DAGOBERTO CALLEGARO
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/45 - Laboratório de Fisiopatologia Neurocirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/62 - Laboratório de Fisiopatologia Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/45 - Laboratório de Fisiopatologia Neurocirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/62 - Laboratório de Fisiopatologia Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
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- Drug-related demyelinating syndromes: understanding risk factors, pathophysiological mechanisms and magnetic resonance imaging findings(2021) RIMKUS, Carolina M.; SCHOEPS, Vinicius Andreoli; BOAVENTURA, Mateus; GODOY, Luis Filipe; APOSTOLOS-PEREIRA, Samira Luisa; CALICH, Ana Luisa; CALLEGARO, Dagoberto; LUCATO, Leandro Tavares; ROVIRA, Alex; SASTRE-GARRIGA, Jaume; LEITE, Claudia da CostaSome drugs and medications can precipitate immune system deregulations, which might be confused with recurrent demyelinating diseases, such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMO), exacerbations of an existing disease, neoplastic lesions or other conditions. In this narrative review we describe some of the most relevant drugs and medications associated with iatrogenic demyelination. The anthelminthic agent levamisole is a frequent cocaine adulterant and can precipitate an exacerbated immune response attacking the central nervous system (CNS). High-efficacy multiple sclerosis (MS) drugs might induce a selective CNS immunosuppression, making it susceptible for opportunistic infections that course with demye-lination, such as progressive multifocal leukoencephalopathy. Sometimes, the interruption of a high-efficacy drug to treat MS can induce a rapid CNS reentry of lymphocytes, exacerbating demyelinating processes and triggering rebound syndromes. Furthermore, selective cytokines inhibition, such as anti-TNF alpha agents, might induce an imbalance between cell death and proliferation inducing a paradoxical increase of CNS tumor necrosis factor (TNF), affecting the activity of lymphocytes, microglia and macrophages, triggering aberrant inflammation and demyelination. Immune checkpoint inhibitors are a new class of antineoplastic drugs that enhance the immune response against tumor cells by an upregulation of T-cell activity. However, this hyperactivation of the immune system might be associated with induction of unwanted autoimmune responses. In this paper we review the risk factors, the possible pathological mechanisms and the magnetic resonance imaging (MRI) findings of these drug-related demyelinating syndromes.
conferenceObject MOG-IgA characterizes a subgroup of patients with central nervous system demyelination(2023) GOMES, Ana Beatriz Ayroza Galvao Ribeiro; KULSVEHAGEN, Laila; LIPPS, Patrick; CAGOL, Alessandro; FUERTES, Nuria Cerda; NEZIRAJ, Tradite; FLAMMER, Julia; LERNER, Jasmine; LECOURT, Anne-Catherine; SIEBENBORN, Nina de Oliveira S.; CORTESE, Rosa; SCHADELIN, Sabine; SCHOEPS, Vinicius; MATOS, Aline; MENDES, Natalia; PEREIRA, Clarissa dos Reis; MONTEIRO, Mario Luiz; PEREIRA, Samira Luisa Dos Apostolos; SCHINDLER, Patrick; CHIEN, Claudia; SCHWAKE, Carolin; SCHNEIDER, Ruth; PAKEERATHAN, Thivya; KIM, Ki Hoon; AKTAS, Orhan; FISCHER, Urs; MEHLING, Matthias; DERFUSS, Tobias; KAPPOS, Ludwig; AYZENBERG, Ilya; RINGELSTEIN, Marius; PAUL, Friedemann; CALLEGARO, Dagoberto; KIM, Ho Jin; KUHLE, Jens; PAPADOPOULOU, Athina; GRANZIERA, Cristina; PROBSTEL, Anne-Katrin- Immunoglobulin A Antibodies Against Myelin Oligodendrocyte Glycoprotein in a Subgroup of Patients With Central Nervous System Demyelination(2023) GOMES, Ana Beatriz Ayroza Galvao Ribeiro; KULSVEHAGEN, Laila; LIPPS, Patrick; CAGOL, Alessandro; CERDA-FUERTES, Nuria; NEZIRAJ, Tradite; FLAMMER, Julia; LERNER, Jasmine; LECOURT, Anne-Catherine; SIEBENBORN, Nina De Oliveira S.; CORTESE, Rosa; SCHAEDELIN, Sabine; SCHOEPS, Vinicius Andreoli; MATOS, Aline de Moura Brasil; MENDES, Natalia Trombini; PEREIRA, Clarissa dos Reis; MONTEIRO, Mario Luiz Ribeiro; APOSTOLOS-PEREIRA, Samira Luisa dos; SCHINDLER, Patrick; CHIEN, Claudia; SCHWAKE, Carolin; SCHNEIDER, Ruth; PAKEERATHAN, Thivya; AKTAS, Orhan; FISCHER, Urs; MEHLING, Matthias; DERFUSS, Tobias; KAPPOS, Ludwig; AYZENBERG, Ilya; RINGELSTEIN, Marius; PAUL, Friedemann; CALLEGARO, Dagoberto; KUHLE, Jens; PAPADOPOULOU, Athina; GRANZIERA, Cristina; PROBSTEL, Anne-KatrinIMPORTANCE Differential diagnosis of patients with seronegative demyelinating central nervous system (CNS) disease is challenging. In this regard, evidence suggests that immunoglobulin (Ig) A plays a role in the pathogenesis of different autoimmune diseases. Yet little is known about the presence and clinical relevance of IgA antibodies against myelin oligodendrocyte glycoprotein (MOG) in CNS demyelination. OBJECTIVE To investigate the frequency of MOG-IgA and associated clinical features in patients with demyelinating CNS disease and healthy controls. DESIGN, SETTING, AND PARTICIPANTS This longitudinal study comprised 1 discovery and 1 confirmation cohort derived from 5 centers. Participants included patients with suspected or confirmed demyelinating diseases and healthy controls. MOG-IgA, MOG-IgG, and MOG-IgM were measured in serum samples and cerebrospinal fluid (CSF) of patients, who were assessed from September 2012 to April 2022. MAIN OUTCOMES AND MEASURES Frequency and clinical features of patients who were seropositive for MOG-IgA and double-seronegative for aquaporin 4 (AQP4) IgG and MOG-IgG. RESULTS After the exclusion of 5 participants with coexisting AQP4-IgG and MOG-IgA, MOG-IgG, and/or MOG-IgM, 1339 patients and 110 healthy controls were included; the median follow-up time was 39 months (range, 0-227 months). Of included patients with isolated MOG-IgA, 11 of 18 were female (61%), and the median age was 31.5 years (range, 3-76 years). Among patients double-seronegative for AQP4-IgG and MOG-IgG (1126/1339; 84%), isolated MOG-IgA was identified in 3 of 50 patients (6%) with neuromyelitis optica spectrum disorder, 5 of 228 patients (2%) with other CNS demyelinating diseases, and 10 of 848 patients (1%) with multiple sclerosis but in none of the healthy controls (0/110). The most common disease manifestation in patients seropositive for isolated MOG-IgA was myelitis (11/17 [65%]), followed by more frequent brainstem syndrome (7/16 [44%] vs 14/75 [19%], respectively; P =.048), and infrequent manifestation of optic neuritis (4/15 [27%] vs 46/73 [63%], respectively; P =.02) vs patients with MOG-IgG. Among patients fulfilling 2017 McDonald criteria for multiple sclerosis, MOG-IgA was associated with less frequent CSF-specific oligoclonal bands (4/9 [44%] vs 325/351 [93%], respectively; P <.001) vs patients with multiple sclerosis who were MOG-IgG/IgA seronegative. Further, most patients with isolated MOG-IgA presented clinical attacks after recent infection or vaccination (7/11 [64%]). CONCLUSION AND RELEVANCE In this study, MOG-specific IgA was identified in a subgroup of patients who were double-seronegative for AQP4-/MOG-IgG, suggesting that MOG-IgA may be a novel diagnostic biomarker for patients with CNS demyelination.
- Management of central nervous system demyelinating diseases during the coronavirus disease 2019 pandemic: a practical approach(2020) APOSTOLOS-PEREIRA, Samira Luisa; SILVA, Guilherme Diogo; DISSEROL, Caio Cesar Diniz; FEO, Lucas Bueno; MATOS, Aline de Moura Brasil; SCHOEPS, Vinicius Andreoli; GOMES, Ana Beatriz Ayroza Galvao Ribeiro; BOAVENTURA, Mateus; MENDES, Maria Fernanda; CALLEGARO, DagobertoBackground: The novelcoronavirus disease 2019(COVID-19) pandemic poses a potential threattopatients with autoimmune disorders, including multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Such patients are usually treated with immunomodulatory or immunosuppressive agents, which may tamper with the organism's normal response to infections. Currently, noconsensus has been reached on how to manage MS and NMOSD patients during the pandemic. Objective: To discuss strategies to manage those patients. Methods: We focus on how to 1) reduce COVID-19 infection risk, such as social distancing, telemedicine, and wider interval between laboratory testing/imaging; 2) manage relapses, such as avoiding treatment of mild relapse and using oral steroids; 3) manage disease-modifying therapies, such as preference for drugs associated with lower infection risk (interferons, glatiramer, teriflunomide, and natalizumab) and extended-interval dosing of natalizumab, when safe; 4) individualize the chosen MS induction-therapy (anti-CD20 monoclonal antibodies, alemtuzumab, and cladribine); 5) manage NMOSD preventive therapies, including initial therapy selection and current treatment maintenance; 6) manage MS/NMOSD patients infected with COVID-19. Conclusions: In the future, real-world case series of MS/NMOSD patients infected with COVID-19 will help us define the best management strategies. For the time being, we rely on expert experience and guidance.