DAGOBERTO CALLEGARO

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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

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  • article 7 Citação(ões) na Scopus
    Clinical and MRI measures to identify non-acute MOG-antibody disease in adults
    (2023) CORTESE, Rosa; BATTAGLINI, Marco; PRADOS, Ferran; BIANCHI, Alessia; HAIDER, Lukas; JACOB, Anu; PALACE, Jacqueline; MESSINA, Silvia; PAUL, Friedemann; WUERFEL, Jens; MARIGNIER, Romain; DURAND-DUBIEF, Francoise; RIMKUS, Carolina de Medeiros; CALLEGARO, Dagoberto; SATO, Douglas Kazutoshi; FILIPPI, Massimo; ROCCA, Maria Assunta; CACCIAGUERRA, Laura; ROVIRA, Alex; SASTRE-GARRIGA, Jaume; ARRAMBIDE, Georgina; LIU, Yaou; DUAN, Yunyun; GASPERINI, Claudio; TORTORELLA, Carla; RUGGIERI, Serena; AMATO, Maria Pia; ULIVELLI, Monica; GROPPA, Sergiu; GROTHE, Matthias; LLUFRIU, Sara; SEPULVEDA, Maria; LUKAS, Carsten; BELLENBERG, Barbara; SCHNEIDER, Ruth; SOWA, Piotr; CELIUS, Elisabeth G.; PROEBSTEL, Anne-Katrin; YALDIZLI, Ozgur; MUELLER, Jannis; STANKOFF, Bruno; BODINI, Benedetta; CARMISCIANO, Luca; SORMANI, Maria Pia; BARKHOF, Frederik; STEFANO, Nicola De; CICCARELLI, Olga
    MRI and clinical features of myelin oligodendrocyte glycoprotein (MOG)-antibody disease may overlap with those of other inflammatory demyelinating conditions posing diagnostic challenges, especially in non-acute phases and when serologic testing for MOG antibodies is unavailable or shows uncertain results. We aimed to identify MRI and clinical markers that differentiate non-acute MOG-antibody disease from aquaporin 4 (AQP4)-antibody neuromyelitis optica spectrum disorder and relapsing remitting multiple sclerosis, guiding in the identification of patients with MOG-antibody disease in clinical practice. In this cross-sectional retrospective study, data from 16 MAGNIMS centres were included. Data collection and analyses were conducted from 2019 to 2021. Inclusion criteria were: diagnosis of MOG-antibody disease; AQP4-neuromyelitis optica spectrum disorder and multiple sclerosis; brain and cord MRI at least 6 months from relapse; and Expanded Disability Status Scale (EDSS) score on the day of MRI. Brain white matter T-2 lesions, T-1-hypointense lesions, cortical and cord lesions were identified. Random forest models were constructed to classify patients as MOG-antibody disease/AQP4-neuromyelitis optica spectrum disorder/multiple sclerosis; a leave one out cross-validation procedure assessed the performance of the models. Based on the best discriminators between diseases, we proposed a guide to target investigations for MOG-antibody disease. One hundred and sixty-two patients with MOG-antibody disease [99 females, mean age: 41 (+/- 14) years, median EDSS: 2 (0-7.5)], 162 with AQP4-neuromyelitis optica spectrum disorder [132 females, mean age: 51 (+/- 14) years, median EDSS: 3.5 (0-8)], 189 with multiple sclerosis (132 females, mean age: 40 (+/- 10) years, median EDSS: 2 (0-8)] and 152 healthy controls (91 females) were studied. In young patients (<34 years), with low disability (EDSS < 3), the absence of Dawson's fingers, temporal lobe lesions and longitudinally extensive lesions in the cervical cord pointed towards a diagnosis of MOG-antibody disease instead of the other two diseases (accuracy: 76%, sensitivity: 81%, specificity: 84%, P < 0.001). In these non-acute patients, the number of brain lesions < 6 predicted MOG-antibody disease versus multiple sclerosis (accuracy: 83%, sensitivity: 82%, specificity: 83%, P < 0.001). An EDSS < 3 and the absence of longitudinally extensive lesions in the cervical cord predicted MOG-antibody disease versus AQP4-neuromyelitis optica spectrum disorder (accuracy: 76%, sensitivity: 89%, specificity: 62%, P < 0.001). A workflow with sequential tests and supporting features is proposed to guide better identification of patients with MOG-antibody disease. Adult patients with non-acute MOG-antibody disease showed distinctive clinical and MRI features when compared to AQP4-neuromyelitis optica spectrum disorder and multiple sclerosis. A careful inspection of the morphology of brain and cord lesions together with clinical information can guide further analyses towards the diagnosis of MOG-antibody disease in clinical practice. In a multicentre MAGNIMS study, Cortese et al. show that brain and cord lesion characteristics on conventional MRI, together with clinical features, can help differentiate non-acute MOG-antibody disease from AQP4-NMOSD and multiple sclerosis, aiding identification of non-acute patients for MOG antibody testing.
  • article 87 Citação(ões) na Scopus
    Myelin injury without astrocytopathy in neuroinflammatory disorders with MOG antibodies
    (2016) KANEKO, Kimihiko; SATO, Douglas Kazutoshi; NAKASHIMA, Ichiro; NISHIYAMA, Shuhei; TANAKA, Satoru; MARIGNIER, Romain; HYUN, Jae-Won; OLIVEIRA, Luana Michelli de; REINDL, Markus; SEIFERT-HELD, Thomas; SEPULVEDA, Maria; SIRITHO, Sasitorn; WATERS, Patrick Joseph; KUROSAWA, Kazuhiro; AKAISHI, Tetsuya; KURODA, Hiroshi; MISU, Tatsuro; PRAYOONWIWAT, Naraporn; BERGER, Thomas; SAIZ, Albert; KIM, Ho Jin; NOMURA, Kyoichi; CALLEGARO, Dagoberto; FUJIHARA, Kazuo; AOKI, Masashi
  • article 168 Citação(ões) na Scopus
    Myasthenia gravis and neuromyelitis optica spectrum disorder A multicenter study of 16 patients
    (2012) LEITE, M. I.; COUTINHO, E.; LANA-PEIXOTO, M.; APOSTOLOS, S.; WATERS, P.; SATO, D.; MELAMUD, L.; MARTA, M.; GRAHAM, A.; SPILLANE, J.; VILLA, A. M.; CALLEGARO, D.; SANTOS, E.; SILVA, A. Martins da; JARIUS, S.; HOWARD, R.; NAKASHIMA, I.; GIOVANNONI, G.; BUCKLEY, C.; HILTON-JONES, D.; VINCENT, A.; PALACE, J.
    Objective: To describe 16 patients with a coincidence of 2 rare diseases: aquaporin-4 antibody (AQP4-Ab)-mediated neuromyelitis optica spectrum disorder (AQP4-NMOSD) and acetylcholine receptor antibody (AChR-Ab)-mediated myasthenia gravis (AChR-MG). Methods: The clinical details and antibody results of 16 patients with AChR-MG and AQP4-NMOSD were analyzed retrospectively. Results: All had early-onset AChR-MG, the majority with mild generalized disease, and a high proportion achieved remission. Fifteen were female; 11 were Caucasian. In 14/16, the MG preceded NMOSD (median interval: 16 years) and 11 of these had had a thymectomy although 1 only after NMOSD onset. In 4/5 patients tested, AQP4-Abs were detectable between 4 and 16 years prior to disease onset, including 2 patients with detectable AQP4-Abs prior to thymectomy. AChR-Abs decreased and the AQP4-Ab levels increased over time in concordance with the relevant disease. AChR-Abs were detectable at NMOSD onset in the one sample available from 1 of the 2 patients with NMOSD before MG. Conclusions: Although both conditions are rare, the association of MG and NMOSD occurs much more frequently than by chance and the MG appears to follow a benign course. AChR-Abs or AQP4-Abs may be present years before onset of the relevant disease and the antibody titers against AQP4 and AChR tend to change in opposite directions. Although most cases had MG prior to NMOSD onset, and had undergone thymectomy, NMOSD can occur first and in patients who have not had their thymus removed.
  • article 712 Citação(ões) na Scopus
    Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders
    (2014) SATO, Douglas Kazutoshi; CALLEGARO, Dagoberto; LANA-PEIXOTO, Marco Aurelio; WATERS, Patrick J.; JORGE, Frederico M. de Haidar; TAKAHASHI, Toshiyuki; NAKASHIMA, Ichiro; APOSTOLOS-PEREIRA, Samira Luisa; TALIM, Natalia; SIMM, Renata Faria; LINO, Angelina Maria Martins; MISU, Tatsuro; LEITE, Maria Isabel; AOKI, Masashi; FUJIHARA, Kazuo
    Objective:To evaluate clinical features among patients with neuromyelitis optica spectrum disorders (NMOSD) who have myelin oligodendrocyte glycoprotein (MOG) antibodies, aquaporin-4 (AQP4) antibodies, or seronegativity for both antibodies.Methods:Sera from patients diagnosed with NMOSD in 1 of 3 centers (2 sites in Brazil and 1 site in Japan) were tested for MOG and AQP4 antibodies using cell-based assays with live transfected cells.Results:Among the 215 patients with NMOSD, 7.4% (16/215) were positive for MOG antibodies and 64.7% (139/215) were positive for AQP4 antibodies. No patients were positive for both antibodies. Patients with MOG antibodies represented 21.1% (16/76) of the patients negative for AQP4 antibodies. Compared with patients with AQP4 antibodies or patients who were seronegative, patients with MOG antibodies were more frequently male, had a more restricted phenotype (optic nerve more than spinal cord), more frequently had bilateral simultaneous optic neuritis, more often had a single attack, had spinal cord lesions distributed in the lower portion of the spinal cord, and usually demonstrated better functional recovery after an attack.Conclusions:Patients with NMOSD with MOG antibodies have distinct clinical features, fewer attacks, and better recovery than patients with AQP4 antibodies or patients seronegative for both antibodies.
  • article 17 Citação(ões) na Scopus
    CSF levels of glutamine synthetase and GFAP to explore astrocytic damage in seronegative NMOSD
    (2020) KLEEREKOOPER, Iris; HERBERT, Megan K.; KUIPERIJ, H. Bea; SATO, Douglas Kazutoshi; FUJIHARA, Kazuo; CALLEGARO, Dagoberto; MARIGNIER, Romain; SAIZ, Albert; SENEL, Makbule; TUMANI, Hayrettin; JONG, Brigit A. De; TRIP, S. Anand; NAKASHIMA, Ichiro; VERBEEK, Marcel M.; PETZOLD, Axel
    Objective To explore levels of astrocytopathy in neuromyelitis optica spectrum disorder (NMOSD) by measuring levels of the astrocytic enzyme glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP), an established astrocytic biomarker known to be associated with disease activity in multiple sclerosis. Methods Cerebrospinal fluid concentrations of GS and GFAP were measured by ELISA in patients with NMOSD (n=39, 28 aquaporin-4 (AQP4)-Ab-seropositive, 3 double-Ab-seronegative, 4 myelin oligodendrocyte glycoprotein (MOG)-Ab-seropositive and 4 AQP4-Ab-seronegative with unknown MOG-Ab-serostatus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and non-neurological controls (n=37). Results GFAP and GS concentrations differed significantly across groups (both p<0.001), showing a similar pattern of elevation in patients with AQP4-Ab-seropositive NMOSD. GS and GFAP were significantly correlated, particularly in patients with AQP4-Ab-seropositive NMOSD (r(s)=0.70, p<0.001). Interestingly, GFAP levels in some patients with double-Ab-seronegative NMOSD were markedly increased. Conclusions Our data indicate astrocytic injury occurs in some patients with double-Ab-seronegative NMOSD, which hints at the possible existence of yet undiscovered astrocytic autoimmune targets. We hypothesise that elevated GS and GFAP levels could identify those double-Ab-seronegative patients suitable to undergo in-depth autoimmune screening for astrocytic antibodies.
  • article 103 Citação(ões) na Scopus
    Treatment of MOG-IgG-associated disorder with rituximab: An international study of 121 patients
    (2020) WHITTAM, Daniel H.; COBO-CALVO, Alvaro; LOPEZ-CHIRIBOGA, A. Sebastian; PARDO, Santiago; GORNALL, Matthew; CICCONI, Silvia; BRANDT, Alexander; BEREK, Klaus; BERGER, Thomas; JELCIC, Ilijas; GOMBOLAY, Grace; OLIVEIRA, Luana Micheli; CALLEGARO, Dagoberto; KANEKO, Kimihiko; MISU, Tatsuro; CAPOBIANCO, Marco; GIBBONS, Emily; KARTHIKEAYAN, Venkatraman; BROCHET, Bruno; AUDOIN, Bertrand; MATHEY, Guillaume; LAPLAUD, David; THOUVENOT, Eric; COHEN, Mikael; TOURBAH, Ayman; MAILLART, Elisabeth; CIRON, Jonathan; DESCHAMPS, Romain; BIOTTI, Damien; ROSTASY, Kevin; NEUTEBOOM, Rinze; HEMINGWAY, Cheryl; FORSYTH, Rob; MATIELLO, Marcelo; WEBB, Stewart; HUNT, David; MURRAY, Katy; HACOHEN, Yael; LIM, Ming; LEITE, M. Isabel; PALACE, Jacqueline; SOLOMON, Tom; LUTTEROTTI, Andreas; FUJIHARA, Kazuo; NAKASHIMA, Ichiro; BENNETT, Jeffrey L.; PANDIT, Lekha; CHITNIS, Tanuja; WEINSHENKER, Brian G.; WILDEMANN, Brigitte; SATO, Douglas Kazutoshi; KIM, Su-Hyun; HUDA, Saif; KIM, Ho Jin; REINDL, Markus; LEVY, Michael; JARIUS, Sven; TENEMBAUM, Silvia; PAUL, Friedemann; PITTOCK, Sean; MARIGNIER, Romain; JACOB, Anu
    Objective: To assess the effect of anti-CD20 B-cell depletion with rituximab (RTX) on relapse rates in myelin oligodendrocyte glycoprotein antibody-associated disorder (MOGAD). Methods: Retrospective review of RTX-treated MOGAD patients from 29 centres in 13 countries. The primary outcome measure was change in relapse rate after starting rituximab (Poisson regression model). Results: Data on 121 patients were analysed, including 30 (24.8%) children. Twenty/121 (16.5%) were treated after one attack, of whom 14/20 (70.0%) remained relapse-free after median (IQR) 11.2 (6.3-14.1) months. The remainder (101/121, 83.5%) were treated after two or more attacks, of whom 53/101 (52.5%) remained relapse-free after median 12.1 (6.3-24.9) months. In this 'relapsing group', relapse rate declined by 37% (95%CI=19-52%, p<0.001) overall, 63% (95%CI=35-79%, p = 0.001) when RTX was used first line (n = 47), and 26% (95%CI=2-44%, p = 0.038) when used after other steroid-sparing immunotherapies (n = 54). Predicted 1-year and 2-year relapse-free survival was 79% and 55% for first-line RTX therapy, and 38% and 18% for second-/third-line therapy. Circulating CD19(+)B-cells were suppressed to <1% of total circulating lymphocyte population at the time of 45/57 (78.9%) relapses. Conclusion: RTX reduced relapse rates in MOGAD. However, many patients continued to relapse despite apparent B-cell depletion. Prospective controlled studies are needed to validate these results.