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Background Chronic leg ulcers affect a large portion of the adult population and cause a significant social and economic impact, related to outpatient and hospital care, absence from work, social security expenses, and reduced quality of life. The correct diagnosis and therapeutic approach are essential for a favorable evolution. Objective To gather the experience of Brazilian dermatologists, reviewing the specialized literature to prepare recommendations for the diagnosis and treatment of the main types of chronic leg ulcers. Methods Seven specialists from six university centers with experience in chronic leg ulcers were appointed by the Brazilian Society of Dermatology to reach a consensus on the diagnosis and therapeutic management of these ulcers. Based on the adapted DELPHI methodology, relevant elements were considered in the diagnosis and treatment of chronic leg ulcers of the most common causes; then, the recent literature was analyzed using the best scientific evidence. Results The following themes were defined as relevant for this consensus - the most prevalent differential etiological diagnoses of chronic leg ulcers (venous, arterial, neuropathic, and hypertensive ulcers), as well as the management of each one. It also included the topic of general principles for local management, common to chronic ulcers, regardless of the etiology. Conclusion This consensus addressed the main etiologies of chronic leg ulcers and their management based on scientific evidence to assist dermatologists and other health professionals and benefit the greatest number of patients with this condition.

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BackgroundStevens-Johnson syndrome and toxic epidermal necrolysis are life-threatening blistering drug reactions with high incidence of ocular sequela. The term ‘Epidermal Necrolysis’ has been recently used to better describe the full spectrum of the disease that includes Stevens-Johnson syndrome and toxic epidermal necrolysis at opposite ends, which differ by the extent of body surface area with epidermal detachment. SCORTEN is a mortality prognosis score for ‘Epidermal Necrolysis’ cases that still needed validation in acquired immunodeficiency syndrome.ObjectiveTo evaluate the SCORTEN performance in acquired immunodeficiency syndrome, and the differences in outcomes between acquired immunodeficiency syndrome and non- acquired immunodeficiency syndrome cohorts.MethodsRetrospective cohort study of AIDS and non-AIDS ‘Epidermal Necrolysis’ cases admitted to a Brazilian reference center from 1990-2014.ResultsFive deaths (16.7%) occurred as a consequence of EN in 30 AIDS patients, and seven (17.9%) in 39 non-AIDS patients, relative risk (RR) .92 (p=1.0). SCORTEN showed great performance, with an Area Under the Receiver Operating Curve (AUC) (ROC) of 0.90 with a 95% confidence interval ranging from .81 to .99. The performance of SCORTEN was better among non- AIDS patients than AIDS patients: AUC non- acquired immunodeficiency syndrome =0.99 (CI 05% 0.96-1.00), AUC acquired immunodeficiency syndrome = 0.74 (CI 95% 0.53-0.95), p=.02.Study LimitationsHeterogeneity of cases, wide variation of systemic corticosteroid doses when used.ConclusionSCORTEN is valid for the Brazilian population, including among those patients with acquired immunodeficiency syndrome, and, as such, its use is recommended for aiding treatment choice in this subgroup of patients.

Corticosteroid or thalidomide adverse effects and aPL and ß2GPI polymorphisms may cause TBE in patients with MB leprosy.

Generalized verrucosis (GV) is a cutaneous manifestation of human papillomavirus (HPV). GV is defined by the presence of over 20 verrucae distributed in various anatomical sites. The condition predominantly affects the digits, where the presence of numerous verrucae may be function-limiting. GV is observed in association with multiple congenital and acquired immunodeficiencies, including GATA2 deficiency (OMIM #614172) (Table 1). 1 GATA2 deficiency is a rare primary immunodeficiency (PID) characterized by hematological cytopenias, including those of Blymphocytes, natural killer cells (NK), and dendritic cells. Patients are prone to developing myeloid leukemia and opportunistic infections, including mycobacterial, HPV, and opportunistic fungal infections. 6 GATA2 deficiency most often manifests during adolescence or young adulthood; the peak age for hemato-immunologic disease manifestations lies between the second and third decade of life. 5 The GATA2 protein is a transcription factor that regulates gene expression in hematopoietic cells, lymphatic development, and dendritic cell differentiation. 2,3 GATA2 mutations appear to cause loss of function of the mutated allele, leading to haploinsufficiency.Germline mutations in the GATA2 gene arise spontaneously but are then transmitted by autosomal dominant inheritance 4 The high rate of de novo GATA2 mutations in patients with myelodysplastic syndromes and the low number of silent carriers are consistent with a disease exhibiting high penetrance and expressivity. 5 We report a case of GV associated with GATA2 deficiency, which worsened after cyclosporine use following bone marrow transplant (BMT), but which was successfully treated with oral acitretin and topical application of trichloroacetic acid.

All excised BCCs fulfilled criteria for MMS indication, among them recurrent and nasal BCCs stood out. The greater number of criteria may be a predictive factor for subclinical extension and can help prioritize indications for MMS.

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