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Lymphomatoid papulosis (LyP) is a benign chronic often relapsing skin condition that belongs to the CD30‐positive cutaneous lymphoproliferative disorders. LyP typically presents as crops of lesions with a tendency to self‐resolve, and morphology can range from solitary to agminated or diffuse papules and plaques to nodules or tumours. The clinical–histological spectrum can range from borderline cases to overlap with primary cutaneous anaplastic cell lymphoma (pcALCL). Histology and immunophenotype commonly show overlap with other CD30‐positive disorders and sometimes may be identical to pcALCL, making its diagnosis more difficult. Patients with LyP have an increased risk of developing a second neoplasm such as mycosis fungoides, pcALCL and/or Hodgkin lymphoma. Clinical correlation allows its proper classification and diagnosis, which is fundamental for treatment and prognosis. This review focuses on the clinical appearance, histopathological features, diagnosis, differential diagnosis and management of LyP.

SEC can present on the trunk and are not limited to the head and neck region. In addition to syringoma-like tadpole structures and glandular differentiation, these tumours can also exhibit squamoid and cribriform growth patterns. Immunostaining in SEC is variable and this variability is believed to stem from this tumour's ability to differentiate along multiple routes, including sweat secretory and/or ductal differentiation.

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Survivors of SJS/TEN suffer from severe physical complications impacting their health and lives that are mostly under recognized and not sufficiently treated by medical professionals.

BackgroundMost cancer patients are treated with radiotherapy, but the treatment can also damage the surrounding normal tissue. Acute skin damage from cancer radiotherapy diminishes patients’ quality of life, yet effective biological interventions for this damage are lacking. Protecting microvascular endothelial cells from irradiation-induced perturbations is emerging as a targeted damage-reduction strategy. Since Angiopoetin-1 signaling through the Tie2 receptor on endothelial cells opposes microvascular perturbations in other disease contexts, we used a preclinical Angiopoietin-1 mimic called Vasculotide to investigate its effect on skin radiation toxicity using a preclinical model.MethodsAthymic mice were treated intraperitoneally with saline or Vasculotide and their flank skin was irradiated with a single large dose of ionizing radiation. Acute cutaneous damage and wound healing were evaluated by clinical skin grading, histology and immunostaining. Diffuse reflectance optical spectroscopy, myeloperoxidase-dependent bioluminescence imaging of neutrophils and a serum cytokine array were used to assess inflammation. Microvascular endothelial cell response to radiation was tested with in vitro clonogenic and Matrigel tubule formation assays. Tumour xenograft growth delay experiments were also performed. Appreciable differences between treatment groups were assessed mainly using parametric and non-parametric statistical tests comparing areas under curves, followed by post-hoc comparisons.ResultsIn vivo, different schedules of Vasculotide treatment reduced the size of the irradiation-induced wound. Although skin damage scores remained similar on individual days, Vasculotide administered post irradiation resulted in less skin damage overall. Vasculotide alleviated irradiation-induced inflammation in the form of reduced levels of oxygenated hemoglobin, myeloperoxidase bioluminescence and chemokine MIP-2. Surprisingly, Vasculotide-treated animals also had higher microvascular endothelial cell density in wound granulation tissue. In vitro, Vasculotide enhanced the survival and function of irradiated endothelial cells.ConclusionsVasculotide administration reduces acute skin radiation damage in mice, and may do so by affecting several biological processes. This radiation protection approach may have clinical impact for cancer radiotherapy patients by reducing the severity of their acute skin radiation damage.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2407-14-614) contains supplementary material, which is available to authorized users.

Thirty-two percent of patients achieved pCR with intralesional IL-2 therapy and had a significantly improved PFS compared with the rest of the cohort, which may be explained by a systemic CD8+ T-cell response.

A 66-year-old female was diagnosed with myelodysplastic syndrome (MDS), specifically refractory cytopenia with multilineage dysplasia. Her bone marrow demonstrated 3% blasts with a complex karyotype and she had transfusion-dependent anaemia and thrombocytopenia. She was started on azacitidine for very high-risk MDS, as determined by her Revised International Prognostic Scoring System score.The first cycle of azacitidine was well tolerated. Three days into her second cycle, multiple erythematous, painful pustular plaques with a violaceous border and central haemorrhagic crusting appeared on her lips, inner nose and upper arms (top). Empirical ciprofloxacin and clindamycin had no clinical benefit and the lesions then progressed to involve her forearms, with three dominant lesions 3-4 cm in diameter.A skin biopsy demonstrated a neutrophilic infiltrate with marked acute inflammation and reactive changes (bottom); microbiological studies were negative. The clinical and pathological presentation was in keeping with pyoderma gangrenosum (PG). She was treated with prednisone and colchicine, and the azacitidine was withheld for 2 months with subsequent healing of the lesions. The forearm lesions recurred when re-challenged with azacitidine, but promptly responded to a second course of prednisone.Neutrophilic dermatoses, including Sweet syndrome and PG, are uncommon but well-documented dermatological sequalae of MDS. However, given the recurrence of skin lesions with therapy, the clinical and pathological picture was most in keeping with PG secondary to azacitidine, rather than to the underlying disease. PG in MDS has also been linked to the administration of granulocyte colony-stimulating factor. While our patient's skin lesions were controlled with concurrent colchicine and corticosteroids, her MDS did not improve with azacitidine and as a result, this drug was stopped after five cycles.