Academic literature on the topic 'Wg 39 r465e 2010'

e12010 Background: While a breast cancer diagnosis is common in many medical settings, it is still uncommon in the U.S. Department of Veterans Affairs (VA) population, namely due to the minority of female veterans and infrequent diagnosis among men (Neumayer L, Schifftner TL, Henderson WG, et al. Breast cancer surgery in Veterans Affairs and selected university medical centers: results of the patient safety in surgery study. J Am Coll Surg. 2007; 204(6): 1235-41.). Currently, few studies describe the outcomes of breast cancer patients in the VA population. Methods: Using the Veterans Health Administration (VHA) datasets, a retrospective, observational study of patients diagnosed with breast cancer during the study period from October 1, 2005 to September 30, 2010 was conducted. Mortality, health care resource use, and costs were assessed for the 12-month follow-up period. Patients' clinical characteristics were assessed descriptively, and mortality rates were calculated using the Kaplan-Meier method. Results: In patients identified with breast cancer (n=11,719), the total follow-up mortality rate reached 17.04% (n=1,993). Mortality by age stratum totaled 26.07% for patients 65 years and over (n=1,192), 10.64% for those age 40 to 64 years (n=711), and 20.22% (n=90) for patients under 39 years. Nearly one-fifth of all breast cancer patients had follow-up inpatient visits (19.00%), which translated into an average inpatient cost of $22,220 annually per patient. While a similar percentage of patients had follow-up emergency room (ER) visits (18.79%), the average ER cost per patient totaled $140.53 annually. Conclusions: Mortality rate is the lowest for U.S. veteran breast cancer patients between ages 40 and 64 and more than doubles for those over age 65. The mortality rate of patients under age 39 years also exceeded the rate of the 40-64 age group, leading to more years of potential life lost. Additionally, inpatient utilization contributes to a high average annual cost incurred by U.S. veteran breast cancer patients. This information may further aid physicians and researchers as the number of female veterans increases.

Abstract Abstract 980 Lenalidomide is an immunomodulatory drug with single agent activity in untreated (Badoux × et al. 2011) and relapsed or refractory CLL (Chanan-Khan A et al. 2006; Ferrajoli A et al. 2008). Lenalidomide enhances NK-cell mediated antibody-dependent cytotoxicity of rituximab against CLL cells in-vitro (Wu L et al. 2008). Based on the potential for synergistic activity between lenalidomide and rituximab and as there are no overlapping toxicities between these two drugs, we designed this phase II trial of lenalidomide and rituximab as salvage therapy for CLL patients (pts). We present a final analysis of responses to therapy. Between 09/2008 and 09/2009, 59 pts with relapsed or refractory CLL were enrolled. All had received prior purine analogue containing therapy, and had indications for therapy according to NCI-WG criteria. Pts were required to have an ECOG performance status ≤ 2 and adequate organ function (serum creatinine ≤ 2mg/dl, bilirubin ≤ 2mg/dl). There was no minimum requirement for neutrophil or platelet count. Pts with HIV, active hepatitis B or C, or tuberculosis within 5 years were excluded. Therapy consisted of 28-day cycles of lenalidomide 10mg p.o. daily starting from day 9 of cycle 1; rituximab 375mg/m2 i.v. was given weekly for 4 weeks starting on day 1 of cycle 1, and on day 1 of cycle 3 to 12 each. The dose of lenalidomide was reduced for grade ≥ 3 hematological toxicity (dose −1: 5mg/day, dose −2: 2.5 mg/day). Lenalidomide was administered for a total of 12 months, but could continue longer if there was benefit to the pts. Allopurinol was administered from days 1 to 14 of cycle 1. The primary endpoint was response according to the 1996 NCI-WG criteria which was determined after 3 and 6 cycles and every 6 cycles thereafter. The median age was 64 years [34–82]. The median number of prior regimens was 2 [1–8]. Almost all pts had previously received rituximab (98%), and either FCR or CFAR (88%). Other pre-treatment characteristics have been previously described (Ferrajoli et al. ASH abstracts 2010). The overall response rate (ORR) is 66% including 6 complete responses (CR, 10%), 10 nodular partial responses (nPR, 17%) and 23 partial responses (PR, 39%). Of 15 pts with del(17p), 2 achieved CR (13%), 2 nPR (13%) and 4 PR (27%) for an ORR of 53%. With a median follow-up of 25 months, 15 pts (25%) remain on therapy with an estimated median time to treatment failure of 24 months. Forty-nine pts are alive with an actuarial 2-year overall survival of 83%. There have been 3 deaths on therapy: 1 stroke, 1 early death with infectious exacerbation of chronic obstructive pulmonary disease and 1 death from an unrelated cardiac arrhythmia. One pt died from pneumocystis pneumonia while receiving immunosuppression for autoimmune haemolysis and 6 pts died following subsequent therapy for progressive disease (n=2) or Richter's transformation (n=4). One patient was diagnosed with colon cancer 10 months are initiation of therapy and another patient developed a myelodysplastic syndrome after 6 months. No other second malignancies have been observed on therapy. Grade ≥3 hematological toxicity included neutropenia (40 pts, 47%), thrombocytopenia (13 pts, 22%), and anemia (6 pts, 10%). Eighteen pts (31%) experienced grade ≥3 infections. There was one episode of grade 3 tumor lysis. All tumor flare (16 pts, 27%) reactions were grade ≤2. Common grade ≤2 non-hematological toxicities included fatigue (42 pts, 71%), diarrhea (23 pts, 39%), rash (16 pts, 27%), sensory peripheral neuropathy (15 pts, 25%) and constipation (13 pts, 22%). The combination of lenalidomide and rituximab leads to durable responses in pts with relapsed and refractory CLL and is active also in pts with del(17p). The combination is feasible, safe and should be investigated further in this group of pts with limited available therapeutic options. Disclosures: Off Label Use: Lenalidomide is an immune modulator being studied in the treatment of relapsed and refractory CLL. Keating:Celgene: Membership on an entity's Board of Directors or advisory committees. O'Brien:Celgene: Consultancy; GSK: Consultancy. Wierda:Genentech: Consultancy, Membership on an entity's Board of Directors or advisory committees. Lerner:Celgene: Membership on an entity's Board of Directors or advisory committees. Ferrajoli:Celgene: Research Funding.

Introdução: A glomerulonefrite difusa aguda é uma glomerulopatia decorrente do dano inflamatório dos componentes glomerulares, comumente encontrada em pacientes pediátricos, com padrão e prevalência variáveis de acordo com idade, sexo, fatores socioeconômicos e geográficos (principalmente nas glomerulonefrites infecciosas ou pós-infecciosas), sendo a causa mais comum de acometimento renal após os seis anos de idade. Porém, faltam dados mundiais precisos sobre a prevalência da síndrome. Objetivo: Traçar o perfil sociodemográfico e clínico dos pacientes pediátricos diagnosticados com esta glomerulonefrite no Hospital Regional Professor Agamenon Magalhães, localizado no município de Serra Talhada, Pernambuco. Material e método: Trata-se de um estudo retrospectivo e descritivo de corte transversal. A coleta de dados foi realizada entre agosto de 2018 a junho de 2019, através da análise dos prontuários dos pacientes pediátricos que foram diagnosticados com glomerulonefrite difusa aguda. Resultados: 29 prontuários foram analisados, correspondendo aos anos 2015 a 2018, sendo 51,72% do sexo masculino, residente em Serra Talhada e em zona rural, com idade média 7,7 anos, todos de etnia parda. Em admissão para atendimento hospitalar 75,86% da amostra apresentou estado geral regular, e apenas 3,45% grave. 34,48% da população estudada apresentou oligúria, 89,66% edema generalizado, 58,62% hipertensão arterial durante admissão, 27,59% cefaleia e 55,17% febre. Conclusão: Os resultados obtidos através da pesquisa destacam a importância de traçar o perfil para guiar os profissionais do serviço na assistência aos pacientes pediátricos acometidos pela patologia abordada. Descritores: Glomerulonefrite; Glomérulos Renais; Pediatria. Referências Costa DMN, Valente LM, Gouveia PAC, Sarinho FW, Fernandes GV, Cavalcante MAGM, et al. Análise comparativa de glomerulopatias primária e secundária no nordeste do Brasil: dados do Registro Pernambucano de Glomerulopatias - REPEG. J. Bras. Nefrol. 2017; 39(1): 29-35. Sim JJ, Batech M, Hever A, Harrison TN, Avelar T, Kanter MH, et al. Distribution of biopsy-proven presumed primary glomerulonephropathies in 2000-2011 among a racially and ethnically diverse US population. Am J Kidney Dis. 2016; 68(4): 533-544. Crensiglova C, Rehme BB, Kinasz LRS, Chula DC, Do Nascimento MM, Soares MFS. Frequência e avaliação clínico-histológica das doenças glomerulares em um hospital terciário da região Sul do Brasil. J Bras Nefrol. 2016; 38(1): 42-48. Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J. Manual de Medicina de Harisson. 19. ed. Porto Alegre: Mc Graw Hill/ Artmed; 2017. Couser WG. Patogênese e tratamento da glomerulonefrite, uma atualização. J Bras Nefrol. 2016; 38(1): 107-122. Figueira F, Alves JGB, Ferreira OS, Maggi RRS, Correia JB. Pediatria. 4ª edição. Rio de Janeiro: MedBook; 2011. Moorani KN, Sherali AR. Histopathological pattern in childhood glomerulonephritis. J Pak Med Assoc. 2010; 60(12): 1006. Rocha LP, Carminati CR, Machado JR, Laterza VL, Reis MA, Corrêa RRM. Prevalence of nephropathies in children and adolescents and alterations in renal biopsies in Minas Gerais, Brazil, from 1996 to 2010. Ann Diagn Pathol. 2017; 17(1): 22-27. Silva VS, Hagemann R, Viero RM. Glomerulonefrites primárias. In: Riella MC. Princípios de Nefrologia e Distúrbios Hidroeletrolíticos. Rio de Janeiro: Guanabara Koogan; 2018. Bertola EA, Simonetti GD, Del Giorno R, Giannini O, Fossali EF, Meoli M, et al. Extrarenal Immune-mediated disorders linked with acute poststreptococcal glomerulonephritis: a systematic review. Clinic Rev Allerg Immunol. 2019;57(2): 294-302. Sethi S, Fervenza FC. Standardized classification and reporting of glomerulonephritis. Nephrol Dial Transplant. 2018;34(2):193-99. Kılıc BD, Akbalık MK, Buyukcelik M, Balat A. Pediatric post-streptococcal glomerulonephritis: Clinical and laboratory data. Pediatr Int. 2018; 60(7):645‐50. Ali el-TM, Babikir AM, El-Assad S, Abdelrahim MB. Prognosis of acute post-streptococcal glomerulonephritis in Sudanese children. Arab J Nephrol Transplant. 2014;7(2):103‐7. Gunasekaran K, Krishnamurthy S, Mahadevan S, Harish BN, Kumar AP. Clinical characteristics and outcome of post-infectious glomerulonephritis in children in Southern India: a prospective study. Indian J Pediatr. 2015;82(10):896‐903. Maia MLA, Vale MLD, Hatanaka E. Recomendações: Atualização de Condutas em Pediatria. Departamento de Nefrologia. Síndrome nefrítica. Departamentos Científicos SPSP, n. 88, p.10-14, 2019.

Abstract Abstract 3899 BACKGROUND: Although chemoimmunotherapy (CIT) has substantially improved response rates, treatment free survival, and overall survival in patients with chronic lymphocytic leukemia (CLL), only 40–50% of patients achieve a complete remission and the majority have residual disease when evaluated using sensitive assays for minimal residual disease (MRD). While these facts generated interest in consolidation strategies for patients with residual disease, previous trials of alemtuzumab-based consolidation found excess morbidity/mortality. In 2008 we began a trial of lenalidomide-based consolidation for patients with previously untreated CLL who had received 6 cycles of CIT induction. Preliminary analysis suggested that lenalidomide consolidation may improve the quality of response and prolong time to retreatment (Shanafelt; ASH 2010), although follow-up was short (median 16 months). METHODS: Eligible patients were previously untreated and had CLL in need of treatment according to the NCI-WG criteria (Blood 111:5446). Treatment schema consisted of 6 cycles of pentostatin (2 mg/m2), cyclophosphamide (600 mg/m2) and rituximab (375 mg/m2) given every 21 days (Blood 109:405). All patients completing 6 cycles of PCR induction, underwent complete restaging including evaluation for MRD using sensitive flow cytometry. Patients subsequently received 6 months of lenalidomide consolidation by daily administration with a starting lenalidomide dose of 5 mg/day and escalation to 10 mg/day after the first cycle as tolerated. Patients again underwent complete restaging including MRD evaluation after 6 months of lenalidomide. At the time of restaging, MRD negative patients entered observation. Those with residual disease continued on lenalidomide and underwent repeat MRD assessment every 3 months until an MRD negative state was achieved. RESULTS: 45 patients were enrolled at Mayo Clinic between 3/2008 and 12/2009 of whom 44 were eligible. Median age was 65 (range: 44–78) and 71% of patients were male. 61% of patients had intermediate Rai risk and 39% high Rai risk. On prognostic testing 32% were CD38+, 52% Zap-70+, 52% IGHV unmutated, and 16% had high risk FISH (del 17p13; del 11q22). Of the 38 eligible patients who completed 6 cycles of PCR induction, 34 (89%) initiated lenalidomide consolidation. Thus by intent to treat analysis, 34/44 (77%) patients starting CIT with PCR were able to receive consolidation therapy. Among the 34 patients who initiated consolidation, the median number of cycles of lenalidomide received was 6 (range: 1–29). Nine of 34 (26%) patients had the lenalidomide dose increased to 10 mg daily while 18 (53%) required a reduction to 5 mg every other day. Five patients are still on lenalidomide at the time of this report. No cases of tumor lysis syndrome or tumor flare reaction were observed. Adverse events deemed at least possibly related to lenalidomide consolidation included 23 (68%) patients with grade 3+ hematologic toxicity and 5 (15%) with grade 3+ non-hematologic toxicity. Among the 34 patients who received at least 1 cycle of lendalidomide, 6 patients have improved the quality of their response including 3 patients who converted from having residual disease to a MRD- state. After a median follow-up of 29 months, 39/44 patients are alive and the median duration of response has not been reached. To date 8/44 (18%) patients have progressed to require additional treatment. Finally, since the eligibility criteria were nearly identical to our historic trial of PCR without lenalidomide consolidation, we conducted an intent to treat analysis that compared all 44 patients in the present trial (i.e. regardless of whether they received lenalidomide consolidation) to the 64 patients previously treated on our PCR trial (Blood 109:405). The demographic and prognostic characteristics of patients in the two studies were similar. With the caveat it represents a comparison across phase II trials, the proportion of patients free of retreatment at 30 months was 79% (95% CI:67–93) for PCR followed by lenalidomide consolidation vs 66% (95% CI: 54–80) for PCR alone (Figure 1). CONCLUSION: Lenalidomide-based consolidation for CLL patients receiving first-line CIT induction appears to improve the quality of response and prolong time to retreatment. Randomized clinical testing of lenalidomide-based consolidation appears warranted. Disclosures: Shanafelt: Celgene: Research Funding; Hospira: Research Funding; Genentech: Research Funding. Off Label Use: PCR-Lenalidomide (off label use of pentostatin and lenalidomide). Tun:Celgene: Research Funding. Kay:Biothera: Research Funding; Clegene: Research Funding; Cephalon: Research Funding; Genentech: Research Funding; Glaxo Smith Kline: Research Funding; Hospira: Research Funding; Novartis: Research Funding; Supergen: Research Funding; Calistoga: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Emergent Biosolutions (Formerly Trubion): Membership on an entity's Board of Directors or advisory committees.

Abstract Abstract 4636 Background: Single agent rituximab has limited activity in chronic lymphocytic at standard doses; however, the addition of rituximab to purine analogues, monoclonal antibodies or steroids has been shown to improve responses and response duration in patients with untreated and relapsed chronic lymphocytic leukemia (CLL). The combination of rituximab and high dose methylprednisone has shown activity in patients with untreated and fludarabine-refractory CLL (Castro 2008, Castro 2009); however, there is limited reported experience with this regimen in elderly patients. These data prompted us to review our center's experience with rituximab in combination with high dose methylprednisone in elderly patients with CLL. Patients and Methods: We retrospectively identified 24 patients 65 years or older with CLL who received rituximab and methylprednisone between July 2002 and April 2010 at MD Anderson Cancer Center. Six patients received this treatment as initial therapy and 18 patients as salvage treatment. Rituximab 375–750 mg/m2 and methylprednisone 500–2000 mg were administered i.v. weekly for 4 weeks. Three patients received further maintenance treatment with rituximab 375–750 mg/m2 and methylprednisone 500 mg/m2 every month or every 3 months until failure of response. Responses were assessed according to 2008 NCI-WG criteria. Estimated progression free survival and OS were analyzed from time of treatment to progression or death using Kaplan-Meier survival curves. Results: The median age was 71 (65 – 87) years and 17 of 24 (71%) had Rai stage III or IV disease. Two patients had concomitant autoimmune hemolytic anemia (AIHA), one patient had immune thrombocytopenic purpura and AIHA was the indication for therapy in one patient. Median β2-microglobulin was 7.7 (2.3 – 21) mg/l and 5 patients had chromosome 17 abnormalities. Previously treated patients had received a median of 3 (1 – 7) prior treatments and 6 (32%) pts were refractory to fludarabine. Responses were observed in 4 of 6 untreated patients (ORR 67%) and included 3 clinical complete responses unconfirmed by bone marrow biopsy (CRu, 50%) and 1 partial response. The estimated median PFS and OS in this group were 13 and 55 months, respectively. Among patients who received rituximab and methylprednisone as salvage therapy, 7 patients achieved a partial response (ORR 39%), 10 (50%) patients failed treatment, 1 patient (6%) received another therapy after 1 cycle for lack of response and 1 patient (6%) was lost to follow-up. In the salvage group, estimated median PFS and OS were 4 and 18 months, respectively. Four deaths occurred 3, 5, 11 and 12 months after rituximab and methylprednisone without further therapy; 3 patients had progressive CLL and the cause of death was unknown in 1 patient. Grade 3 or 4 neutropenia, anemia and thrombocytopenia occurred in 6 (33%), 3 (14%) and 1 (5%) of evaluable patients. Four patients (17%) experienced grade 3 or 4 infections (3 pneumonia and 1 colonic abscess), 5 patients experienced minor infections and 3 patients experienced viral reactivations (1 CMV, 1 HSV, 2 VZV). There were four grade 3 or 4 non-hematological adverse events including grade 4 gastrointestinal and pulmonary hemorrhage (1), colitis (1), steroid myopathy (1) and peripheral edema (1). All grade 3 or 4 complication occurred in salvage patients. Conclusions: Based on our experience, rituximab and methylprednisone therapy can be safely administered to older patients with CLL. As previously reported by Castro et al, higher response rates were seen in untreated patients, whereas responses were less frequent and shorter lasting in patients with relapsed disease, although this group had high risk disease based on β2-microglobulin levels. Additional studies are required to explore the benefit of this regimen in elderly patients with CLL. Disclosures: Off Label Use: Ofatumumab and lenalidomide in patients with relapsed chronic lymphocytic leukemia. O'Brien:Celgene: Consultancy; Genentech BioOncology: Consultancy. Wierda:Celgene: Consultancy, Membership on an entity's Board of Directors or advisory committees; Genentech BioOncology: Advisory Board, Consultancy, Speakers Bureau. Estrov:Celgene: Consultancy. Keating:Celgene: Consultancy; Genentech: Consultancy. Ferrajoli:Celgene: Research Funding; Genentech: Research Funding.

Introdução: A pneumonia nosocomial é definida como infecção do parênquima pulmonar que ocorre depois de aproximadamente 48 horas de internação e os principais microrganismos envolvidos nessa infecção são bastonetes Gram-negativos, é a complicação mais comum que ocorre entre os pacientes internados em UTIs, e os microrganismos que podem gerar essas infecções respiratórias estão predispostos à colonizar do biofilme bucal. Objetivo: Realizar uma revisão de literatura acerca da Pneumonia Nosocomial relacionada à odontologia, a fim de compreender fatores como aspectos gerais, tipos de bactérias mais frequentes, fisiopatologia, epidemiologia e o tratamento. Metodologia: As buscas foram realizadas no período de 10 de Janeiro a 10 de Maio de 2019, foram utilizados artigos científicos retirados das bases de dados: SCIELO, MEDLINE, LILACS, e monografias que atendiam aos requisitos. Os artigos utilizados como referências bibliográficas foram do período entre 2008 a 2018, com exceção de artigos clássicos. A pesquisa foi realizada tanto na língua portuguesa, como em inglês e espanhol. Foram utilizados como descritores para a busca: "Pneumonia Nosocomial", "Pneumoia Hospitalar”, “Pneumonia Hospitalar e Odontologia”, “Odontologia Hospitalar”, “Pneumonia associada à ventilação mecânica”,e com um resultado de 43 artigos utilizados. Conclusão: Portanto, a Pneumonia nosocomial pode ter relação com a cavidade bucal, deste modo é necessário a implantação do cirurgião dentista no âmbito hospitalar e na Unidade Terapia Intensiva (UTI) para o melhor controle dos microrganismos que colonizam a boca na forma de biofilme bucal e que se proliferam rapidamente quando não é feita higiene adequada e/ou fazem uso de medicações que geram hipossalivação. Descritores: Pneumonia Nosocomial; Unidade Terapia Intensiva; Odontologia. Referências Batista SA, Silva Junior A, Ferreira MF, Agostini M, Torres SR. Alterações orais em pacientes internados em unidades de terapia intensiva. Rev Bras Odontol. 2015;71(2):156-59. Padovani MCRL, Souza SAB, Santanna GR, Guaré RO. Protocolo de cuidados bucais na unidade de tratamento intensivo (UTI) neonatal. Rev Bras Pesq Saúde.2012;14(1):71-80. Gandolfo MC, Pessole T, Mendes G, Albara MF, Fontana A, Freisleben EV et al. Uso dos colutórios em Odontologia. Ação Odonto.2017;2:21. Muniz KGG. Atividade antimicrobiana in vitro de enxaguatórios bucais sobre bactérias do biofilme dentário [Mmonografia]. Campina Grande: Centro de Ciências Biológicas e da Saúde - Universidade Estadual da Paraíba; 2014. Andrade DP, Pallos D, Forte LFBP, Ricardo LH. A doxiciclina como adjuvante no tratamento da periodontite. IJD. Int J Dent. 2009;8(4):202-10. Morais TMN, Silva A, Avi ALRO, Souza PHR, Knobel E, Camargo LFH. A importância da atuação odontológica em pacientes internados em unidade de terapia intensiva. Rev Bras Ter Intensiva. 2010; 18(4):412-17. Soh KL, Shariff Ghazali S, Soh KG, Abdul Raman R, Sharif Abdullah SS, Ong SL. Oral care practice for the ventilated patients in intensive care units: a pilot survey. J Infect Dev Ctries. 2012;6(4):333-39. ANVISA − Agência Nacional de Vigilância Sanitária. Ministério da Saúde. Pediatria: Prevenção e controle de infecção hospitalar/ Ministério da Saúde, Agência Nacional de Vigilância Sanitária. – Brasília: Ministério da Saúde, 2011. Oliveira LCBS, Carneiro PPM, Fischer RG, Tinoco BEM. A presença de patógenos respiratórios no biofilme bucal de pacientes com pneumonia nosocomial. Rev bras ter intensiva. 2010;19(4):428-33. Bernardo WM, Nobre MRC, Jatene FB. A prática clinica baseada em evidências. Parte II: buscando as evidências em fontes de informação. Rev Assoc Med Bras. 2004;50(1):104-8. Sachdev M, Ready D, Brealey D, Ryu J, Bercades G, Nagle J, Borja-Boluda S, Agudo E, Petrie A, Suvan J, Donos N, Singer M, Needleman I. Changes in dental plaque following hospitalisation in a critical care unit: an observational study. Crit Care. 2013;17(5):R189. Dewhirst FE, Chen T, Izard J, Paster BJ, Tanner AC, Yu WH, Lakshmanan A, Wade WG. The human oral microbiome. J Bacteriol. 2010; 192(19):5002-17. Palmer RJ Jr. Composition and development of oral bacterial communities. Periodontol 2000. 2014;64(1):20-39. Pina-Vaz I, Barros J, Noites R, Villa-Vigil A, Pintado M, Carvalho MF. Estratégias anti-microbianas na prevenção e tratamento da infecção oral. Universidade Católica Portuguesa. Ciências da Saúde. 2011;14(55):1-12. Culler HF, Mota CM, Abe CM, Elias WP, Sircili MP, Franzolin MR. Atypical enteropathogenic Escherichia coli strains form biofilm on abiotic surfaces regardless of their adherence pattern on cultured epithelial cells. Biomed Res Int. 2014;2014:845147. Silva ACB, Cruz JS, Sampaio FC, Araújo DAM. Detecção de estreptococos orais em biofilme dental de crianças cárie-ativas e livres de cárie. Braz J Microbiol. 2008;39(4):648-51. Romeiro RL, Majewski M, Molina F, Junqueira JC, Oliveira L, Jorge AOC. Aderência de C. albicans, C. dubliniensis e C. glabrata à superfície de implantes lisos e rugosos. ImplantNews, 2009;6(1):33-37. Cruz MK, Morais TMN, Trevisani DM. Clinical assessment of the oral cavity of patients hospitalized in an intensive care unit of an emergency hospital. Rev bras ter intensiva. 2014;26(4):379-83. Bellissimo-Rodrigues F, Bellissimo-Rodrigues WT, Viana JM, Teixeira GC, Nicolini E, Auxiliadora-Martins M et al. Effectiveness of oral rinse with chlorhexidine in preventing nosocomial respiratory tract infections among intensive care unit patients. Infect Control Hosp Epidemiol. 2009;30(10):952-8. Alotaibi AK, Alshayiqi M, Ramalingam S. Does the presence of oral care guidelines affect oral care delivery by intensive care unit nurses? A survey of Saudi intensive care unit nurses. Am J Infect Control. 2014;42(8):921-22. Oliveira AC, Kovner CT, Silva RS. Infecção hospitalar em unidade de tratamento intensivo de um hospital universitário brasileiro Rev Latinoam Enfermagem. 2010;18(2):97-104. Figueiredo DA, Vianna RPT, Nascimento JA. Epidemiologia da infecção hospitalar em uma unidade de terapia intensiva de um hospital público municipal de João Pessoa-PB. Rev Bras Ciênc Saúde. 2013;17:233-40. Ribas RM, Gontijo Filho PP, Cezário RC, Silva PF, Langoni DRP, Duque AS. Fatores de risco para colonização por bactérias hospitalares multiresistentes em pacientes críticos, cirúrgicos e clínicos em um hospital universitário brasileiro. Rev Med Minas Gerais. 2009;19:193-7. Douglas IS, Price CS, Overdier KH, Wolken RF, Metzger SW, Hance KR, Howson DC. Rapid automated microscopy for microbiological surveillance of ventilator-associated pneumonia. Am J Respir Crit Care Med. 2015;191(5):566-73. Moreira BSG, Silva RMO, Esquivel DN, Fernandes JD. Pneumonia associada à ventilação mecânica: medidas preventivas conhecidas pelo enfermeiro. Rev Baiana Enferm.2011;25:99-106. Rodrigues PMA, Carmo NE, Santos LRC, Knibel MF. Pneumonia associada à ventilação mecânica: epidemiologia e impacto na evolução clínica de pacientes em uma unidade de terapia intensiva. J bras pneumol. 2009;35(11):1084-91. Palomar MÁLF, Olaechea P, López Pueyo MJ, Gimeno R, Gracia Arnillas MP, et al. Estudio nacional de vigilancia de infección nosocomial en servicios de medicina intensiva. Sociedad Española de Medicina Intensiva Crítica y Unidades Coronarias (SEMICYUC) Grupo de trabajo de enfermedades infecciosas y sepsis. 2015. Klepser ME. Aerosolized antibiotics for the treatment of nosocomial pneumonia. Medscape Medical News. 2012. Vardakas KZ, Matthaiou DK, Falagas ME. Incidence, characteristics and outcomes of patients with severe community acquired-MRSA pneumonia. Eur Respir J. 2009;34(5):1148-58. Écila CM, Silvânia PO, Beatriz RMS, Patrick LNS, Adriana CO. Incidência da pneumonia associada à ventilação mecânica em unidade de terapia intensiva. Medicina (Ribeirão Preto, Online), 2017;50(1):39-46. Souza AS. Prevalência de pneumonia associada à assistência à saúde em unidades de terapia intensiva [dissertação]. Campo Grande: Universidade Federal de Mato Grosso de Sul; 2012. Favarin SS, Camponogara S. Perfil dos pacientes internados na unidade de terapia intensiva adulto de um hospital universitário. Rev Enferm UFSM. 2012; 2:320-9. Souza AF, Guimarães AC, Ferreira EF. Avaliação da implementação de novo protocolo de higiene bucal em um centro de terapia intensiva para prevenção de pneumonia associada à ventilação mecânica. REME Rev Min Enferm. 2013;17:177-84. Amaral SM, Cortês Ade Q, Pires FR. Nosocomial pneumonia: importance of the oral environment. J Bras Pneumol. 2009;35(11):1116-24. Munro CL, Grap MJ, Jones DJ, McClish DK, Sessler CN. Chlorhexidine, toothbrushing, and preventing ventilator-associated pneumonia in critically ill adults. Am J Crit Care. 2009;18(5):428-37. Scannapieco FA, Yu J, Raghavendran K, Vacanti A, Owens SI, Wood K, Mylotte JM. A randomized trial of chlorhexidine gluconate on oral bacterial pathogens in mechanically ventilated patients. Crit Care. 2009;13(4):R117. Lorente L, Lecuona M, Jiménez A, Palmero S, Pastor E, Lafuente N, Ramos MJ, Mora ML, Sierra A. Ventilator-associated pneumonia with or without toothbrushing: a randomized controlled trial. Eur J Clin Microbiol Infect Dis. 2012;31(10):2621-29. Özçaka Ö, Başoğlu OK, Buduneli N, Taşbakan MS, Bacakoğlu F, Kinane DF. Chlorhexidine decreases the risk of ventilator-associated pneumonia in intensive care unit patients: a randomized clinical trial. J Periodontal Res. 2012;47(5):584-92. Bezerra EL, Lima AIF, Nóbrega ARR, Barroso DN, Donadi HA, Santos JGS et al. Prevalência de pneumonia em pacientes de uma unidade de terapia intensiva de um hospital- escola de fortaleza – CE. Rev Bras Promoç Saúde. 2012;25(2):20-4. Rosenthal VD, Rodrigues C, Álvarez-Moreno C, Madani N, Mitrev Z, Ye G et al. Effectiveness of a multidimensional approach for prevention of ventilator-associated pneumonia in adult intensive care units from 14 developing countries of four continents: findings of the International Nosocomial Infection Control Consortium. Crit Care Med. 2012;40(12):3121-28. Resende MM, Monteiro SG, Callegari B, Figueiredo PM, Monteiro CR, Monteiro-Neto V. Epidemiology and outcomes of ventilator-associated pneumonia in northern Brazil: an analytical descriptive prospective cohort study. BMC Infect Dis. 2013;13:119.

Background The long‐term impact of weight gain (WG) on cardiovascular outcomes among patients with atrial fibrillation (AF) is unclear. Methods and Results We studied 62 871 (mean age, 72±12, 43% women) adult patients with AF evaluated at the University of Pittsburgh Medical Center between January 1, 2010, and May 13, 2021. Serial body mass index, risk factors, comorbidities, and subsequent death and hospitalization were ascertained and stratified according to percentage WG (≥0% to <5%, ≥5% to <10%, and ≥10%). Over 4.9±3.19 years of follow‐up, 27 114 (43%) patients gained weight (61%, ≥0% to <5%; 23%, ≥5% to <10%; 16%, ≥10%). Patients with progressive WG were incrementally younger ( P <0.001) women (40%, 42%, and 47%) with lower median household income ( P =0.002) and active smoking (8%, 13% and 13%), and they were less likely to be on a non–vitamin K oral anticoagulant (39%, 37%, and 32%). WG was incrementally associated with a significant increase in risk of hospitalization for AF (≥10% WG; hazard ratio [HR], 1.2 [95% CI, 1.2–1.3]; P <0.0001), heart failure (≥10% WG; HR, 1.44 [95% CI, 1.3–1.6]; P <0.001; ≥5% to <10% WG; HR, 1.17 [95% CI, 1.1–1.2]; P <0.001), myocardial infarction (≥10% WG; HR, 1.2 [95% CI, 1.3–1.6]; P <0.001) and all‐cause stroke (4.2%, 4.3%, and 5.6%) despite significantly lower mean CHADS 2 Vasc score (2.9±1.7, 2.7±1.6, and 2.7±1.7). Patients with more WG were significantly more likely to receive cardiac and electrophysiologic interventions. Conclusions Among patients with AF, WG is incrementally associated with increased hospitalization for cardiovascular causes, particularly heart failure, stroke, myocardial infarction, and AF.

Introduction: The National Institute of Neurological Disorders and Stroke (NINDS) Common Data Element (CDE) project provides standardized data collection formats for neuroscience clinical research. Goals are to increase harmonization, efficiency, and data quality in studies, and facilitate collaboration through data sharing and analysis. Stroke-specific CDEs were developed in 2010. The Stroke Oversight Committee (OC) reviewed Core CDEs in 2015. Subarachnoid hemorrhage and unruptured cerebral aneurysms (SAH)-specific CDEs were developed in 2017. In 2018, the Stroke OC recommended that Stroke CDEs be updated to Version 2.0. Methods: NINDS in August 2018, convened the Stroke V2.0 Working Group (WG) consisting of over 50 international subject matter experts. Each domain-specific subgroup: Biospecimens, Biomarkers, and Laboratory Tests; Hospital Course and Acute Therapies; Imaging; Long Term Therapies; Medical History and Prior Health Status; Outcomes and Endpoints; Stroke Presentation and Vital Signs; and Stroke Types and Subtypes, reviewed Stroke V1.0 and SAH CDEs relevant to their purview. Subgroups met regularly to discuss updates to existing Stroke CDEs, addition of new instruments and case report forms (CRFs), and harmonization with SAH CDEs. Draft V2.0 recommendations were posted for public review from February 26 to April 8, 2020. The WG considered public feedback before V2.0 was finalized. Results: This comprehensive review led to updates across CDEs and additions to therapies, outcomes, and imaging domains including Imaging Acquisition and SAH Surgical/Procedural Interventions CRFs and Fugl-Meyer Assessment and PROMIS-29 outcome measures. Following review of 39 V1.0 Stroke outcome measures, 11 were reclassified. Stroke V2.0 CDE recommendations include revised and new template CRFs, data dictionaries, instrument informational documents and guidance documents. Stroke V2.0 was posted to the NINDS CDE website in summer 2020. Conclusions: Updates to the NINDS CDEs based on scientific advancements and user feedback ensure they remain a useful resource. The Stroke v2.0 CDEs provide a current tool for clinical investigators across research domains. NINDS encourages CDE use to standardize research data collection across studies.