ESTER CERDEIRA SABINO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/46 - Laboratório de Parasitologia Médica, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/46 - Laboratório de Parasitologia Médica, Hospital das Clínicas, Faculdade de Medicina - Líder
43 resultados
Resultados de Busca
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- Prevalence and laboratorial determinants of the clinical relevance of antibodies of undetermined specificity(2019) CONRADO, Marina Cavalcanti de Albuquerque da Veiga; CARDOSO, Regina A.; DEZAN, Marcia Regina; OLIVEIRA, Valeria Brito; NETO, Abel da Costa; ZIZA, Karen Chinoca; KRIEGER, Jose Eduardo; PEREIRA, Alexandre Costa; SABINO, Ester Cerdeira; ROCHA, Vanderson; MENDRONE-JUNIOR, Alfredo; DINARDO, Carla LuanaBackground and Objectives Antibodies of unknown specificity (AUS) are frequently identified in the pre-transfusion testing. These antibodies can be insignificant or potentially cause post-transfusion haemolysis. Information about the prevalence of clinically relevant AUS is still lacking. Our aim was to predict the potential clinical relevance of AUS using the monocyte monolayer assay (MMA) and to identify the clinical and laboratorial determinants of AUS' significance. Materials and Methods Antibodies of unknown specificity identified at a single institution from 2015-2017 were evaluated through MMA. A monocyte index (MI) of more than 5% was predictive of potential post-transfusion haemolysis. Results Thirty-two patients with AUS were included in the study. Of the studied AUS, 37 center dot 5% (12/32) presented with a monocyte index (MI) more than 5%. In the group of significant AUS, 41 center dot 7% of the patients presented with sickle cell disease (SCD) and the AUS were associated with Rh antibodies in 75% of the cases. In the group of insignificant AUS, only 10% of the patients had SCD and the association with Rh antibodies was detected in 20% of the cases. The presence of Rh antibodies was independently associated with the AUS clinical relevance (P = 0 center dot 012). Conclusion More than one-third of the AUS are potentially clinically relevant, and the association with Rh antibodies is predictive of AUS relevance. Services must honour AUS in the pre-transfusion process in order to ensure transfusion safety.
- Diversity of RH and transfusion support in Brazilian sickle cell disease patients with unexplained Rh antibodies(2019) DINARDO, Carla L.; KELLY, Shannon; DEZAN, Marcia R.; RIBEIRO, Ingrid H.; CASTILHO, Shirley L.; SCHIMIDT, Luciana C.; VALGUEIRO, Maria do C.; PREISS, Liliana R.; CUSTER, Brian; SABINO, Ester C.; WESTHOFF, Connie M.BACKGROUND Genetic diversity in the RH genes among sickle cell disease (SCD) patients is well described but not yet extensively explored in populations of racially diverse origin. Transfusion support is complicated in patients who develop unexpected Rh antibodies. Our goal was to describe RH variation in a large cohort of Brazilian SCD patients exhibiting unexpected Rh antibodies (antibodies against RH antigens to which the patient is phenotypically positive) and to evaluate the impact of using the patient's RH genotype to guide transfusion support. STUDY DESIGN AND METHODS Patients within the Recipient Epidemiology and Evaluation Donor Study (REDS)-III Brazil SCD cohort with unexpected Rh antibodies were selected for study. RHD and RHCE exons and flanking introns were sequenced by targeted next-generation sequencing. RESULTS Fifty-four patients with 64 unexplained Rh antibodies were studied. The majority could not be definitively classified as auto- or alloantibodies using serologic methods. The most common altered RH were RHD*DIIIa and RHD*DAR (RHD locus) and RHCE*ce48C, RHCE*ce733G, and RHCE*ceS (RHCE locus). In 53.1% of the cases (34/64), patients demonstrated only conventional alleles encoding the target antigen: five of 12 anti-D (41.7%), 10 of 12 anti-C (83.3%), 18 of 38 anti-e (47.4%), and one of one anti-E (100%). CONCLUSION RHD variation in this SCD cohort differs from that reported for African Americans, with increased prevalence of RHD*DAR and underrepresentation of the DAU cluster. Many unexplained Rh antibodies were found in patients with conventional RH allele(s) only. RH genotyping was useful to guide transfusion to determine which patients could potentially benefit from receiving RH genotyped donor units.
conferenceObject Changes in Gene Expression in Response to Red Blood Cell Transfusions in Chronically Transfused Sickle Cell Disease Patients(2019) KELLY, Shannon; DINARDO, Carla; DENG, Xutao; BELISARIO, Andre; PROIETTI, Anna Carneiro; LOUREIRO, Paula; MOTA, Rosimere Afonso; FLOR-PARK, Miriam V.; MAXIMO, Claudia; SABINO, Ester; CUSTER, Brian- Evaluation of Galectin-3 and Myocardial Fibrosis in Patients with Hypertrophic Cardiomyopathy(2019) ANTUNES, Murillo de Oliveira; ARTEAGA-FERNÁNDEZ, Edmundo; FERNANDES, Fabio; SOFFIATTI, Carla David; BUCK, Paula de Cássia; SABINO, Ester Cerdeira; MOREIRA, Carlos Henrique Valente; MADY, CharlesAbstract Background: Galectin-3 is the designation given to the protein that binds to ß-galactosides, expressed by activated macrophages and described as a cardiac fibrosis mediator. In hypertrophic cardiomyopathy (HCM), myocardial fibrosis is an independent predictor of adverse outcome; however, the association between Galectin-3 and myocardial fibrosis has not been studied in this cardiopathy. Objective: To evaluate the association of Galectin-3 and the presence of myocardial fibrosis in a patient with hypertrophic cardiomyopathy. Methods: Galectin-3 was measured in automated equipment using the Elisa technique in 100 participants divided into two groups: 50 patients with hypertrophic cardiomyopathy and 50 healthy control subjects. All patients with hypertrophic cardiomyopathy underwent magnetic nuclear resonance with the late enhancement technique to investigate myocardial fibrosis. For the statistical analysis, p values < 0.05 were considered statistically significant. Results: Galectin-3 levels were low and did not show significant differences between patients with hypertrophic cardiomyopathy and the control group, 10.3 ± 3.1 ng/dL and 11.3 ± 2.6 ng/dL (p = 0.12) respectively. Myocardial fibrosis was a common finding and was identified in 84% (42/50) of patients with HCM, but no differences were observed between Galectin-3 levels when comparing patients with and without fibrosis, 10.3 ± 2.4 ng/dL and 10.1 ± 2.1 ng/dL (p = 0.59). Conclusion: The results did not show an association between Galectin-3 and myocardial fibrosis in patients with hypertrophic cardiomyopathy, suggesting that non-inflammatory mechanisms of myocardial fibrosis formation and cardiac remodeling are involved in this cardiopathy.
conferenceObject Whole exome sequencing of Chagas disease cardiomyopathy families reveals accumulation of rare variants in mitochondrial and inflammation-associated genes(2019) CUNHA-NETO, E.; MARQUET, S.; FRADE, A. Farage; FERREIRA, A. Mota; OUARHACHE, M.; IANNI, B.; FERREIRA, L. Rodrigues Pinto; RIGAUD, V. Oliveira-Carvalho; ALMEIDA, R. Ribeiro; CANDIDO, D.; TORRES, M.; GALLARDO, F.; FERNANDES, R.; MADY, C.; BUCK, P.; CARDOSO, C.; SANTOS-JUNIOR, O. R.; OLIVEIRA, L. C.; OLIVEIRA, C. D. L.; NUNES, M. do Carmo; ABEL, L.; KALIL, J.; RIBEIRO, A. L. P.; SABINO, E. C.; CHEVILLARD, C.- Interpreting HIV diagnostic histories into infection time estimates: analytical framework and online tool(2019) GREBE, Eduard; FACENTE, Shelley N.; BINGHAM, Jeremy; PILCHER, Christopher D.; POWRIE, Andrew; GERBER, Jarryd; PRIEDE, Gareth; CHIBAWARA, Trust; BUSCH, Michael P.; MURPHY, Gary; KASSANJEE, Reshma; WELTE, Alex; WELTE, Alex; SEMPA, Joseph; MATTEN, David; BRAND, Hilmarie; CHIBAWARA, Trust; MURPHY, Gary; HALL, Jake; MCKINNEY, Elaine; BUSCH, Michael P.; GREBE, Eduard; FACENTE, Shelley; HAMPTON, Dylan; KEATING, Sheila; LEBEDEVA, Mila; PILCHER, Christopher D.; MARSON, Kara; KASSANJEE, Reshma; LAEYENDECKER, Oliver; QUINN, Thomas; BURNS, David; LITTLE, Susan; SANDS, Anita; HALLETT, Tim; OWEN, Sherry Michele; PAREKH, Bharat; SEXTON, Connie; PRICE, Matthew; KAMALI, Anatoli; LOEB, Lisa; MARTIN, Jeffrey; DEEKS, Steven G.; HOH, Rebecca; BARTOLOMEI, Zelinda; SANTOS, Breno; ZABTOSKI, Kellin; LIRA, Rita de Cassia Alves; SPERHACKE, Rosa Dea; MOTTA, Leonardo R.; PAGANELLA, Machline; KALLAS, Esper; TOMIYAMA, Helena; TOMIYAMA, Claudia; COSTA, Priscilla; NUNES, Maria A.; REIS, Gisele; SAUER, Mariana M.; CERQUEIRA, Natalia; NAKAGAWA, Zelinda; FERRARI, Lilian; AMARAL, Ana P.; MILANI, Karine; KARIM, Salim S. Abdool; KARIM, Quarraisha Abdool; NDUNGU, Thumbi; MAJOLA, Nelisile; SAMSUNDER, Natasha; NANICHE, Denise; MANDOMANDO, Inacio; MACETE, Eusebio V.; SANCHEZ, Jorge; LAMA, Javier; DUERR, Ann; CAPOBIANCHI, Maria R.; SULIGOI, Barbara; STRAMER, Susan; WILLIAMSON, Phillip; VERMEULEN, Marion; SABINO, EsterBackground It is frequently of epidemiological and/or clinical interest to estimate the date of HIV infection or time-since-infection of individuals. Yet, for over 15 years, the only widely-referenced infection dating algorithm that utilises diagnostic testing data to estimate time-since-infection has been the 'Fiebig staging' system. This defines a number of stages of early HIV infection through various standard combinations of contemporaneous discordant diagnostic results using tests of different sensitivity. To develop a new, more nuanced infection dating algorithm, we generalised the Fiebig approach to accommodate positive and negative diagnostic results generated on the same or different dates, and arbitrary current or future tests - as long as the test sensitivity is known. For this purpose, test sensitivity is the probability of a positive result as a function of time since infection. Methods The present work outlines the analytical framework for infection date estimation using subject-level diagnostic testing histories, and data on test sensitivity. We introduce a publicly-available online HIV infection dating tool that implements this estimation method, bringing together 1) curatorship of HIV test performance data, and 2) infection date estimation functionality, to calculate plausible intervals within which infection likely became detectable for each individual. The midpoints of these intervals are interpreted as infection time 'point estimates' and referred to as Estimated Dates of Detectable Infection (EDDIs). The tool is designed for easy bulk processing of information (as may be appropriate for research studies) but can also be used for individual patients (such as in clinical practice). Results In many settings, including most research studies, detailed diagnostic testing data are routinely recorded, and can provide reasonably precise estimates of the timing of HIV infection. We present a simple logic to the interpretation of diagnostic testing histories into infection time estimates, either as a point estimate (EDDI) or an interval (earliest plausible to latest plausible dates of detectable infection), along with a publicly-accessible online tool that supports wide application of this logic. Conclusions This tool, available at , is readily updatable as test technology evolves, given the simple architecture of the system and its nature as an open source project.
- A generalizable method for estimating duration of HIV infections using clinical testing history and HIV test results(2019) PILCHER, Christopher D.; PORCO, Travis C.; FACENTE, Shelley N.; GREBE, Eduard; DELANEY, Kevin P.; MASCIOTRA, Silvina; KASSANJEE, Reshma; BUSCH, Michael P.; MURPHY, Gary; OWEN, S. Michele; WELTE, Alex; MATTEN, David; BRAND, Hilmarie; CHIBAWARA, Trust; MCKINNEY, Elaine; HALL, Jake; BUSCH, Michael; KEATING, Sheila; LEBEDEVA, Mila; HAMPTON, Dylan; PILCHER, Christopher; FACENTE, Shelley; MARSON, Kara; LAEYENDECKER, Oliver; QUINN, Thomas; BURNS, David; LITTLE, Susan; SANDS, Anita; HALLETT, Tim; OWEN, Sherry Michele; PAREKH, Bharat; SEXTON, Connie; PRICE, Matthew; KAMALI, Anatoli; LOEB, Lisa; MARTIN, Jeffrey; DEEKS, Steven G.; HOH, Rebecca; BARTOLOMEI, Zelinda; CERQUEIRA, Natalia; SANTOS, Breno; ZABTOSKI, Kellin; LIRA, Rita de Cassia Alves; SPERHACKE, Rosa Dea; MOTTA, Leonardo R.; PAGANELLA, Machline; KALLAS, Esper; TOMIYAMA, Helena; TOMIYAMA, Claudia; COSTA, Priscilla; NUNES, Maria A.; REIS, Gisele; SAUER, Mariana M.; NAKAGAWA, Zelinda; FERRARI, Lilian; AMARAL, Ana P.; MILANI, Karine; KARIM, Salim S. Abdool; KARIM, Quarraisha Abdool; NDUNGU, Thumbi; MAJOLA, Nelisile; SAMSUNDER, Natasha; NANICHE, Denise; MANDOMANDO, Inicio; V, Eusebio Macete; SANCHEZ, Jorge; LAMA, Javier; DUERR, Ann; CAPOBIANCHI, Maria R.; SULIGOI, Barbara; STRAMER, Susan; WILLIAMSON, Phillip; VERMEULEN, Marion; SABINO, EsterObjective: To determine the precision of new and established methods for estimating duration of HIV infection. Design: A retrospective analysis of HIV testing results from serial samples in commercially available panels, taking advantage of extensive testing previously conducted on 53 seroconverters. Methods: We initially investigated four methods for estimating infection timing: method 1, 'Fiebig stages' based on test results from a single specimen; method 2, an updated '4th gen' method similar to Fiebig stages but using antigen/antibody tests in place of the p24 antigen test; method 3, modeling of 'viral ramp-up' dynamics using quantitative HIV-1 viral load data from antibody-negative specimens; and method 4, using detailed clinical testing history to define a plausible interval and best estimate of infection time. We then investigated a 'two-step method' using data from both methods 3 and 4, allowing for test results to have come from specimens collected on different days. Results: Fiebig and '4th gen' staging method estimates of time since detectable viremia had similar and modest correlation with observed data. Correlation of estimates from both new methods (3 and 4), and from a combination of these two ('two-step method') was markedly improved and variability significantly reduced when compared with Fiebig estimates on the same specimens. Conclusion: The new 'two-step' method more accurately estimates timing of infection and is intended to be generalizable to more situations in clinical medicine, research, and surveillance than previous methods. An online tool is now available that enables researchers/clinicians to input data related to method 4, and generate estimated dates of detectable infection.
- Lack of evidence of seronegative infection in an endemic area of Chagas disease(2019) OLIVEIRA, Lea Campos de; LEE, Tzong-Hae; FERREIRA, Ariela Mota; BIERRENBACH, Ana Luiza; SOUZA-BASQUEIRA, Marcela de; OLIVEIRA, Claudia Di Lorenzo; CARDOSO, Clareci Silva; MOREIRA, Carlos Henrique Valente; OIKAWA, Marcio K.; RIBEIRO, Antonio Luiz P.; BUSCH, Michael P.; SABINO, Ester CerdeiraThe diagnosis of Chagas disease is based on the detection of Trypanosoma cruzi (T. cruzi)-specific antibodies. Nonetheless, there is concern about the sensitivity of current serological assays due to reports of T. cruzi PCR positivity among seronegative individuals. The aim of this study was to evaluate if T. cruzi seronegative infections occur in endemic areas. We recruited 2,157 individuals that were identified as having Chagas disease in a public health system database of an endemic region in Brazil. All participants were interviewed and 2,091 had a sample collected for serological and PCR testing. From these, 149 (7.1%) had negative serological results. PCR was positive in 610 samples (31.4%) of the 1,942 seropositive samples but in none of the 149 samples from seronegative participants. True T. cruzi seronegative infections seem to be rare (95% CI 0-3.7) and should not be a concern for blood supply, which relies on antibody screening.
- Molecular characterization of viruses associated with encephalitis in Sao Paulo, Brazil(2019) FERREIRA, Jerenice E.; FERREIRA, Suzete C.; ALMEIDA-NETO, Cesar; NISHIYA, Anna S.; ALENCAR, Cecilia S.; GOUVEIA, Gisele R.; CAIAFFA-FILHO, Helio; GOMES, Helio; SANTOSID, Raimunda Telma de Macedo; WITKIN, Steven S.; MENDRONE-JUNIOR, Alfredo; SABINO, Ester C.The objective of this study was to characterize the prevalence of viral encephalitis due to arbovirus infection of the Togaviridae and Flaviviridae families in Sao Paulo, Brazil. A total of 500 cerebrospinal fluid (CSF) samples collected between August 2012 and January 2013, from patients with symptoms of acute encephalitis were analyzed. Findings suggestive of viral encephalitis-elevations in cell concentration, glucose and total protein-were observed in 234 (46.8%) samples, designated as Group 1. The remaining 266 samples comprised Group 2. All samples were tested for Flaviviruses (dengue virus 1, 2, 3 and 4, yellow fever virus and West Nile virus), Alphavirus (NS5 region) and enterovirus by RT-PCR and for herpesviruses and enteroviruses using CLART(-)Entherpex. A presumptive viral etiological agent was detected in 26 samples (5.2%), 18 (8.0%) in Group 1 and 8 (3.0%) in Group 2. In Group 1 human herpesviruses were detected in 9 cases, enteroviruses in 7 cases, dengue viruses (DENV) in 2 CSFs and St. Louis encephalitis virus (SLEV) in one case. In Group 2 there were 3 CSFs positive for human herpesviruses, 2 for enteroviruses, 2 for DENV and 1 for SLEV. Detection of arboviruses, even though present in a minority of infected patients, identifies these viruses as a probable etiological agent of encephalitis. This is of special concern in regions where this class of viruses is endemic and has been linked to other recent epidemics.
- Human sapovirus GI.2 and GI.3 from children with acute gastroenteritis in northern Brazil(2019) CILLI, Audrey; LUCHS, Adriana; LEAL, Elcio; GILL, Danielle; MILAGRES, Flavio Augusto de Padua; KOMNINAKIS, Shirley Vasconcelos; BRUSTULIN, Rafael; TELES, Maria da Aparecida Rodrigues; LOBATO, Marcia Cristina Alves Brito Sayao; CHAGAS, Rogerio Togisaki das; ABRAO, Maria de Fatima Neves dos Santos; SOARES, Cassia Vitoria de Deus Alves; DENG, Xutao; DELWART, Eric; SABINO, Ester Cerdeira; COSTA, Antonio Charlys daHuman sapoviruses (HSaV) are considered important causative agents of acute gastroenteritis in humans worldwide. However, knowledge of the genetic characteristics of the whole genome of HSaV in Brazil is limited. Here we report the complete genome sequences of six HSaVs GI.2 and two GI.3 strains obtained from children with acute gastroenteritis in the Northern region of Brazil. Next generation sequencing was used to obtain the full genome and molecular characterization of the genome was performed. Phylogenetic analysis of the genome was also performed. Only one complete HSaV GI.2 genome characterization in the country precedes that of the present study. This is the first complete genome sequence of genotype GI.3 in Brazil. The data obtained in this investigation can contribute to the augmentation of the database on the molecular diversity of HSaVs strains circulating in Brazil, and to the improvement of current typing protocols.