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1.
Rev. Assoc. Med. Bras. (1992) ; 66(3): 338-344, Mar. 2020. graf
Article in English | SES-SP, LILACS, SES-SP | ID: biblio-1136202

ABSTRACT

SUMMARY The first confirmed case of coronavirus disease 2019 (COVID-19) in Brasil was reported on February 25th, 2020, and by April 3rd, 8076 were confirmed in the country. As COVID-19 disease incidence escalates in Brasil, management of cancer patients requires immediate action and oncology clinics are urged to establish a contingency plan. We have installed a COVID-19 Management Committee to elaborate and implement best practices to assist cancer outpatients as well as to provide a safe environment for clinical staff and other employees at the outpatient clinics. The challenges of cancer treatment in the midst of COVID-19 global pandemic highlight the importance of a rapid response by institutions, where organizational structure, strategic planning, agility in guidelines implementation and alternative ways to protect and support clinical staff, employees and patients may be the key to mitigate pandemic effects.


RESUMO O primeiro caso confirmado de Doença Associada ao Coronavírus 2019 (COVID-19) no Brasil foi confirmado em 25 de fevereiro de 2020 e em 3 de abril já haviam 8076 casos confirmados no país. A medida que a incidência de COVID-19 aumenta no Brasil, o tratamento de pacientes com câncer exige ação imediata e as clínicas oncológicas são instadas a estabelecer um plano de contingência. Instalamos um Comitê de Manejo de COVID-19 para elaborar e implementar as melhores práticas para ajudar pacientes ambulatoriais com câncer, bem como proporcionar um ambiente seguro para a equipe clínica e outros funcionários das clínicas ambulatoriais. Os desafios do tratamento do câncer em meio à pandemia global do COVID-19 destacam a importância de uma resposta rápida das instituições, onde a estrutura organizacional, o planejamento estratégico, a agilidade na implementação de diretrizes e formas alternativas de proteger e apoiar a equipe clínica, funcionários e pacientes podem ser a chave para mitigar os efeitos da pandemia.


Subject(s)
Humans , Pneumonia, Viral/prevention & control , Coronavirus Infections/prevention & control , Pandemics/prevention & control , Betacoronavirus , Medical Oncology/standards , Neoplasms/therapy , Risk Management , Brazil , Coronavirus Infections , Medical Oncology/methods , Medical Oncology/organization & administration
2.
Clinics ; 75: e1777, 2020. tab, graf
Article in English | LILACS | ID: biblio-1133470

ABSTRACT

OBJECTIVES: To evaluate the molecular testing and treatment patterns in a retrospective cohort of newly diagnosed treatment-naïve patients with locally advanced or metastatic non-small-cell lung cancer (NSCLC). METHODS: This is an observational retrospective cohort study conducted across 10 cancer centers in Brazil. Treatment-naïve patients with locally advanced or metastatic NSCLC were enrolled from January to December 2014. The following data were collected from the medical records of patients from diagnosis until the last record (death, loss to follow-up, or the end of the maximum follow-up period): demographics; medical history; smoking status; disease characteristics; previous treatments; and molecular testing patterns and results. The overall survival (OS) was also estimated. Results: A total of 391 patients from 8 different Brazilian states were included, with a median age of 64.1 years (23.7-98.7), with most patients being males (60.1%). The smoking status of 74.2% of patients was a 'former' or 'current smoker'. Stage IV NSCLC at diagnosis was observed in 82.4% of patients, with 269 of them (68.8%) presenting adenocarcinoma (ADC). Among the stage IV ADC patients, 54.0% were referred for molecular testing. Among the patients with an available epidermal growth factor receptor (EGFR) mutation status, 31 (24.0%) were EGFR-positive. The first-line treatment was a platinum-based chemotherapy for 98 patients (25.1%), while non-platinum-based regimens were used in 54 patients (13.8%). OS data were available for 370 patients, with a median OS of 10.8 months. Never smokers had a significantly higher median OS versus current or former smokers (14.6 versus 9.1 months; log-rank p=0.003). Among the patients for whom molecular testing data were available, those with EGFR-positive results had a longer median OS (34.6 versus 12.8 months; log-rank p=0.003). Conclusion: Our findings provide relevant information for prescribers and policy decision-makers by highlighting the unmet needs of patients and the importance of molecular testing in newly diagnosed locally advanced or metastatic lung adenocarcinoma. We also highlight the respective EGFR-tyrosine kinase inhibitor treatment when the result is positive and the areas in which further efforts are required to grant access to effective treatment.


Subject(s)
Humans , Male , Middle Aged , Carcinoma, Non-Small-Cell Lung/diagnosis , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/drug therapy , Lung Neoplasms/genetics , Lung Neoplasms/drug therapy , Brazil , Retrospective Studies , Molecular Diagnostic Techniques , Protein Kinase Inhibitors , Mutation
3.
Rev. bras. ter. intensiva ; 23(2): 176-182, abr.-jun. 2011. ilus, tab
Article in Portuguese | LILACS-Express | LILACS | ID: lil-596441

ABSTRACT

OBJETIVO: O objetivo deste estudo foi caracterizar e quantificar a acidose metabólica causada pela expansão volêmica inicial na reanimação de pacientes com sepse grave e choque séptico. MÉTODOS: Uma coleta de sangue para caracterização físico-química do equilíbrio ácido-básico antes e após a expansão volêmica com 30 mL/kg de solução salina a 0,9 por cento. O diagnóstico e a quantificação da acidose metabólica foram feitas com o uso do "standard base excess" (SBE). RESULTADOS: Oito pacientes com 58 ± 13 anos e APACHE II de 20 ± 4 foram expandidos com 2000 ± 370 mL de solução salina a 0,9 por cento. Houve queda do pH de 7,404 ± 0,080 para 7,367 ± 0,086 (P=0,018) associada a elevação da PCO2 de 30 ± 5 mmHg para 32 ± 2 mmHg (P=0,215) e queda do SBE de -4,4 ± 5,6 para -6,0 ± 5,7 mEq/L (P=0,039). Esta queda do SBE foi associada ao poder acidificante de dois fatores: elevação não significativa do "strong ion gap" (SIG) de 6,1 ± 3,4 para 7,7 ± 4,0 mEq/L (P=0,134) e queda não significativa do "strong ion diference" aparente inorgânico (SIDai) de 40 ± 5 para 38 ± 4 mEq/L (P=0,318). Em contraposição, houve queda da albumina sérica de 3,1 ± 1,0 para 2,6 ± 0,8 mEq/L (P=0,003), que teve um poder alcalinizante sobre o SBE. A elevação do cloro sérico de 103 ± 10 para 106 ± 7 mEq/L (P<0,001) gerou a queda do SIDai. CONCLUSÃO: A reanimação inicial de pacientes com sepse grave e choque séptico com 30 mL/Kg de solução salina a 0,9 por cento é associada a piora da acidose metabólica aferida pelo SBE. Esta piora do SBE pode ser atribuída a uma elevação dos ânions não mensuráveis e do cloro sérico.


OBJECTIVE: The aim of this study was to characterize and quantify metabolic acidosis that was caused by initial volume expansion during the reanimation of patients with severe sepsis and septic shock. METHODS: A blood sample was drawn for physicochemical characterization of the patient's acid-base equilibrium both before and after volume expansion using 30 mL/kg 0.9 percent saline solution. The diagnosis and quantification of metabolic acidosis were based on the standard base excess (SBE). RESULTS: Eight patients with a mean age of 58 ± 13 years and mean APACHE II scores of 20 ± 4 were expanded using 2,000 ± 370 mL of 0.9 percent saline solution. Blood pH dropped from 7.404 ± 0.080 to 7.367 ± 0.086 (p=0.018), and PC O2 increased from 30 ± 5 to 32 ± 2 mmHg (p=0.215); SBE dropped from -4.4 ± 5.6 to -6.0 ± 5.7 mEq/L (p=0.039). The drop in SBE was associated with the acidifying power of two factors, namely, a significant increase in the strong ion gap (SIG) from 6.1 ± 3.4 to 7.7 ± 4.0 mEq/L (p = 0.134) and a non-significant drop in the apparent inorganic strong ion differences (SIDai) from 40 ± 5 to 38 ± 4 mEq/L (p = 0.318). Conversely, the serum albumin levels decreased from 3.1 ± 1.0 to 2.6 ± 0.8 mEq/L (p = 0.003) with an alkalinizing effect on SBE. Increased serum chloride levels from 103 ± 10 to 106 ± 7 mEq/L (p < 0.001) led to a drop in SIDai. CONCLUSION: Initial resuscitation using 30 mL/kg of 0.9 percent saline solution for patients with severe sepsis and septic shock is associated with worsened metabolic acidosis, as measured by SBE. This worsened SBE can be ascribed to a serum increase in the levels of unmeasurable anions and chloride.

4.
Rev. bras. hematol. hemoter ; 32(supl.2): 95-98, jun. 2010. ilus
Article in Portuguese | LILACS | ID: lil-560725

ABSTRACT

Anemia é uma complicação quase universal nos pacientes em estágios avançados de doença renal crônica (DRC). Ela está associada com maior número de internações hospitalares, maior mortalidade e pior qualidade de vida dos pacientes. Ela tem várias causas, sendo deficiência de eritropoetina e ferro as duas principais causas. A condição inflamatória presente na DRC interfere com a ação da eritropoetina e com a absorção intestinal de ferro e mobilização de ferro dos estoques, devido ao aumento de hepcidina. A correção parcial (não completa) da anemia promove melhores resultados nos pacientes com DRC.


Anemia is an almost universal complication of patients in advanced stages of chronic kidney disease (CKD). It is associated with more hospitalizations, increased mortality and worse quality of life. Although there are several causes, erythropoietin and iron deficiency are the most common. The inflammatory condition present in CKD interferes with the action of erythropoietin, intestinal iron absorption and iron mobilization from deposits, due to increased hepcidin concentrations. Partial but incomplete correction of anemia promotes better outcomes in patients with CKD.


Subject(s)
Humans , Anemia , Iron Deficiency , Neoplasms
5.
Rev. bras. mastologia ; 20(1): 15-21, jan.-mar. 2010. tab, graf
Article in Portuguese | LILACS | ID: lil-558628

ABSTRACT

O tamoxifeno (TMX),consagrado como terapia padrão no tratamento de pacientes portadoras de câncer de mama com receptores hormonais positivos, é convertido por metabolização primária e secundária no metabólito endoxifeno, que apresenta afinidade muito maior pelos receptores hormonais e é o maior responsável pelos efeitos antitumorais desta droga. A biotransformação do TMX em endoxifeno é dependente da subunidade 2D6 do citocromo P-450 (CYP2D6), cujo gene apresenta inúmeros polimorfismos que reduzem a atividade metabólica dessa via biológica, resultando em menores níveis de seu produto ativo e, possivelmente, da resposta terapêutica ao uso do TMX. Objetivo: O objetivo deste estudo foi determinar a frequência dos polimorfismos CYP2D6*3, *4, *5, *6 e *10 e dos fenótipos de metabolização da droga TMX em pacientes portadoras de câncer de mama atendidas pelos autores no Centro de Oncologia do Hospital Sírio Libanês (HSL), além de revisar os dados sobre este tema disponíveis na literatura. Métodos: Amostras de sangue periférico de 30 pacientes foram enviadas a laboratório de referência para pesquisa dos polimorfismos descritos de CYP2D6 pela técnica de reação em cadeia da polimerase e digestão por enzimas de restrição (PCR-RFLP). Resultados: Os resultados mostraram heterozigose para polimorfismo CYP2D6*4 e *10 em 33 e 38% das mulheres, respectivamente. Utilizando a classificação de fenótipos de metabolização de TMX previamente descrita determinamos que 27% das mulheres avaliadas foram categorizadas com perfil de metabolização intermediária da droga, e 3% como metabolizadoras pobres, as quais, segundo dados atuais, parecem estar duas vezes mais sujeitas a desenvolverem recorrência de câncer de mama durante tratamento com TMX. Foi documentada uma elevada e inesperada prevalência de heterozigose do polimorfismo *10 na população estudada. Conclusões: Estudos prospectivos estão em andamento, visando definir o papel do perfil dos polimorfismos de CYP2D6 na escolha...


Tamoxifen (TMX), established as standard therapy in treating patients with breast cancer with hormone receptor positive, is converted by metabolism in primary and secondary metabolite endoxifeno, which has much higher affinity for hormone receptors and is most responsible the antitumor effects of this drug. Biotransformation of TMX in endoxifeno 2D6 is dependent on the subunit of cytochrome P-450 (CYP2D6), whose gene has many polymorphisms that reduce the metabolic activity of this biological pathway, resulting in lower levels of its active product, and possibly therapeutic response to use of TMX. Objective: The objective of this study was to determine the frequency of CYP2D6 polymorphisms * 3, * 4, * 5, * 6 and * 10 and phenotypes of drug metabolizing TMX in patients with breast cancer treated by the authors at the Centre for Oncology Syrian Lebanese Hospital (HSL), and review the data on this subject available in the literature. Methods: Blood samples from 30 patients were sent to reference laboratory for research of CYP2D6 polymorphisms described the technique of polymerase chain reaction and restriction enzyme digestion (PCR-RFLP). Results: Results showed heterozygosity for polymorphic CYP2D6 * 4 and * 10 in 33 women and 38% respectively. Using the classification of phenotypes of metabolism of TMX described previously determined that 27% of the women studied were categorized with a profile of intermediate metabolites of the drug, and 3% as poor metabolizers, which, according to current data seem to be two times more likely to develop recurrence of breast cancer during treatment with TMX. It was documented and an unexpected high prevalence of heterozygous * 10 polymorphism in the population. Conclusions: Prospective studies are underway, aimed at defining the role of the profile of CYP2D6 polymorphisms on the choice of strategy hormonal therapy in women with breast cancer.


Subject(s)
Humans , Female , /physiology , /metabolism , Breast Neoplasms/therapy , Polymorphism, Genetic , Tamoxifen/analysis , Tamoxifen/therapeutic use , /biosynthesis , Tamoxifen/metabolism
7.
Rev. Soc. Cardiol. Estado de Säo Paulo ; 19(4): 544-554, out.-dez. 2009. tab, graf
Article in Portuguese | LILACS | ID: lil-559941

ABSTRACT

Nas últimas décadas, o advento de estratégias de tratamento para diversos tipos de tumores permitiu aos pacientes oncológicos longa sobrevida, possibilitando o desenvolvimento de complicações cardiovasculares em grande número de pacientes. A incidência e a gravidade das lesões dependem do quimioterápico administrado, da dose cumulativa empregada, da presença prévia ou não de cardiomiopatias, da existência de comorbidades e da utilização de outros tratamentos utilizados, tais como a radioterapia. A quimioterapia pode levar a toxicidade cardiovascular, manisfestada pela ocorrência de miocardiopatia com ou sem insuficiência cardíaca, disfunção endotelial e arritmias. Apesar de os efeitos dos quimioterápicos e de a incidência de cardiomiopatia estarem bem documentados, ainda não existem estudos específicos direcionados para o tratamento dessa população de pacientes. A base do tratamento proposto tem sido a mesma utilizada para outras formas de agressões miocárdicas, ou seja, fundamentada no uso de inibidor da enzima de conversão. betabloqueador e diuréticos.


Over the last decades, the advent of new and effective treatments for different tumor types has enabled oncologic patients to live longer, however, a large number of these patients develop cardiovascular complications. The incidence and severity of the lesions depend on the type of chemotherapy drug used, cumulative dose, presence of coexisting cardiac disease, others co- morbidities and the association with other treatments such as radiotherapy. Chemotherapy may lead to cardiovascular toxicity, which is manifested by cardiomyopathy with or without heart failure, endothelial lesion and arrhythmias. Although the potential cardiac effects of chemotherapy and cardiomyopathy have been well documented, there is a lack of specific studies focusing on the treatment of this population of patients. The proposed therapy has been the same as that used in other types of myocardial lesions, i.e., the use of angiotensin converting enzyme, betablockers and diuretics.


Subject(s)
Male , Cardiomyopathies/complications , Heart Failure/complications , Heart Failure/chemically induced , Drug Therapy/adverse effects , Drug Therapy/methods , Anthracyclines/administration & dosage , Risk Factors
8.
Rev. bras. mastologia ; 19(2): 76-82, abr.-jun. 2009. ilus
Article in Portuguese | LILACS | ID: lil-559982

ABSTRACT

O câncer de mama é a neoplasia maligna mais comum entre as mulheres, e sua incidência vem aumentando de maneira consistente nas últimas décadas. A melhor compreensão anatomopatológica e molecular do câncer de mama vem permitindo observar que os diferentes subtipos desta doença apresentam características clínicas e prognósticas diferentes, além de perfil de resposta aos tratamentos diferenciados para cada subtipo. Neste artigo, serão revistos os principais aspectos clínicos, laboratoriais e terapêuticos do subgrupo de câncer de mama triplo-negativo; subgrupo de doença definido, do ponto de vista imunoistoquímico, pela ausência de receptores hormonais ou de HER-2. Esse tipo de câncer de mama representa novo desafio para os profissionais envolvidos no tratamento multidisciplinar dessa neoplasia, e vem tornando-se foco de inúmeros estudos destinados a permitir sua melhor compreensão e ao desenho de estratégias terapêuticas mais eficientes.


Breast cancer is the most common cancer among women; the incidence of such disease is increasing through the last decades. Recently, several advances regarding the understanding of the pathology and molecular biology of breast cancer directed us to a new understanding of the disease pathologic mechanisms, leading to a molecular classification and, consequently, a novel way to treat the patients. In this review we will focus on the main clinical, laboratorial and therapeutical aspects of the triple negative breast cancer, as well as on the differences and similarities among triple negative, basal-like and BRCA1 linked breast cancers.


Subject(s)
Humans , Genes, BRCA1/physiology , Breast Neoplasms/genetics , Breast Neoplasms/pathology , Breast Neoplasms/therapy , Gene Expression , Immunohistochemistry , Breast Neoplasms/classification , Breast Neoplasms/drug therapy , Survival
9.
Rev. bras. mastologia ; 18(2): 73-83, abr.-jun. 2008. tab
Article in Portuguese | LILACS | ID: lil-550121

ABSTRACT

O receptor do fqtor de crescimento epidérmico humano tipo 2 (HER-2) é um receptor trasnsmembranacom atividade tirosina quinase, tal molécula encontra-se hiper-expressa em aproximadamente 20% a 25% dos carcinomas invasivos de mama. Os pacientes que apresentam esta característica molecular apresentam padrão de sensibilidade a agentes antineoplásicos diferente dos outros tumores e também um pior prognóstico. O trastuzumabe (Herceptin, Genentech) é um anticorpo monoclonal humanizado do tipo IgG1, direcionado à porção extracelular do HER-2. A adição do trastuzumabe à quimioterapia resulta aumento na sobrevida das pacientes, seja na doença metastática ou no tratamento adjuvante. Infelizmente, uma importante fração destas pacientes não atinge resposta à terapia inicial com trastuzumabe e a vasta maioria daquelas que responde inicialmente desenvolverão resistência em um perído de um ano. Nesta revisão, iremos discutir os mecanismos moleculares que levam à resistência a este agente, assim como as possibilidades terapêuticas que emergem deste conhecimento.


The human epidermal growth factor receptor 2 (HER-2) is a transmembrane receptor with tyrosine-kinase activity overexpressed in about 20-25% of invasive carcinomas of the breast. Patientes with such tumors have different responses to therapeutic agents and a worse outlook, with reduced progression-free and overall survival, when compared with patients harboring HER-2 negative tumors. Trastuzumab (Herceptin, Genentech) is a humanized IgG1 monoclonal antibody against the extracellular domain of HER-2. The combined use of trastuzumab and chemotherapy has resulted in an increase in overall survival rates in the metastatic setting. Unfortunately, a sizable fraction of patients do not respond to initial therapy with trastuzumab, either as a single agent or in combination with chemotherapy, and the vast majority of patients initially responding eventually develop resistance to treatment within 1 year. This review will discuss several molecular mechanisms that can lead to development of trastuzumab resistance, as well as the possibility of exploring these aberrations as therapeutic targets that could help avoid or overcome resistance to trastuzumab, thus enhancing the therapeutic arsenal and the life expectancy of patients with HER2-positive breast cancer.


Subject(s)
Humans , Male , Female , Antibodies, Monoclonal/adverse effects , Antibodies, Monoclonal/metabolism , Antibodies, Monoclonal , Antibodies, Monoclonal/therapeutic use , Breast Neoplasms/therapy , ErbB Receptors , /analysis , Protein Kinases , Drug Resistance
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