. Après l’échec des corticostéroïdes topiques, du tacrolimus topique, de la photothérapie et de la ciclosporine, le dupilumab était instauré (600 mg puis 300 mg toutes les deux semaines) et permettait une amélioration significative de la DA (EASI 80 à 4 mois), une amélioration rapide du prurit sur les lésions d’AP (EVA = 2/10 à 3 mois) et une rémission complète (RC) des lésions d’AP à 6 mois. Une femme de 30 ans atteinte de DA sévère (EASI à 25/72) et d’asthme depuis l’enfance présentait un prurit féroce. L’examen physique montrait des lésions de DA associées à de petites papules pigmentées monomorphes, fermes et très prurigineuses sur les avant-bras et la face antérieure des jambes. L’EVA prurit sur les lésions d’AP était de 9/10. Le dupilumab entraînait une amélioration clinique significative (EASI 75 à 3 mois), une amélioration rapide du prurit (EVA = 2/10 à 3 mois) et une RC des lésions d’AP à 5 mois. Dans les deux cas, la tolérance du dupilumab était bonne et l’efficacité était maintenue sur la DA et l’AP à 10 mois de suivi. L’AP est une dermatose prurigineuse chronique rare caractérisée par des papules et des plaques hyperkératosiques et pigmentées touchant généralement la face antérieure des jambes. Le prurit est généralement sévère et met en jeu l’inflammation de type 2 au travers d’une expression accrue des récepteurs épidermiques de l’interleukine (IL)-31 (un récepteur de cytokine Th2) entraînant possiblement une hypersensibilité des fibres nerveuses cutanées. L’examen histologique de l’AP montre des dépôts amorphes dans le derme papillaire qui peuvent provenir de la kératine de kératinocytes apoptotiques transformés par des macrophages et des fibroblastes. Les corticostéroïdes topiques ou oraux, les rétinoïdes, la ciclosporine, le tacrolimus, la capsaïcine, le laser et la photothérapie sont d’efficacité incertaine. Le dupilumab, approuvé pour le traitement de la DA modérée à sévère, est un anticorps monoclonal humain dirigé contre la sous-unité alpha des récepteurs de l’IL-4 et de l’IL-13 qui régule l’inflammation de type 2. À ce jour, un seul cas d’AP traité par dupilumab a été rapporté. Des essais thérapeutiques pourraient être menés pour démontrer son efficacité dans le traitement de l’AP.

Chronic graft-versus-host disease (cGVHD) remains the main cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (AHSCT). cGVHD is a multisystem, immune-mediated disease characterized by tissue fibrosis and immune dysregulation of T and B cells (MacDonald et al., 2017MacDonald K.P. Hill G.R. Blazar B.R. Chronic graft-versus-host disease: biological insights from preclinical and clinical studies.Blood. 2017; 129: 13-21Crossref PubMed Scopus (120) Google Scholar). The pathophysiology of cGVHD involves homeostatic abnormalities of thymus-derived regulatory T cells (tTregs, described as CD4+ FOXP3+ IL-2Ra/CD25hi IL-7Ra/CD127low), including low tTreg numbers, decreased thymic export, and increased susceptibility to Fas-mediated apoptosis (Matsuoka et al., 2010Matsuoka K. Kim H.T. McDonough S. Bascug G. Warshauer B. Koreth J. et al.Altered regulatory T cell homeostasis in patients with CD4+ lymphopenia following allogeneic hematopoietic stem cell transplantation.J Clin Invest. 2010; 120: 1479-1493Crossref PubMed Scopus (166) Google Scholar). In addition, cGVHD is associated with elevated levels of IL-7 and functional IL-2 deficiency (Matsuoka et al., 2013Matsuoka K. Koreth J. Kim H.T. Bascug G. McDonough S. Kawano Y. et al.Low-dose interleukin-2 therapy restores regulatory T cell homeostasis in patients with chronic graft-versus-host disease.Sci Transl Med. 2013; 5: 179ra43Crossref PubMed Scopus (294) Google Scholar). Treatment of cGVHD with low-dose subcutaneous IL-2 has proven to be safe and increase tTreg numbers (Koreth et al., 2011Koreth J. Matsuoka K. Kim H.T. McDonough S.M. Bindra B. Alyea 3rd, E.P. et al.Interleukin-2 and regulatory T cells in graft-versus-host disease.N Engl J Med. 2011; 365: 2055-2066Crossref PubMed Scopus (731) Google Scholar). The role of other cell subpopulations with regulatory functions and their possible usage for the treatment of cGVHD is under investigation (Schneidawind et al., 2013Schneidawind D. Pierini A. Negrin R.S. Regulatory T cells and natural killer T cells for modulation of GVHD following allogeneic hematopoietic cell transplantation.Blood. 2013; 122: 3116-3121Crossref PubMed Scopus (65) Google Scholar). Type 1 adaptive regulatory T cells (Tr1s) are FOXP3-negative CD4 T cells that secrete high amounts of IL-10, have immunosuppressive properties, and are found more frequently in AHSCT recipients with persistent mixed chimerism than in those with complete donor chimerism (Gagliani et al., 2013Gagliani N. Magnani C.F. Huber S. Gianolini M.E. Pala M. Licona-Limon P. et al.Coexpression of CD49b and LAG-3 identifies human and mouse T regulatory type 1 cells.Nat Med. 2013; 19: 739-746Crossref PubMed Scopus (473) Google Scholar). In addition to IL-10, Tr1s produce high amounts of TGF-β and variable levels of IFN-γ, but no IL-2 or IL-4 (Groux et al., 1997Groux H. O'Garra A. Bigler M. Rouleau M. Antonenko S. de Vries J.E. et al.A CD4+ T-cell subset inhibits antigen-specific T-cell responses and prevents colitis.Nature. 1997; 389: 737-742Crossref PubMed Scopus (3068) Google Scholar). Coexpression of CD49b and LAG-3 was described as a specific surrogate marker of Tr1s (Gagliani et al., 2013Gagliani N. Magnani C.F. Huber S. Gianolini M.E. Pala M. Licona-Limon P. et al.Coexpression of CD49b and LAG-3 identifies human and mouse T regulatory type 1 cells.Nat Med. 2013; 19: 739-746Crossref PubMed Scopus (473) Google Scholar), facilitating their study in humans. A phase I clinical study demonstrated the efficacy of in vitro engineered Tr1-like cells (host antigen–specific IL-10–anergized T cells) after AHSCT (Bacchetta et al., 2014Bacchetta R. Lucarelli B. Sartirana C. Gregori S. Lupo Stanghellini M.T. Miqueu P. et al.Immunological outcome in haploidentical-HSC transplanted patients treated with IL-10-anergized donor T cells.Front Immunol. 2014; 5: 16Crossref PubMed Scopus (102) Google Scholar, Zhang and Hill, 2019Zhang P. Hill G.R. Interleukin-10 mediated immune regulation after stem cell transplantation: mechanisms and implications for therapeutic intervention.Semin Immunol. 2019; 44: 101322Crossref PubMed Scopus (3) Google Scholar), but the role of Tr1s in human cGVHD needs to be further investigated. Herein, we prospectively analyzed Tr1 and tTreg frequency, phenotype, and function in the peripheral blood of 14 AHSCT patients with active cGVHD, 11 with cGVHD in remission, 12 without cGVHD, and 12 healthy donors. All samples were collected following written informed consent according to the Declaration of Helsinki. This study received the agreement of the local ethics committee. Tr1s were defined as CD3+CD4+CD45RA−CD49b+LAG3+ and tTregs as CD3+CD4+CD25hiCD127−. Patients’ characteristics are summarized in Supplementary Table S1. Tr1 frequencies were higher in AHSCT patients with active cGVHD than in patients with cGVHD in remission (10% and 2.3%, respectively; P < 0.001), patients without cGVHD (3.8%, P < 0.001), and healthy donors (4.0%, P < 0.001) (Figure 1a and b). Conversely, tTreg frequencies were lower in patients with active cGVHD than patients with cGVHD in remission (5.5% and 9.5%, respectively; P = 0.03), patients without cGVHD (11.2%, P = 0.02), and healthy donors (10.9%, P = 0.01) (Figure 1b). Therefore, the Tr1:tTreg ratio was reversed in patients with active cGVHD compared with patients with cGVHD in remission (2.0 and 0.4, respectively; P < 0.001), patients without cGVHD (0.4, P < 0.001), and healthy donors (0.5, P < 0.001) (Figure 1b). Three patients experienced partial remission of cGVHD after low-dose IL-2 treatment and showed an early drop in Tr1 frequencies (from 24% to 13% on average) and increase in tTreg frequencies (from 6% to 13.2% on average) one week after treatment. Two of these patients were further analyzed 12 and 24 months later while they had ongoing remission of cGVHD. Notably, the frequencies of Tr1s and tTregs and the Tr1:tTreg ratio remained at values comparable to those in healthy donors (Figure 1c). In all study subjects, Tr1s expressed lower levels of IL-2Rα than tTregs (P < 0.001) but higher levels than conventional T cells (P < 0.001). Conversely, levels of IL-7Rα in Tr1s were higher than in tTregs (P < 0.001) but similar to those in conventional T cells (Figure 1d). These results are consistent with the previously observed increased levels of IL-7 in patients with cGVHD (Matsuoka et al., 2013Matsuoka K. Koreth J. Kim H.T. Bascug G. McDonough S. Kawano Y. et al.Low-dose interleukin-2 therapy restores regulatory T cell homeostasis in patients with chronic graft-versus-host disease.Sci Transl Med. 2013; 5: 179ra43Crossref PubMed Scopus (294) Google Scholar), which could stimulate Tr1 expansion. They are also in line with the absence of expansion of Tr1s after IL-2 treatment. The mechanisms that lead to Tr1 drop after IL-2 treatment remain to be understood but could involve IL-7 deprivation, as IL-7 levels were shown to decrease in the serum of patients treated with IL-2 (Matsuoka et al., 2013Matsuoka K. Koreth J. Kim H.T. Bascug G. McDonough S. Kawano Y. et al.Low-dose interleukin-2 therapy restores regulatory T cell homeostasis in patients with chronic graft-versus-host disease.Sci Transl Med. 2013; 5: 179ra43Crossref PubMed Scopus (294) Google Scholar). Next, we measured IL-10 secretion of CD4 T cells following anti-CD3/CD28 stimulation, as described previously (Gagliani et al., 2013Gagliani N. Magnani C.F. Huber S. Gianolini M.E. Pala M. Licona-Limon P. et al.Coexpression of CD49b and LAG-3 identifies human and mouse T regulatory type 1 cells.Nat Med. 2013; 19: 739-746Crossref PubMed Scopus (473) Google Scholar). As shown in Figure 2a and b, patients with active cGVHD had increased frequencies of IL-10–secreting CD4 T cells compared with patients with cGVHD in remission (2.6% vs. 0.5%, respectively; P = 0.02), patients without cGVHD (1.0%, P = 0.03), and healthy donors (1.4%, P = 0.19). The proportions of IL-10–secreting cells correlated with those of Tr1s across all patient groups (r = 0.7, P = 0.003, Figure 2c), and IL-10–secreting cells were significantly enriched within the CD45RA−CD49b+LAG3+ subset of CD4 T cells (Figure 2d). Finally, we assessed the suppressive capacity of bead-purified IL-10–secreting CD4 T cells on autologous CD4 T-cell proliferation in response to anti-CD3/CD28 stimulation. As shown in Figure 2e, IL-10+ CD4 T cells significantly suppressed autologous CD4 T-cell proliferation as compared with IL-10− CD4 T cells. Altogether, these data indicate that CD3+CD4+CD45RA−CD49b+LAG3+ cells have the hallmark functional properties of Tr1s, and that Tr1s are expanded in active cGVHD. Several papers reported an impaired recovery of circulating functional CD4+CD25+ tTregs in patients with active cGVHD compared with patients without cGVHD after AHSCT or healthy donors (Alho et al., 2016Alho A.C. Kim H.T. Chammas M.J. Reynolds C.G. Matos T.R. Forcade E. et al.Unbalanced recovery of regulatory and effector T cells after allogeneic stem cell transplantation contributes to chronic GVHD.Blood. 2016; 127: 646-657Crossref PubMed Scopus (91) Google Scholar, Matsuoka et al., 2013Matsuoka K. Koreth J. Kim H.T. Bascug G. McDonough S. Kawano Y. et al.Low-dose interleukin-2 therapy restores regulatory T cell homeostasis in patients with chronic graft-versus-host disease.Sci Transl Med. 2013; 5: 179ra43Crossref PubMed Scopus (294) Google Scholar, Matsuoka et al., 2010Matsuoka K. Kim H.T. McDonough S. Bascug G. Warshauer B. Koreth J. et al.Altered regulatory T cell homeostasis in patients with CD4+ lymphopenia following allogeneic hematopoietic stem cell transplantation.J Clin Invest. 2010; 120: 1479-1493Crossref PubMed Scopus (166) Google Scholar, Zorn et al., 2005Zorn E. Kim H.T. Lee S.J. Floyd B.H. Litsa D. Arumugarajah S. et al.Reduced frequency of FOXP3+ CD4+CD25+ regulatory T cells in patients with chronic graft-versus-host disease.Blood. 2005; 106: 2903-2911Crossref PubMed Scopus (366) Google Scholar). The role of Tr1s in the maintenance of immune tolerance to non–self-antigens after AHSCT may be complex (Gagliani et al., 2013Gagliani N. Magnani C.F. Huber S. Gianolini M.E. Pala M. Licona-Limon P. et al.Coexpression of CD49b and LAG-3 identifies human and mouse T regulatory type 1 cells.Nat Med. 2013; 19: 739-746Crossref PubMed Scopus (473) Google Scholar, Roncarolo et al., 2011Roncarolo M.G. Gregori S. Lucarelli B. Ciceri F. Bacchetta R. Clinical tolerance in allogeneic hematopoietic stem cell transplantation.Immunol Rev. 2011; 241: 145-163Crossref PubMed Scopus (63) Google Scholar), especially as the functional plasticity of these cell subsets has been demonstrated. In inflammatory conditions, IL-10–producing Tr1s can derive from the differentiation of tTregs (Le Buanec et al., 2011Le Buanec H. Gougeon M.L. Mathian A. Lebon P. Dupont J.M. Peltre G. et al.IFN-α and CD46 stimulation are associated with active lupus and skew natural T regulatory cell differentiation to type 1 regulatory T (Tr1) cells.Proc Natl Acad Sci USA. 2011; 108: 18995-19000Crossref PubMed Scopus (35) Google Scholar). Immunoregulatory mechanisms are generally induced in the context of immune activation and inflammation. We may then speculate that increased Tr1 levels could represent a compensatory mechanism to (i) the inflammatory environment and (ii) the impaired Treg recovery in these patients. Notably, the increase in Tr1 levels may not be sufficient to circumvent ongoing cGVHD. Thus, our data do not preclude that Tr1s may play a beneficial role to prevent cGVHD and be used in an adoptive transfer therapy. Additional in situ studies of Tr1 localization and proportion in skin tissue would improve our understanding of the regulatory properties of Tr1s in the setting of cGVHD. Future in vivo studies should allow us to optimize adoptive transfer strategies to treat this disease. Datasets related to this article can be found at https://flowrepository.org/experiments/2596, hosted at Flow Repository. Nana Talvard-Balland: http://orcid.org/0000-0001-8590-6351 Aurélien Sutra Del Galy: http://orcid.org/0000-0002-4716-1472 David Michonneau: http://orcid.org/0000-0003-4553-3065 Helene Le Buanec: http://orcid.org/0000-0002-2139-0357 Francois Chasset: http://orcid.org/0000-0003-2580-8607 Marie Robin: http://orcid.org/0000-0001-7655-4083 Régis Peffault de Latour: http://orcid.org/0000-0001-6222-4753 Alienor Xhaard: http://orcid.org/0000-0002-4449-989X Flore Sicre de Fontbrune: http://orcid.org/0000-0003-2000-1556 Nathalie Parquet: http://orcid.org/0000-0002-4254-9857 Sophie Duchez: http://orcid.org/0000-0003-1629-1810 Valérie Schiavon: http://orcid.org/0000-0001-8466-774X Michel Rybojad: http://orcid.org/0000-0002-6276-7261 Anne Bergeron-Lafaurie: http://orcid.org/0000-0003-2156-254X Martine Bagot: http://orcid.org/0000-0002-0400-1954 Armand Bensussan: http://orcid.org/0000-0002-0409-2497 Sophie Caillat-Zucman: http://orcid.org/0000-0002-4535-3550 Gérard Socié: http://orcid.org/0000-0002-2114-7533 Jean-David Bouaziz: http://orcid.org/0000-0002-4993-2461 Adèle de Masson: http://orcid.org/0000-0001-7828-6211 The authors state no conflict of interest. The authors thank Christelle Doliger and Niclas Setterblad (Plateforme Technologique de l’Institut de Recherche Saint-Louis). This work was supported by Société Française de Dermatologie and Association d’Entraide des Greffés de Moëlle Osseuse. Nana Talvard-Balland was supported by the Ligue Nationale contre le Cancer. Adèle de Masson was supported by the Institut National du Cancer/Institut Thématique Multi-Organismes Cancer. Conceptualization: ADM, JDB, GS, SCZ, HLB; Data Curation: ADM, HLB, SD, VS; Formal Analysis: ADM, NTB, JDB; Investigation: ADM, NTB, JDB; Writing - Original Draft Preparation: ADM, JDB, NTB, GS, SCZ; Writing - Review and Editing: NTB, ASDG, DM, HLB, FC, MR, RPDL, AX, FSDF, NP, SD, VS, AB, MB, AB, SCZ, GS, JDB, ADM This prospective study was conducted at Saint-Louis Hospital from January 2014 to June 2015. The diagnosis and staging of chronic graft-versus-host disease were made at study inclusion using the National Institutes of Health criteria (Lee et al., 2015Lee S.J. Wolff D. Kitko C. Koreth J. Inamoto Y. Jagasia M. et al.Measuring therapeutic response in chronic graft-versus-host diseaseNational Institutes of Health consensus development project on criteria for clinical trials in chronic graft-versus-host disease: IV. The 2014 Response Criteria Working Group report.Biol Blood Marrow Transplant. 2015; 21: 984-999Abstract Full Text Full Text PDF PubMed Scopus (163) Google Scholar). All samples were collected following written informed consent. This study received the agreement of the local ethics committee. Patients’ characteristics are shown in Supplementary Table S1. Peripheral blood mononuclear cells were isolated by density gradient centrifugation (LSM, PAA Laboratories) and stained using combinations of the following antibodies: anti-CD3-Krome Orange (clone UCHT1), anti-CD4 TITC (SFCI12T4D11), and anti-CD25 PE-Cy7 (B1.49.9) (all from Beckman Coulter, Brea, CA); anti-CD45RA PerCP-Cy5.5 (HI100, Biolegend, San Diego, CA); anti-CD127 APC-eFluor 780 (eBio-RDR5), anti-CD49b APC (P1H5), and anti-Foxp3 PE (PCH101) (all from eBioscience, San Diego, CA); anti-LAG3 PE or PerCP (polyclonal goat IgG, R&D Systems, Minneapolis, MN); and Fixable Viability Stain 450 (BD Biosciences, San Jose, CA). Fluorescence minus one was used as control. Data were acquired on a BD Canto II cytometer (Becton Dickinson, Franklin Lakes, NJ) and analyzed using FlowJo Software version X. Thymus-derived regulatory T cells, conventional T cells, and type 1 adaptive regulatory T cells were identified as live CD3+CD4+CD25hiCD127lo cells, CD3+CD4+CD25loCD127+ cells, and CD3+CD4+CD45RA−CD49b+LAG3+ cells, respectively. CD4 T cells were isolated from freshly isolated peripheral blood mononuclear cells using the CD4 T-cell isolation kit (Miltenyi Biotec). Cell purity was shown to be >95% by flow cytometry. CD4 T cells were plated at 106 cells/ml in complete RMPI 1640 medium and stimulated for 72 hours at 37 °C using plate-bound anti-CD3 antibody (1 μg/ml, OKT3, eBioscience) and soluble anti-CD28 antibody (10 μg/ml, CD28.2, BD Biosciences). After 72 hours, cells were washed and assessed for IL-10 production by flow cytometry or further enriched where indicated, using the IL-10 secretion assay (Miltenyi Biotec) according to provider’s recommendations. Purified CD4 T cells were labeled with CellTrace CFSE (0.5 μM, Life Technologies, Carlsbad, CA). IL-10–secreting CD4 T cells (suppressor cells) were enriched as described previously and added to autologous carboxyfluorescein succinimidyl ester–labeled CD4 T cells (responder cells) in a 1:1 ratio. IL-10–negative CD4 T cells were used as negative control. Cells were then stimulated for 5 days as described previously and proliferation of CD4 T cells was assessed by carboxyfluorescein succinimidyl ester dilution. Statistical analyses were performed using Prism (GraphPad) for Windows. Medians were compared between two groups using nonparametric Mann-Whitney U tests. P-value < 0.05 was considered significant. Abbreviations: ALL, acute lymphocytic leukemia; AML, acute myelogenous leukemia; cGVHD, chronic graft-versus-host disease; HSCT, hematopoietic stem cell transplantation; MAC, myeloablative conditioning; MDS, myelodysplastic syndrome; MM, multiple myeloma; MMF, mycophenolate mofetil; MPS, myeloproliferative syndrome; MTX, methotrexate; MUD, matched unrelated donor; NA, not applicable; NHL, non-Hodgkin lymphoma; RIC, reduced-intensity conditioning.

Abstract Coronavirus 19 (COVID-19) was declared as a pandemic viral infection by the World Health organization on March 11th 2020. Usual clinical manifestations of COVID-19 infection include fever, fatigue, myalgia, headache, diarrhea, dry cough, dyspnea that may lead to acute respiratory distress syndrome and death (1). Skin symptoms of COVID-19 have been poorly described but may include erythematous rash, urticaria and chicken pox like lesions (2-7). Angiotensin-converting enzyme 2 (ACE2) is a cellular receptor for COVID-19.

In metropolitan France, nearly 20 new cases of leprosy are diagnosed each year. The incidence of tuberculosis in France is 8/100,000 inhabitants and there are very few accounts of association of these two mycobacteria. Herein we report a case of co-infection with borderline tuberculoid (BT) leprosy and disseminated tuberculosis diagnosed in metropolitan France.A male subject presented with diffuse painless infiltrated erythematous plaques. The biopsy revealed perisudoral and perineural lymphohistiocytic epithelioid cell granuloma as well as acid-alcohol-fast bacilli on Ziehl staining. PCR was positive for Mycobacterium leprae, confirming the diagnosis of leprosy in the BT form. The staging examination revealed predominantly lymphocytic left pleural effusion, right-central necrotic adenopathy without histological granuloma, negative screening for BK, a positive QuantiFERON-TB™ test, and a positive intradermal tuberculin reaction. The clinical and radiological results militated in favour of disseminated tuberculosis. Combined therapy (rifampicin, isoniazid, ethambutol and pyrazinamide) together with clofazimine resulted in regression of both cutaneous and extra-cutaneous lesions. This rare co-infection combines leprosy, often present for several years, and tuberculosis (usually pulmonary) of subsequent onset. The pathophysiological hypothesis is that of cross-immunity (with anti-TB immunity protecting against subsequent leprosy and vice versa), supported by the inverse correlation of the two levels of prevalence and by the protection afforded by tuberculosis vaccination. In most cases, treatment for TB and leprosy improves both diseases. Patients presenting leprosy should be screened for latent tuberculosis in order to avoid reactivation, particularly in cases where corticosteroid treatment is being given.

To the Editor: Coronavirus disease 19 (COVID-19), a pneumonia associated with severe acute respiratory syndrome coronavirus 2 (SARS-Cov2), was first identified in Wuhan, China, in December 2019, and was characterized as a pandemic by the World Health Organization on March 11, 2020. Fever, dry cough, dyspnea, fatigue, anorexia, ageusia, and anosmia are common symptoms of COVID-19. Reported skin manifestations of COVID-19 include erythematous lesions, sometimes with dengue-like petechiae,1 and urticaria and chickenpox-like vesicles.

Scleromyxedema is a rare skin and systemic mucinosis that is usually associated with monoclonal gammopathy (MG). In this French, multicenter, retrospective study of 33 patients, we investigated the clinical and therapeutic features of MG-associated scleromyxedema. Skin molecular signatures were analyzed using a transcriptomic approach. Skin symptoms included papular eruptions (100%), sclerodermoid features (91%), and leonine facies (39%). MG involved an IgG isotype in all patients, with a predominant λ light chain (73%). Associated hematologic malignancies were diagnosed in 4/33 patients (12%) (smoldering myeloma, n=2; chronic lymphoid leukemia, n=1; and refractory cytopenia with multilineage dysplasia n=1). Carpal tunnel syndrome (33%), arthralgia (25%) and dermato-neuro syndrome (DNS) (18%) were the most common systemic complications. One patient with mucinous cardiopathy died of acute heart failure. Intravenous immunoglobulin (HDIVig) treatment alone or in combination with steroids appeared to be quite effective in nonsevere cases (clinical complete response achieved in 13/31 patients). Plasma cell-directed therapies using lenalidomide and/or bortezomib with dexamethasone and HDIVig led to a significant improvement in severe cases (HDIVig-refractory or cases with central nervous system or cardiac involvement). The emergency treatment of DNS with combined plasmapheresis, HDIVig, and high-dose corticosteroids induced the complete remission of neurological symptoms in 4/5 patients. Quantitative reverse transcriptase-PCR (RT-PCR) analysis of 6 scleromyxedema skin samples showed significantly higher profibrotic pathway levels (transforming growth factor β (TGFβ) and collagen-1) than in healthy skin. Prospective studies targeting plasma cell clones and/or fibrotic pathways are warranted for long-term scleromyxedema management.

Journal of the European Academy of Dermatology and VenereologyVolume 34, Issue 8 p. e348-e350 Letter to the Editor Did Whatsapp® reveal a new cutaneous COVID-19 manifestation? T.A. Duong, Corresponding Author T.A. Duong [email protected] orcid.org/0000-0003-2221-9903 Dermatology Department, Henri Mondor Hospital, Créteil, France Chaire Avenir Santé numérique, Equipe 8 IMRB U955, INSERM, Université Paris Est Créteil, Créteil, France Correspondence: T.A. Duong. E-mail: [email protected]Search for more papers by this authorC. Velter, C. Velter orcid.org/0000-0002-7270-3886 Dermatology Department, Henri Mondor Hospital, Créteil, France Equal contributionSearch for more papers by this authorM. Rybojad, M. Rybojad Dermatology Department, Paris University, Saint-Louis Hospital, Paris, France Equal contributionSearch for more papers by this authorC. Comte, C. Comte Dermatology Department, Paris University, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorM. Bagot, M. Bagot Dermatology Department, Paris University, Saint-Louis Hospital, Paris, France INSERM U976 Human Immunology, Pathophysiology and Immunotherapy, Université de Paris, Paris, FranceSearch for more papers by this authorL. Sulimovic, L. Sulimovic President of the SNDV (syndicat national des dermatologues vénéréologues)/on behalf of SNDV Corona group, Paris, France Equal contributionSearch for more papers by this authorJ.D. Bouaziz, J.D. Bouaziz orcid.org/0000-0002-4993-2461 Dermatology Department, Paris University, Saint-Louis Hospital, Paris, France INSERM U976 Human Immunology, Pathophysiology and Immunotherapy, Université de Paris, Paris, France Equal contributionSearch for more papers by this author T.A. Duong, Corresponding Author T.A. Duong [email protected] orcid.org/0000-0003-2221-9903 Dermatology Department, Henri Mondor Hospital, Créteil, France Chaire Avenir Santé numérique, Equipe 8 IMRB U955, INSERM, Université Paris Est Créteil, Créteil, France Correspondence: T.A. Duong. E-mail: [email protected]Search for more papers by this authorC. Velter, C. Velter orcid.org/0000-0002-7270-3886 Dermatology Department, Henri Mondor Hospital, Créteil, France Equal contributionSearch for more papers by this authorM. Rybojad, M. Rybojad Dermatology Department, Paris University, Saint-Louis Hospital, Paris, France Equal contributionSearch for more papers by this authorC. Comte, C. Comte Dermatology Department, Paris University, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorM. Bagot, M. Bagot Dermatology Department, Paris University, Saint-Louis Hospital, Paris, France INSERM U976 Human Immunology, Pathophysiology and Immunotherapy, Université de Paris, Paris, FranceSearch for more papers by this authorL. Sulimovic, L. Sulimovic President of the SNDV (syndicat national des dermatologues vénéréologues)/on behalf of SNDV Corona group, Paris, France Equal contributionSearch for more papers by this authorJ.D. Bouaziz, J.D. Bouaziz orcid.org/0000-0002-4993-2461 Dermatology Department, Paris University, Saint-Louis Hospital, Paris, France INSERM U976 Human Immunology, Pathophysiology and Immunotherapy, Université de Paris, Paris, France Equal contributionSearch for more papers by this author First published: 24 April 2020 https://doi.org/10.1111/jdv.16534Citations: 32 Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1Ghanchi A. Adaptation of the National Plan for the Prevention and Fight against pandemic influenza to the 2020 COVID-19 epidemic in France. Disaster Med Public Health Prep 2020; 7: 1–9. 10.1017/dmp.2020.82 Google Scholar 2Lan J, Song Z, Miao X et al. Skin damage among healthcare workers managing coronavirus disease-2019. J Am Acad Dermatol 2020; 82: 1215–1216. 10.1016/j.jaad.2020.03.014 CASPubMedWeb of Science®Google Scholar 3Recalcati S. Cutaneous manifestations in COVID- 19: a first perspective. J Eur Acad Dermatol Venereol 2020. https://doi.org/10.1111/jdv.16387 10.1111/jdv.16387 Web of Science®Google Scholar 4Radi G, Diotallevi F, Campanati A, Offidani A. Global coronavirus pandemic (2019-nCOV): implication for an Italian medium size dermatological clinic of a ii level hospital. J Eur Acad Dermatol Venereol 2020. https://doi.org/10.1111/jdv.16386 10.1111/jdv.16386 PubMedWeb of Science®Google Scholar 5Chen Y, Pradhan S, Xue S. What are we doing in the dermatology outpatient department amidst the raging of the 2019 novel coronavirus?J Am Acad Dermatol 2020; 82: 1034. 10.1016/j.jaad.2020.02.030 CASPubMedWeb of Science®Google Scholar 6Eliezer M, Hautefort C, Hamel A-L et al. Sudden and complete olfactory loss function as a possible symptom of COVID-19. JAMA Otolaryngol Head Neck Surg 2020; in press. 10.1001/jamaoto.2020.0832 PubMedWeb of Science®Google Scholar 7Ohannessian R, Duong TA, Odone A. Global telemedicine implementation and integration within health systems to fight the COVID-19 pandemic: a call to action. JMIR Public Health Surveill 2020; 6: e18810. 10.2196/18810 PubMedGoogle Scholar 8Tang L, Bie B, Park S-E, Zhi D. Social media and outbreaks of emerging infectious diseases: a systematic review of literature. 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L'infection à SARS-CoV-2 (COVID-19), pneumonie associée au virus SARS-Cov2, a été identifiée pour la première fois à Wuhan, en Chine en décembre 2019, et a été qualifiée de pandémie par l'Organisation mondiale de la santé (OMS) le 11 mars 2020. Nous avons réalisé une étude rétrospective observationnelle à l'échelle nationale des lésions cutanées rencontrées lors de la pandémie de COVID-19 en France du 18 mars au 9 avril 2020 dans un cadre ambulatoire. Les patients ont donné leur consentement éclairé pour la publication de leurs photographies et cette étude a été approuvée par le CPP de l'hôpital Bichat, Paris. Deux cent soixante-dix-sept patients ont été recrutés, dont la moitié étaient des hommes, l'âge médian était de 27 ans (2–98). Les lésions ont été classées en six catégories : urticaire (n = 26, 9 %), vésicules (n = 41, 15 %), lésions acrales (n = 142, 51 %), morbilliformes (n = 25, 9 %), pétéchiales (n = 7, 3 %), livedo reticularis (n = 4, 1 %) et autres (n = 41, 15 %). Certains patients présentaient des signes cutanés correspondant à plusieurs catégories. Les lésions acrales étaient particulièrement fréquentes (n = 142). Les lésions ressemblant à des engelures étaient les plus fréquentes des lésions acrales (n = 106/142, 75 %). Des lésions vésiculaires acrales (de type dyshidrose) étaient signalées dans 20 cas (14 %). Une acrodynie était présente dans 18 cas (6 %), parfois isolée. Parmi les 277 patients, 34 avaient subi une PCR nasopharyngée SARS-Cov-2, dont 25 étaient positives (74 %). Sept de ces 25 (28 %) avaient des lésions acrales. Parmi les patients sans test PCR positif, 115 patients présentaient des symptômes extracutanés évocateurs et/ou avaient signalé un contact étroit avec un patient atteint de COVID-19. L'examen histologique de 3 lésions de type engelures révélait une dermatite lichénoïde avec un infiltrat mononucléé périvasculaire et eccrine et des microthrombi vasculaires dans 2 cas. Notre étude apporte une description de la riche symptomatologie cutanée liée au SARS-Cov-2. Bien que le nombre de patients testés ne nous permette pas de tirer des conclusions définitives concernant un lien direct entre le SARS-Cov-2 et ces lésions cutanées, l'épidémie inattendue de lésions cutanées acrales dans ce contexte épidémique suggère un lien dont la physiopathologie mérite de futures investigations.

We describe a unique case of human T-lymphotropic virus 1 (HTLV-1)-associated infective dermatitis-like lesions in systemic lupus erythematosus. This suggests that some lupus patients may have immunological abnormalities resembling to those described in chronic HTLV-1 infection.

Background Blau syndrome (BS) is a rare monogenic autoinflammatory disease caused by NOD2 mutations. BS classically presents in early childhood as a triad of granulomatous polyarthritis, uveitis and skin involvement. Joint and ocular involvement have been characterized by several cohort studies but only very little data are available on skin lesions. Objectives We aimed to provide a detailed clinical and microscopic analysis of skin manifestations and to study whether they may contribute to an early diagnosis. Methods We conducted a retrospective multicentre study in a French cohort of 21 patients diagnosed with genetically confirmed BS. Results Skin involvement was the first clinical manifestation of BS in 15/16 patients with dermatological manifestations. The presence of skin lesions was associated with significant shorter age at diagnosis (P = 0.03) and diagnostic delay (P = 0.04). Dermatological assessment allowed an earlier diagnosis (P = 0.001) and reduces the diagnostic delay (P = 0.007). Early skin lesions had a homogeneous, stereotypical clinical presentation, namely non-confluent erythematous or pigmented millimetric papules in 13/14(93%) patients. In contrast, skin lesions occurring during later disease stages had a more heterogeneous clinical presentation, including ichthyosiform dermatosis, panniculitis, livedoid lesions and vasculitis. Whatever their time of occurrence and the clinical aspect, all biopsied showed histologically presence of granuloma. Conclusion Skin involvement in BS is the earliest clinical manifestation of the BS in the large majority of patients. The recognition of dermatological manifestations as granulomatous skin lesions and early dermatological expertise are the key to an early diagnosis of BS. In view of our results, it seems reasonable to propose a simplified view of skin lesions of BS in which the granuloma is the key structure.

INTRODUCTION:In metropolitan France, nearly 20 new cases of leprosy are diagnosed each year. The incidence of tuberculosis in France is 8/100,000 inhabitants and there are very few accounts of association of these two mycobacteria. Herein we report a case of co-infection with borderline tuberculoid (BT) leprosy and disseminated tuberculosis diagnosed in metropolitan France.PATIENTS AND METHODS:A male subject presented with diffuse painless infiltrated erythematous plaques. The biopsy revealed perisudoral and perineural lymphohistiocytic epithelioid cell granuloma as well as acid-alcohol-fast bacilli on Ziehl staining. PCR was positive for Mycobacterium leprae, confirming the diagnosis of leprosy in the BT form. The staging examination revealed predominantly lymphocytic left pleural effusion, right-central necrotic adenopathy without histological granuloma, negative screening for BK, a positive QuantiFERON-TB™ test, and a positive intradermal tuberculin reaction. The clinical and radiological results militated in favour of disseminated tuberculosis. Combined therapy (rifampicin, isoniazid, ethambutol and pyrazinamide) together with clofazimine resulted in regression of both cutaneous and extra-cutaneous lesions. This rare co-infection combines leprosy, often present for several years, and tuberculosis (usually pulmonary) of subsequent onset. The pathophysiological hypothesis is that of cross-immunity (with anti-TB immunity protecting against subsequent leprosy and vice versa), supported by the inverse correlation of the two levels of prevalence and by the protection afforded by tuberculosis vaccination. In most cases, treatment for TB and leprosy improves both diseases. Patients presenting leprosy should be screened for latent tuberculosis in order to avoid reactivation, particularly in cases where corticosteroid treatment is being given.

Les lymphomes B cutanés primitifs de la zone marginale (LBCPZM) correspondent à une prolifération lympho-plasmocytaire cutanée clonale d'évolution en général indolente. Ils se manifestent le plus souvent par des papules et des nodules érythémateux. Les amyloses cutanées (AC) correspondent à des dépôts amyloïdes visibles en coloration Rouge Congo ou par biréfringence vert pomme en lumière polarisée. L'association LBCPZM et AC a été peu rapportée. Étude rétrospective multicentrique de la base de données de deux services d'anatomie pathologique. Les critères d'inclusion étaient : – infiltrat lympho-plasmocytaire ; – monotypie de la chaîne légère Kappa ou Lambda ; – dépôts amyloïdes cutanés. Entre 1996 et 2019, six observations ont été recensées : 5 hommes et une femme ; âge médian 44 ans (29–58) ; suivi moyen 6 ans (0,23–21). Les lésions étaient des plaques ou des nodules violacés uniques ou multiples (n = 5) localisés sur les membres inférieurs (n = 4), le tronc (n = 1) ou le visage (n = 1). Tous les patients, sauf un, ont eu au moins une des associations thérapeutiques locales ou générales : – radiothérapie, bêtaméthasone, cryothérapie et laser (n = 2) ; – rituximab et cyclophosphamide suivi de chlorambucil (n = 1) ; la récurrence à 8 ans a conduit à associer rituximab et bendamustine avec une efficacité partielle ; – un patient (6) a rechuté 5 ans après l'exérèse chirurgicale et a alors reçu des séances de radiothérapie, des cures de rituximab et de la bendamustine sans efficacité ; – un patient (5) a reçu du rituximab (réponse partielle) puis du bortézomib et de la dexaméthasone (rémission complète). La réponse a été le plus souvent partielle (n = 5). On notait une rémission complète (n = 1) avec bortézomib et dexaméthasone (RC). Notre travail souligne la rareté de cette association, sa difficulté diagnostique et l'absence de traitement spécifique disponible. Le clinicien favorisera le traitement chirurgical ou local.

En métropole, près de 20 nouveaux cas de lèpre sont diagnostiqués chaque année. L’incidence de la tuberculose en France est de 7,2/100 000 habitants et l’association des deux mycobactéries a été exceptionnellement rapportée. Nous rapportons un cas de co-infection avec lèpre borderline tuberculoïde (BT) et tuberculose disséminée diagnostiqué en France métropolitaine. Un homme de 34 ans, originaire d’Inde, consultait pour des plaques érythémateuses infiltrées et hypoesthésiques du visage, du tronc, des membres supérieurs, de la cuisse droite et du lobule de l’oreille droite. La biopsie cutanée montrait un granulome épithélioïde lympho-histiocytaire à tropisme péri-sudoral et péri-nerveux, et la coloration de Ziehl mettait en évidence des bacilles acido-alcoolo-résistants. La PCR Mycobacterium leprae était positive, confirmant le diagnostic de lèpre, BT d’après la présentation clinico-biologique. Le patient présentait une altération de l’état général fébrile et des douleurs abdominales, ne s’intégrant pas dans le cadre de la lèpre. La tomodensitométrie montrait un épanchement pleural gauche de moyenne abondance, une adénopathie hilaire droite de 11 mm à centre nécrotique et un épanchement péritonéal. La ponction pleurale trouvait un exsudat lymphocytaire et la biopsie ganglionnaire ne montrait pas de granulome. L’examen direct, la culture et la PCR BK étaient négatifs dans les biopsies bronchique et cutanée, et les BK crachats. Le test du Quantiféron® et l’intradermoréaction à la tuberculine étaient positifs. Le tableau clinico-radiologique était en faveur d’une tuberculose disséminée, selon la définition de l’Organisation mondiale de la santé (OMS). Un traitement associant polychimiothérapie anti-lépreuse (PCT) et quadrithérapie antituberculeuse (rifampicine, isoniazide, ethambutol, pyrazinamide, clofazimine) était débuté. Quelques jours après, une réaction de réversion (diplégie faciale), justifiait une corticothérapie à 1 mg/kg/j. À 12 mois était notée une régression complète des lésions cutanées, extra-cutanées et de la diplégie faciale. Au total, moins de 200 cas de co-infection lèpre et tuberculose ont été rapportés, avec un âge médian de 37 ans [18–69]. La lèpre est inaugurale dans 89 % des cas, et la tuberculose dans 6 % des cas, avec un intervalle médian de 12 mois [0,5–300] ; les 2 infections sont simultanées dans 5 % des cas. La lèpre est lépromateuse dans 80 % des cas et tuberculoïde dans 20 % des cas. La tuberculose est pleuropulmonaire dans 90 % des cas, rarement cutanéo-muqueuse. Plusieurs hypothèses physiopathologiques historiques ont été avancées, celle de l’immunité croisée et celle de la mortalité de la co-infection. De même zone d’endémie, cette co-infection doit être connue car elle peut être fatale. Un cas de lèpre doit faire rechercher une tuberculose latente afin de limiter l’émergence de formes résistantes à la rifampicine et d’éviter une réactivation, a fortiori si une corticothérapie est associée.

Journal of the European Academy of Dermatology and VenereologyVolume 33, Issue 8 p. e303-e304 Letter to the Editor Dramatic improvement of generalized prurigo nodularis with dupilumab A. Calugareanu, A. Calugareanu Dermatology Department, Saint-Louis Hospital, APHP, Paris, FranceSearch for more papers by this authorM. Jachiet, M. Jachiet Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorC. Lepelletier, C. Lepelletier Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorA. De Masson, A. De Masson Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorM. Rybojad, M. Rybojad Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorM. Bagot, M. Bagot Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorJ.D. Bouaziz, Corresponding Author J.D. Bouaziz jean-david.bouaziz@aphp.fr Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceCorrespondence: J.D. Bouaziz. E-mail: jean-david.bouaziz@aphp.frSearch for more papers by this author A. Calugareanu, A. Calugareanu Dermatology Department, Saint-Louis Hospital, APHP, Paris, FranceSearch for more papers by this authorM. Jachiet, M. Jachiet Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorC. Lepelletier, C. Lepelletier Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorA. De Masson, A. De Masson Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorM. Rybojad, M. Rybojad Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorM. Bagot, M. Bagot Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceSearch for more papers by this authorJ.D. Bouaziz, Corresponding Author J.D. Bouaziz jean-david.bouaziz@aphp.fr Dermatology Department, Saint-Louis Hospital, APHP, Paris, France Université Paris Diderot-Paris VII, Sorbonne Paris Cité, Paris, FranceCorrespondence: J.D. Bouaziz. E-mail: jean-david.bouaziz@aphp.frSearch for more papers by this author First published: 20 March 2019 https://doi.org/10.1111/jdv.15584Citations: 21Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume33, Issue8August 2019Pages e303-e304 RelatedInformation

Neutrophilic dermatoses (ND) are a group of conditions characterized by an aseptic accumulation of polymorphonuclear leukocytes in the skin. Occurrence of ND in association with myeloid malignancies, mainly myelodysplastic syndrome and myelogenous acute leukemia, is not rare and is often associated with a poor prognosis. Recent findings have improved understanding of the pathophysiology of myeloid malignancy-associated ND. We review the clinical spectrum of myeloid malignancy-associated ND with an emphasis on recently identified mechanisms. Myeloid leukemia cells retain the potential for terminal differentiation into polymorphonuclear leukocytes in the skin. Many studies suggest a clonal link between myeloid malignancies and ND. Activation of autoinflammatory pathways (NOD-like receptor family pyrin domain-containing-3, Familial Mediterranean Fever Gene) in the clonal cells of myeloid disorders may also be involved in this setting.

Journal of the European Academy of Dermatology and VenereologyVolume 32, Issue 11 p. e402-e403 Letter to the Editor Chronic oral lichenoid erosions revealing haematological malignancies E. Ouedraogo, E. Ouedraogo Dermatology Department, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorJ. Gottlieb, J. Gottlieb Dermatology Department, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorA. de Masson, A. de Masson Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorC. Lepelletier, C. Lepelletier Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorM. Jachiet, M. Jachiet Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorM. Rybojad, M. Rybojad Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorM. Bagot, M. Bagot Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorL. Galicier, L. Galicier Paris VII Sorbonne Paris Cité University, Paris, France Immunology Department, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorJ.-D. Bouaziz, Corresponding Author J.-D. Bouaziz jean-david.bouaziz@aphp.fr Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceCorrespondence: J.-D. Bouaziz. E-mail: jean-david.bouaziz@aphp.frSearch for more papers by this author E. Ouedraogo, E. Ouedraogo Dermatology Department, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorJ. Gottlieb, J. Gottlieb Dermatology Department, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorA. de Masson, A. de Masson Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorC. Lepelletier, C. Lepelletier Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorM. Jachiet, M. Jachiet Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorM. Rybojad, M. Rybojad Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorM. Bagot, M. Bagot Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceSearch for more papers by this authorL. Galicier, L. Galicier Paris VII Sorbonne Paris Cité University, Paris, France Immunology Department, Saint-Louis Hospital, Paris, FranceSearch for more papers by this authorJ.-D. Bouaziz, Corresponding Author J.-D. Bouaziz jean-david.bouaziz@aphp.fr Dermatology Department, Saint-Louis Hospital, Paris, France Paris VII Sorbonne Paris Cité University, Paris, FranceCorrespondence: J.-D. Bouaziz. E-mail: jean-david.bouaziz@aphp.frSearch for more papers by this author First published: 06 April 2018 https://doi.org/10.1111/jdv.14992Citations: 1Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume32, Issue11November 2018Pages e402-e403 RelatedInformation