SANDRA FATIMA MENOSI GUALANDRO

(Fonte: Lattes)
Índice h a partir de 2011
12
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina - Docente
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/31 - Laboratório de Genética e Hematologia Molecular, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 10 de 53
  • article 29 Citação(ões) na Scopus
    3rd GUIDELINE FOR PERIOPERATIVE CARDIOVASCULAR EVALUATION OF THE BRAZILIAN SOCIETY OF CARDIOLOGY
    (2017) GUALANDRO, D. M.; YU, P. C.; CARAMELLI, B.; MARQUES, A. C.; CALDERARO, D.; FORNARI, L. S.; PINHO, C.; FEITOSA, A. C. R.; POLANCZYK, C. A.; ROCHITTE, C. E.; JARDIM, C.; VIEIRA, C. L. Z.; NAKAMURA, D. Y. M.; IEZZI, D.; SCHREEN, D.; ADAM, Eduardo L.; D'AMICO, E. A.; LIMA, M. Q.; BURDMANN, E. A.; PACHON, E. I. M.; BRAGA, F. G. M.; MACHADO, F. S.; PAULA, F. J.; CARMO, G. A. L.; FEITOSA-FILHO, G. S.; PRADO, G. F.; LOPES, H. F.; FERNANDES, J. R. C.; LIMA, J. J. G.; SACILOTTO, L.; DRAGER, L. F.; VACANTI, L. J.; ROHDE, L. E. P.; PRADA, L. F. L.; GOWDAK, L. H. W.; VIEIRA, M. L. C.; MONACHINI, M. C.; MACATRAO-COSTA, M. F.; PAIXAO, M. R.; OLIVEIRA JR., M. T.; CURY, P.; VILLACA, P. R.; FARSKY, P. S.; SICILIANO, R. F.; HEINISCH, R. H.; SOUZA, R.; GUALANDRO, S. F. M.; ACCORSI, T. A. D.; MATHIAS JR., W.
  • article 12 Citação(ões) na Scopus
    Paraoxonases (PON) 1, 2, and 3 Polymorphisms and PON-1 Activities in Patients with Sickle Cell Disease
    (2019) REICHERT, Cadiele Oliana; MACEDO, Carolina Garcia de; LEVY, Debora; SINI, Bruno Carnevale; MONTEIRO, Andreia Moreira; GIDLUND, Magnus; MASELLI, Luciana Morganti Ferreira; GUALANDRO, Sandra Fatima Menosi; BYDLOWSKI, Sergio Paulo
    (1) Background: Oxidative stress, chronic inflammation, vasoocclusion, and free iron are all features present in sickle cell disease. Paraoxonases (PON) are a family (PON-1, PON-2, PON-3) of antioxidant enzymes with anti-inflammatory action. Here, for the first time, we described PON-1 activities and PON-1, PON-2, PON-3 polymorphisms in patients with sickle cell disease, homozygous for HbSS, compared with healthy controls. (2) Methods: The groups were matched for age and gender. PON-1 activities (arylesterase and paraoxonase) were determined by enzymatic hydrolysis of phenylcetate and paraoxon, respectively. Polymorphisms were determined by Restriction Fragment Length Polymorphism- Polymerase Chain Reaction (RFLP-PCR). (3) Results: Plasma cholesterol and fractions, ApoA1 and ApoB levels were all decreased in sickle cell disease patients, while anti-oxidized low-density lipoprotein (LDL) antibodies and C-reactive protein were increased. Serum arylesterase activity was lower in sickle cell disease patients when compared with healthy controls. In patients, paraoxonase activity was higher in those with PON-1 RR Q192R polymorphism. In these patients, the increase of serum iron and ferritin levels and transferrin saturation were less pronounced than those observed in patients with QQ or QR polymorphism. No differences were observed with PON-1 L55M, and PON-2 and PON-3 polymorphisms. Multivariate regression analysis showed that transferrin and ferritin concentrations correlated with arylesterase and paraoxonase activities. (4) Conclusions: Both transferrin and ferritin were the main predictors of decreased arylesterase and paraoxonase activities in patients with sickle cell disease. LDL oxidation increased, and RR PON-1 Q192R polymorphism is likely to be a protective factor against oxidative damage in these patients.
  • article 6 Citação(ões) na Scopus
    Economic burden of sickle cell disease in Brazil
    (2022) SILVA-PINTO, Ana Cristina; COSTA, Fernando F.; GUALANDRO, Sandra Fatima Menosi; FONSECA, Patricia Belintani Blum; GRINDLER, Carmela Maggiuzzu; SOUZA FILHO, Homero C. R.; BUENO, Carolina Tosin; CANCADO, Rodolfo D.
    Background Sickle cell disease (SCD) may cause several impacts to patients and the whole society. About 4% of the population has the sickle cell trait in Brazil, and 60,000 to 100,000 have SCD. However, despite recognizing the significant burden of disease, little is known about SCD costs. Objective To estimate SCD societal costs based on disease burden modelling, under Brazilian societal perspective. Methods A disease burden model was built considering the societal perspective and a one-year time horizon, including direct medical and indirect costs (morbidity and mortality). The sum of life lost and disability years was considered to estimate disability-adjusted life years (DALYs). Data from a public database (DATASUS) and the prevalence obtained from literature or medical experts were used to define complications prevalence and duration. Costs were defined using data from the Brazilian public healthcare system table of procedures and medications (SIGTAP) and the human capital method. Results Annual SCD cost was 413,639,180 USD. Indirect cost accounted for the majority of burden (70.1% of the total; 290,158,365 USD vs 123,480,816 USD). Standard of care and chronic complications were the main source of direct costs among adults, while acute conditions were the main source among children. Vaso-occlusive crisis represented the complication with the highest total cost per year in both populations, 11,400,410 USD among adults and 11,510,960 USD among children. Conclusions SCD management may impose an important economic burden on Brazilian society that may reach more than 400 million USD per year.
  • article 4 Citação(ões) na Scopus
    Fc gamma R2B B2.4 haplotype predicts increased risk of red blood cell alloimmunization in sickle cell disease patients
    (2020) COSTA NETO, Abel; SANTOS, Flavia; RIBEIRO, Ingrid; OLIVEIRA, Valeria; DEZAN, Marcia; KASHIMA, Simone; COVAS, Dimas; PEREIRA, Alexandre; FONSECA, Guilherme; MOREIRA, Frederico; KRIEGER, Jose; GUALANDRO, Sandra; ROCHA, Vanderson; MENDRONE JR., Alfredo; DINARDO, Carla L.
    BACKGROUND Red blood cell (RBC) alloimmunization is an important transfusion complication which is prevalent among sickle cell disease (SCD) patients. Autoimmune diseases are a known risk factor for RBC alloimmunization, suggesting that autoimmunity and post-transfusion alloantibody development occur through similar physiopathological pathways. Polymorphisms in the Fc gamma R2B gene have already been associated with several autoimmune disorders and hypothetically could be associated with RBC alloimmunization. Our goal was to evaluate if important polymorphisms of Fc gamma R2B have an impact on the risk of RBC alloimmunization among SCD patients. STUDY DESIGN AND METHODS This was a case-control study in which alloimmunized and non-alloimmunized SCD patients were compared in terms of the genotype frequency of the Fc gamma R2B polymorphisms -386G/C, -120 T/A, and 695C/T, genotyped through direct Sanger sequencing. RESULTS A total of 237 patients met the eligibility criteria, 120 cases (alloimmunized) and 117 controls (non-alloimmunized). RBC alloimmunization was associated with female sex (p < 0.001), lifetime number of RBC units transfused (p = 0.002) and 120 T/A Fc gamma R2B genotype (p = 0.031). The Fc gamma R2B promoter region haplotype 2B.4 (386C120A) was positively associated with RBC alloimunization (p = 0.045). The logistic regression (LR) model identified female sex (OR 10.03, CI 95% 5.16-19.49; p < 0.001) and Fc gamma R2B 2B.4 haplotype (OR 4.55, CI95% 1.1118.65; p = 0.035) as independent predictors of RBC alloimmunization in SCD patients. CONCLUSION SCD patients with the Fc gamma R2B 2B.4 haplotype had over a fourfold higher risk for RBC alloimmunization. This highlights the role played by Fc gamma R2B on RBC alloimmunization and may be helpful in identifying the immune responders.
  • conferenceObject
    Acute anemia and cardiovascular events after vascular surgery
    (2013) CALDERARO, D.; GUALANDRO, S. M.; GUALANDRO, D. M.; YU, P. C.; CARMO, G. L. A.; MARQUES, A. C.; D'AMICO, E. A.; ROCHA, T. R. F.; CARAMELLI, B.; PASTANA, A. F.
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    NIH Bayesian Score As a Stratification Tool in Sickle Cell Disease - Results from a Single Center Cohort in Brazil
    (2017) FONSECA, Guilherme Henrique Hencklain; GRACA, Lutu Ima Viana da; SOUZA, Rogerio; SUGANUMA, Liliana Mitie; ROCHA, Vanderson; GUALANDRO, Sandra Fatima
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    Burden of Sickle Cell Disease: A Brazilian Societal Perspective Analysis
    (2020) PINTO, Ana Cristina Silva; COSTA, Fernando Ferreira; GUALANDRO, Sandra Fatima Menosi; FONSECA, Patricia Belintani Blum; BUENO, Carolina Tosin; CANCADO, Rodolfo D.
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    A Polymorphism in Toll-like Receptor 2 Gene Is Associated with Occurrence of Bacterial Infections in Sickle Cell Disease Patients
    (2018) TOZATTO-MAIO, Karina; GIROT, Robert; LY, Indou Deme; ROCHA, Vanderson; PINTO, Ana Cristina Silva; DIAGNE, Ibrahima; BENZERARA, Yahia; DINARDO, Carla Luana; KASHIMA, Simone; ARAUJO, Itaua Leston; KENZEY, Chantal; FONSECA, Guilherme Henrique Hencklain; RODRIGUES, Evandra; VOLT, Fernanda; JARDULI, Luciana Ribeiro; RUGGERI, Annalisa; MARIASELVAM, Christina Mary; GUALANDRO, Sandra Fatima Menosi; ELAYOUBI, Hanadi; CUNHA, Renato; CAPPELLI, Barbara; SIMOES, Belinda Pinto; GLUCKMAN, Eliane; TAMOUZA, Ryad
  • article 1 Citação(ões) na Scopus
    Novel Insights into the Pathophysiology and Treatment of Sickle Cell Disease
    (2023) ARAUJO, Aderson da Silva; PINTO, Ana Cristina Silva; LOBO, Clarisse Lopes de Castro; FIGUEIREDO, Maria Stella; GUALANDRO, Sandra Fatima Menosi; SAAD, Sara Teresinha Olalla; CANCADO, Rodolfo Delfini
    The polymerization of hemoglobin under deoxygenation is the main pathophysiological event in sickle cell diseases, described more than 70 years ago. The last two decades have seen a major increase in knowledge about the cascade of events that follow the polymerization of hemoglobin and the ensuing sickling of red blood cells. Several distinctive therapeutic targets have been discovered as a result, and a few drugs with innovative mechanisms of action are already on the market, while several others are the focus of ongoing trials. The aim of this narrative review is to describe some of the more recent data in the SCD literature regarding pathophysiology and novel treatments.
  • article 4 Citação(ões) na Scopus
    A Toll-like receptor 2 genetic variant modulates occurrence of bacterial infections in patients with sickle cell disease
    (2019) TOZATTO-MAIO, Karina; GIROT, Robert; LY, Indou D.; ROCHA, Vanderson; PINTO, Ana C. Silva; DIAGNE, Ibrahima; BENZERARA, Yahia; DINARDO, Carla L.; KASHIMA, Simone; LESTON-ARAUJO, Itaua; KENZEY, Chantal; FONSECA, Guilherme H. H.; RODRIGUES, Evandra S.; VOLT, Fernanda; JARDULI, Luciana R.; RUGGERI, Annalisa; MARIASELVAM, Christina M.; GUALANDRO, Sandra F. M.; ELAYOUBI, Hanadi; CUNHA, Renato; CAPPELLI, Barbara; MALMEGRIM, Kelen C. R.; SIMOES, Belinda P.; GLUCKMAN, Eliane; TAMOUZA, Ryad
    Despite adequate immunization and penicillin prophylaxis, bacterial infections remain a leading cause of morbidity and mortality in patients with sickle cell disease (SCD). Besides hyposplenism, inflammatory and genetic factors might modulate their susceptibility to bacterial infections. We performed a candidate gene association of single nucleotide polymorphisms (SNPs) located in Toll-like receptor (TLR) genes, encoding prominent molecules for innate immune responses, with the occurrence of bacterial infections in patients with SCD. A cohort followed in centres in Brazil, France and Senegal (n=430) was divided in two groups: patients who presented at least one episode of bacterial infection (n=235) and patients who never had bacterial infections (n=195). There were no differences in gender or age distribution among the groups. The frequency of the TLR2 rs4696480 TA genotype was significantly lower in the infected group (50% vs. 67%, odds ratio [OR]=050, 95% confidence interval [CI] 034-075, P<0001), and the TT genotype was significantly higher in the infected group (15% vs. 5%, OR=318, 95% CI 153-661, P<0001). Previous reports demonstrated higher secretion of inflammatory factors in cells from AA individuals, lower occurrence and severity of immune diseases in T carriers. The rs4696480 TA genotype might stand between deleterious effects of over inflammatory response (AA genotype) and inefficient responses (TT genotype) to infectious agents in SCD settings.