ROBERTO TAKAOKA
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
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- When does atopic dermatitis warrant systemic therapy? Recommendations from an expert panel of the International Eczema Council(2017) SIMPSON, Eric L.; BRUIN-WELLER, Marjolein; FLOHR, Carsten; ARDERN-JONES, Michael R.; BARBAROT, Sebastien; DELEURAN, Mette; BIEBER, Thomas; VESTERGAARD, Christian; BROWN, Sara J.; CORK, Michael J.; DRUCKER, Aaron M.; EICHENFIELD, Lawrence F.; FOELSTER-HOLST, Regina; GUTTMAN-YASSKY, Emma; NOSBAUM, Audrey; REYNOLDS, Nick J.; SILVERBERG, Jonathan I.; SCHMITT, Jochen; SEYGER, Marieke M. B.; SPULS, Phyllis I.; STALDER, Jean-Francois; SU, John C.; TAKAOKA, Roberto; TRAIDL-HOFFMANN, Claudia; THYSSEN, Jacob P.; SCHAFT, Jorien van der; WOLLENBERG, Andreas; IRVINE, Alan D.; PALLER, Amy S.Background: Although most patients with atopic dermatitis (AD) are effectively managed with topical medication, a significant minority require systemic therapy. Guidelines for decision making about advancement to systemic therapy are lacking. Objective: To guide those considering use of systemic therapy in AD and provide a framework for evaluation before making this therapeutic decision with the patient. Methods: A subgroup of the International Eczema Council determined aspects to consider before prescribing systemic therapy. Topics were assigned to expert reviewers who performed a topic-specific literature review, referred to guidelines when available, and provided interpretation and expert opinion. Results: We recommend a systematic and holistic approach to assess patients with severe signs and symptoms of AD and impact on quality of life before systemic therapy. Steps taken before commencing systemic therapy include considering alternate or concomitant diagnoses, avoiding trigger factors, optimizing topical therapy, ensuring adequate patient/caregiver education, treating coexistent infection, assessing the impact on quality of life, and considering phototherapy. Limitations: Our work is a consensus statement, not a systematic review. Conclusion: The decision to start systemic medication should include assessment of severity and quality of life while considering the individual's general health status, psychologic needs, and personal attitudes toward systemic therapies.
conferenceObject Adult atopic dermatitis: Evaluation of TH17 and TH22 cytokines in peripheral blood mononuclear cells induced by staphylococcal enterotoxins A and B(2012) ORFALI, Raquel Lean; RIVITTI, Evandro; SATO, Maria Notomi; TAKAOKA, Roberto; AOKI, ValeriaObjective: Evaluation of interleukins (IL) 17, 22, and 23 induced by Staphylococcus aureus enterotoxin stimulation in peripheral blood mononuclear cells (PBMC) of adults with atopic dermatitis. Background: Atopic dermatitis (AD) is a chronic, inflammatory disease with a high prevalence and complex etiopathogenesis.S aureusis present in 80% to 100% of AD patients, and secretes exotoxins that might relate to its pathogenesis. TH17 has been described as playing a major role in inflammatory diseases with a close relationship to bacterial pathogens, as well as TH22 in modulating the immunopathogenesis of some skin diseases. Methods: Thirty-eight AD patients (mean age, 28.55), 19 female and 19 male, and 40 healthy controls (mean age, 34.1), 21 females and 19 males (without personal or family history of atopy and negative prick-test) were selected. Hanifin and Rajka’s criteria were used to diagnose AD. Disease severity was established according to EASI (Eczema Area and Severity Index). IL-17, IL-22, and IL-23 production from PBMC after staphylococcal enterotoxins A (SEA) and B (SEB), and phytohemaglutinin (PHA) stimuli and IL-22 serum levels were measured by ELISA. Results: In AD patients, there was increased IL-22 levels in sera as well as in vitro secretion by PBMC after SEA and SEB stimuli, when compared to healthy controls. No correlation between IL-22 levels and EASI was observed (P ≤ .05). Conclusion: These findings suggest an involvement of TH22 subtype in the pathogenesis of adults with AD, especially because of its link to S aureus enterotoxins.