Myelodysplasia Cutis Versus Leukemia Cutis

Osio, Amélie; Battistella, Maxime; Feugeas, Jean-Paul; Cuccuini, Wendy; Noguera, Maria Elena; Petrella, Tony; Raffoux, Emmanuel; Janin, Anne; Pennamen, Vignon

doi:10.1038/jid.2015.146

Cited by 39 publications

(51 citation statements)

References 14 publications

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“…Discriminant features (clinical, histological and survival) were observed between the two groups. They propose that these patients have myelodysplasia cutis, a cutaneous specific manifestation, different from leukaemia cutis . For clinicians, myelodysplasia cutis may better characterize patients with cutaneous infiltration by immature myeloid cells than histiocytoid Sweet syndrome.…”

Section: Sweet Syndromementioning

confidence: 99%

Pyoderma gangrenosum and Sweet syndrome: the prototypic neutrophilic dermatoses

Wallach¹,

Vignon‐Pennamen

2015

Br J Dermatol

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Pyoderma gangrenosum, a dramatic ulcerative skin disease, and Sweet syndrome, a papular dermatosis, were described independently. It was subsequently shown that they share many characteristics, including clinical overlap and the frequent association with multisystemic disorders. The group of the neutrophilic dermatoses encompasses these two dermatoses, as well as other conditions having in common an aseptic neutrophilic infiltrate predominating in the epidermis and/or the dermis and/or the subcutis. Some patients also experience neutrophilic infiltrates in other organs, defining the neutrophilic disease. Recent research suggests that the neutrophilic dermatoses could be considered as the cutaneous expression of the autoinflammation, an aberrant hyperproduction of interleukin-1. Autoinflammation is responsible for monogenic diseases, and is also involved in the mechanism of many polygenic conditions, including the neutrophilic dermatoses.

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Section: Sweet Syndromementioning

confidence: 99%

Pyoderma gangrenosum and Sweet syndrome: the prototypic neutrophilic dermatoses

Wallach¹,

Vignon‐Pennamen

2015

Br J Dermatol

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“…H‐SS is a histological variant of SS differing from classical neutrophilic SS by a dermal infiltrate mostly made of immature cells of the myeloid lineage, which has been associated with myeloid malignancies 3–5 . We recently observed that the skin immature myeloid cells seen in this H‐SS variant were clonally related to the myeloid malignancy, and we proposed to designate this H‐SS variant occurring in patients with MDS as ‘myelodysplasia cutis’ 6 . Herein we report a descriptive case with identification of clonal skin myeloid cells by next‐generation sequencing (NGS) and highlight important nuances between myelodysplasia cutis, H‐SS and leukaemia cutis.…”

Section: Figurementioning

confidence: 99%

“…This is, to our knowledge, the first reported case of myelodysplasia cutis with detailed clinicohistological features, in which NGS analyses confirmed the clonality of the dysplastic myeloid infiltrates in both the blood and skin. Most patients with myelodysplasia cutis present with relapsing erythematous papules and plaques, fever and arthralgia 6 . The histological features of myelodysplasia cutis include a papillary dermal oedema and a perivascular and periadnexal inflammatory infiltrate of T cells and polymorphic, dysplastic myeloid cells (pseudo‐Pelger–Hüet abnormalities) expressing myeloid markers such as CD33, CD68, CD163 and myeloperoxidase, but no blastic marker (CD34, CD56 or CD117) 6 .…”

Section: Figurementioning

confidence: 99%

“…Most patients with myelodysplasia cutis present with relapsing erythematous papules and plaques, fever and arthralgia 6 . The histological features of myelodysplasia cutis include a papillary dermal oedema and a perivascular and periadnexal inflammatory infiltrate of T cells and polymorphic, dysplastic myeloid cells (pseudo‐Pelger–Hüet abnormalities) expressing myeloid markers such as CD33, CD68, CD163 and myeloperoxidase, but no blastic marker (CD34, CD56 or CD117) 6 . In our case, the perivascular inflammatory infiltrate may have misled to a diagnosis of MDS‐associated vasculitis.…”

Section: Figurementioning

confidence: 99%

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Identification of clonal skin myeloid cells by next‐generation sequencing in myelodysplasia cutis

et al. 2020

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number 16_136). CPRD collects deidentified patient data from a network of general practitioner practices across the UK. Primary care data are linked to a range of other health-related data to provide a longitudinal, representative UK population health dataset. The data encompass 50 million patients, including 14 million currently registered patients. Additional methods and results are available upon direct request. In our cohort there were 12 057, 17 614 and 80 854 patients in the whole of the UK living with MM, SCC or BCC, respectively. The prevalence of MM was 0Á3%, SCC had a prevalence of 0Á4%, and BCC had the highest prevalence at 1Á8%. Over the 10-year study period, there was a 36% increase in the age-adjusted incidence of MM, a 34% increase in SCC and a 21% increase of BCC. Sex-stratified incidence per 100 000 person years (PYs) was age-adjusted (SEM) for 2004 and then 2014 [for MM, 15Á8 (0Á9) to 26Á4 (1Á0) for men and 22Á4 (1Á1) to 25Á5 (1Á0) for women; for SCC, 48Á2 (1Á4) to 66Á0 (1Á6) for men and 25Á4 (1Á2) to 32Á6 (1Á2) for women; and for BCC, 161Á2 (2Á6) to 201Á1 (2Á7) for men and 124Á0 (2Á5) to 143Á8 (2Á5) for women].

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“…In most cases, cutaneous leukaemic infiltration indicates that the disease will progress within a few months of the diagnosis of leukaemia cutis (Osio et al, 2015;Peña-Romero et al, 2016). Both the current patients had a short time from diagnosis to death.…”

Section: Discussionmentioning

confidence: 99%