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dc.contributor.advisorTorres Dueñas, Diegospa
dc.contributor.advisorHiguera Cobos, Juan Diegospa
dc.contributor.advisorOchoa Vera, Miguel Enriquespa
dc.contributor.authorCorrea Gómez, David Fernandospa
dc.coverage.spatialFloridablanca (Santander, Colombia)spa
dc.date.accessioned2020-08-22T01:28:30Z
dc.date.available2020-08-22T01:28:30Z
dc.date.issued2020
dc.identifier.urihttp://hdl.handle.net/20.500.12749/7193
dc.description.abstract“Estudio anidado al proyecto de investigación “Valor pronóstico de los polimorfismos de la Metaloproteinasa de Matriz extracelular-9 (MMP-9: SNP-1562C/T), su inhibidor tisular endógeno (TIMP-1: SNP-372T/C), MMP-2 (– 1575 A/G) y de la Acuaporina 5 (AQP5: SNP-1364A/C) en pacientes sépticos.” Introducción: La disfunción cardiovascular asociada a la sepsis tiene un papel fundamental a nivel diagnóstico y pronóstico. Varios biomarcadores se han estudiado para objetivar la disfunción cardiovascular en la sepsis tales como la troponina, péptidos natriuréticos y parámetros ecocardiográficos. Se han encontrado moléculas como las acuaporinas y su polimorfismo AQP-5 SNP- 1364A/C que se han asociado a la fisiopatología de la sepsis y que impactan en la mortalidad. Objetivo: Determinar la asociación entre polimorfismo de la AQP-5 SNP-1364A/C con la disfunción cardiovascular en pacientes adultos con sepsis. Materiales y Métodos: Estudio analítico de corte transversal anidado a la cohorte del estudio “Valor pronóstico de los polimorfismos de la Metaloproteinasa de Matriz extracelular-9 (MMP-9: SNP-1562C/T), su inhibidor tisular endógeno (TIMP-1: SNP- 372T/C), MMP-2 (– 1575 A/G) y de la Acuaporina 5 (AQP5: SNP-1364 A/C) en pacientes sépticos.” Se calculó la asociación del NT pro BNP, troponina I disfunción sistólica /diastólicas medidas por variables ecocardiográficas con el polimorfismo AQP-5 -SNP1364A/C en pacientes con sepsis. Resultados: Se analizó 540 registros. La mediana de edad de los pacientes fue de 59 años con un rango de edad entre 45-74 años. La mediana de NT-pro BNP fue 762 (RIQ: 215.5-3284), de la troponina I 0.1 (RIQ: 0.1- 0.1). El origen más frecuente de la sepsis fue tracto urinario (34.4%). El 14.63% de los pacientes fallecieron. La disfunción sistólica estuvo presente en 29.64 %, la disfunción diastólica 66.1%. El 76.67% fueron manejados en unidad de cuidados intensivo, 22.04% presentaron choque séptico. La asociación entre el polimorfismo de la AQP-5 -SNP1364A/C con la disfunción sistólica (RP:0.94; IC 95%= 0.64- 1.3 Valor P: 0.4503), disfunción diastólica, (RP: 0.93; IC 95%= 0 .75- 1.14 Valor P: 0.2909) Troponina I (RP: 1.2; IC 95%= 0 .75- 2.1 Valor P: 0.2006 ) y NT-proBNP (RP: 1.0; IC 95%= 0 .90- 1.15 Valor P: 0.4169). Conclusiones: No se encontró una asociación estadísticamente significativa entre el polimorfismo AQP-5 -SNP1364A/C con los biomarcadores de lesión miocárdica y variables ecocardiográficas en pacientes con sepsis. A partir de los hallazgos, la metodología de análisis y la evidencia es necesario reorientar las estrategias de investigación alrededor, de la relacion polimorfismo de la AQP-5 -SNP1364A/C con la disfunción cardiovascular incluyendo más pacientes para evaluar su asociación.spa
dc.description.tableofcontentsRESUMEN 9 SUMMARY 11 INTRODUCCIÓN 12 PLANTEAMIENTO DEL PROBLEMA Y JUSTIFICACIÓN 15 MARCO TEÓRICO Y ESTADO DEL ARTE 18 Definición y epidemiologia de la Sepsis 18 Fisiopatología de la sepsis: 22 Disfunción cardiaca asociada a la sepsis 29 Disfunción cardiaca asociada a la sepsis, fisiopatología: 31 Alteraciones hemodinámicas en miocardiopatía séptica 34 Definición de cardiomiopatía séptica 35 Métodos diagnósticos de cardiomiopatía séptica: 37 Biomarcadores de origen cardiogénico 38 Manifestaciones ecocardiográficas 40 Acuaporinas conceptos generales 42 Acuaporinas de origen cardiaco: 43 Acuaporinas cardiacas asociada a la sepsis: 45 OBJETIVOS 47 Objetivos específicos 47 METODOLOGÍA PROPUESTA 48 Tipo de estudio: 48 Población 48 Muestra 49 Recolección de la información 50 Procesamiento y control de calidad 52 Procesamiento y análisis estadístico 52 CONSIDERACIONES ÉTICAS 54 RESULTADOS 56 Características de base 56 Desenlaces primarios 57 Asociación entre el polimorfismo de la AQP-5 -SNP1364A/C con la disfunción sistólica medida por ecocardiograma. 57 Asociación entre el polimorfismo de la AQP-5 -SNP1364A/C con la disfunción diastólica medida por ecocardiograma. 57 Asociación entre el polimorfismo de la AQP-5 -SNP1364A/C con la troponina I.................................................................................................................................................. 58 Asociación entre el polimorfismo de la AQP-5 -SNP1364A/C con el NT- pro BNP. .................................................................................................................................................. 58 DISCUSIÓN 59 CONCLUSIONES 66 BIBLIOGRAFÍA 67 TABLAS 78 FIGURAS 82 ANEXOS 83 CRONOGRAMA 85 CARTAS AUTORIZACIÓN 86spa
dc.format.mimetypeapplication/pdfspa
dc.language.isospaspa
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.5/co/*
dc.titleAsociación entre el polimorfismo de la AQP-5 -1364A/C con la disfunción cardiovascular en pacientes con sepsisspa
dc.title.translatedAssociation between AQP-5 -1364A / C polymorphism with cardiovascular dysfunction in patients with sepsiseng
dc.degree.nameEspecialista en Medicina Internaspa
dc.publisher.grantorUniversidad Autónoma de Bucaramanga UNABspa
dc.rights.localAbierto (Texto Completo)spa
dc.publisher.facultyFacultad Ciencias de la Saludspa
dc.publisher.programEspecialización en Medicina Internaspa
dc.description.degreelevelEspecializaciónspa
dc.type.driverinfo:eu-repo/semantics/masterThesis
dc.type.localTesisspa
dc.type.coarhttp://purl.org/coar/resource_type/c_bdcc
dc.subject.keywordsInternal medicineeng
dc.subject.keywordsMedicineeng
dc.subject.keywordsMedical scienceseng
dc.subject.keywordsHealth scienceseng
dc.subject.keywordsSepsiseng
dc.subject.keywordsTroponin Ieng
dc.subject.keywordsMortalityeng
dc.subject.keywordsHeart failure systoliceng
dc.subject.keywordsHeart failure diastoliceng
dc.subject.keywordsVentricular dysfunctioneng
dc.subject.keywordsSeptic shockeng
dc.subject.keywordsAquaporin 5eng
dc.subject.keywordsInfectionseng
dc.subject.keywordsHematologyeng
dc.subject.keywordsHearteng
dc.identifier.instnameinstname:Universidad Autónoma de Bucaramanga - UNABspa
dc.identifier.reponamereponame:Repositorio Institucional UNABspa
dc.type.hasversioninfo:eu-repo/semantics/acceptedVersion
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.rights.accessrightshttp://purl.org/coar/access_right/c_abf2spa
dc.relation.references1. Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, et al. Definitions for Sepsis and Organ Failure and Guidelines for the Use of Innovative Therapies in Sepsis. Chest. 1992 Jun;101(6):1644-55.spa
dc.relation.references2. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive Care Med. 2003 Apr;29(4):530-8.spa
dc.relation.references3. Singer M. The new sepsis consensus definitions (Sepsis-3): the good, the not- so-bad, and the actually-quite-pretty. Intensive Care Med. 2016 Dec;42(12):2027- 9.spa
dc.relation.references4. Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, et al. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23,;315(8):762-74.spa
dc.relation.references5. Parrillo JE, Parker MM, Natanson C, Suffredini AF, Danner RL, Cunnion RE, et al. Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Annals of internal medicine. 1990 Aug 1,;113(3):227.spa
dc.relation.references6. Nayer J, Aggarwal P, Galwankar S. Utility of point-of-care testing of natriuretic peptides (brain natriuretic peptide and n-terminal pro-brain natriuretic peptide) in the emergency department. International Journal of Critical Illness and Injury Science. 2014 Sep 1,;4(3):209-15.spa
dc.relation.references7. Bessière F, Khenifer S, Dubourg J, Durieu I, Lega J. Prognostic value of troponins in sepsis: a meta-analysis. Intensive Care Med. 2013 Jul;39(7):1181-9.spa
dc.relation.references8. Rump K, Adamzik M. Function of aquaporins in sepsis: a systematic review. Cell & bioscience. 2018;8(1):10.spa
dc.relation.references9. R. Madonna, J jiangi YJ gengi. Attenuated expression of gelsolin in association with induction of aquaporin-l and nitric oxide synthase in dysfunctional hearts of aging mice exposed to endotoxin. ;25.spa
dc.relation.references10. Montiel V, Montiel V, Leon Gomez E, Leon Gomez E, Bouzin C, Bouzin C, et al. Genetic deletion of aquaporin-1 results in microcardia and low blood pressure in mouse with intact nitric oxide-dependent relaxation, but enhanced prostanoids- dependent relaxation. Pflugers Arch - Eur J Physiol. 2014 Feb;466(2):237-51.spa
dc.relation.references11. Adamzik M, Frey UH, Möhlenkamp S, Scherag A, Waydhas C, Marggraf G, et al. Aquaporin 5 Gene Promoter −1364A/C Polymorphism Associated with 30-day Survival in Severe Sepsis. Anesthesiology. 2011 Apr;114(4):912-7.spa
dc.relation.references12. Adamzik M, Frey U, Bitzer K, Jakob H, Baba H, Schmieder R, et al. A novel- 1364A/C aquaporin 5 gene promoter polymorphism influences the responses to salt loading of the renin-angiotensin-aldosterone system and of blood pressure in young healthy men. Basic Res Cardiol. 2008 Nov;103(6):598-610.spa
dc.relation.references13. Martin Arsanios D, Barragan AF, Garzón DA, Cuervo Millán F, Pinzón J, Ramos Isaza E, et al. Actualización en sepsis y choque séptico: nuevas definiciones y evaluación clínica. Acta Colombiana de Cuidado Intensivo. 2017 Jul;17(3):158-83.spa
dc.relation.references14. Mayr FB, Yende S, Angus DC. Epidemiology of severe sepsis. Virulence. 2014 Jan 1,;5(1):4-11.spa
dc.relation.references15. National Inpatient Hospital Costs: The Most Expensive Conditions by Payer, 2011. The HCUP Report : Healthcare Cost and Utilization Project (HCUP): Statistical Briefs;2013 ASI 4186-20.160;Statistical Brief No. 160. 2013.spa
dc.relation.references16. Liu V, Escobar GJ, Greene JD, Soule J, Whippy A, Angus DC, et al. Hospital Deaths in Patients With Sepsis From 2 Independent Cohorts. JAMA. 2014 Jul 2,;312(1):90-2.spa
dc.relation.references17. Martin GS. Sepsis, severe sepsis and septic shock: changes in incidence, pathogens and outcomes. Expert Review of Anti-infective Therapy. 2012 Jun 1,;10(6):701-6.spa
dc.relation.references18. Paoli C, Reynolds M, Sinha M, Gitlin M, Crouser E. Epidemiology and Costs of Sepsis in the United States—An Analysis Based on Timing of Diagnosis and Severity Level. Critical Care Medicine. 2018 Dec;46(12):1889-97.spa
dc.relation.references19. Ortíz G, Dueñas C, Rodríguez F, Barrera L, de La Rosa G, Dennis R, et al. Epidemiology of sepsis in Colombian intensive care units. Biomedica : revista del Instituto Nacional de Salud. 2014 Jan;34(1):40.spa
dc.relation.references20. Rudiger A, Singer M. Mechanisms of sepsis-induced cardiac dysfunction. Critical Care Medicine. 2007 Jun;35(6):1599-608.spa
dc.relation.references21. Charpentier J, Luyt C, Fulla Y, Vinsonneau C, Cariou A, Grabar S, et al. Brain natriuretic peptide: A marker of myocardial dysfunction and prognosis during severe sepsis. Critical Care Medicine. 2004 Mar;32(3):660-5.spa
dc.relation.references22. Flynn A, Chokkalingam Mani B, Mather PJ. Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms. Heart failure reviews. 2010 Nov;15(6):605-11.spa
dc.relation.references23. Francisco J. Romero-Bermejo, Manuel Ruiz-Bailen, Julian Gil-Cebrian, Maria J. Huertos-Ranchal. Sepsis-induced Cardiomyopathy. Current Cardiology Reviews. 2011 Aug;7(3):163-83.spa
dc.relation.references24. Angus DC, van der Poll T. Severe Sepsis and Septic Shock. New England journal of medicine. 2013;369(9):840-51.spa
dc.relation.references25. Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, et al. Definitions for Sepsis and Organ Failure and Guidelines for the Use of Innovative Therapies in Sepsis. Chest. 1992 Jun;101(6):1644-55.spa
dc.relation.references26. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Critical Care Medicine. 2003 Jan 1,;31(4):1250-6.spa
dc.relation.references27. Rabello, Lígia Sarmet Cunha Farah, Rosolem MdM, Leal JV, Soares M, Lisboa T, Salluh JIF. Entendendo o conceito PIRO: da teoria à prática clínica - Parte 1. Revista Brasileira de Terapia Intensiva. 2009 Dec;21(4):425-31.spa
dc.relation.references28. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23,;315(8):801-10.spa
dc.relation.references29. Vincent J, Prof, Opal SM, Prof, Marshall JC, Prof, Tracey KJ, Prof. Sepsis definitions: time for change. Lancet, The. 2013;381(9868):774-5.spa
dc.relation.references30. Carré JE, Singer M. Cellular energetic metabolism in sepsis: the need for a systems approach. Biochimica et biophysica acta. 2008 Jul;1777(7-8):763.spa
dc.relation.references31. Laguado-Nieto MA, Amaris-Vergara AA, Vargas-Ordoñez JE, Rangel-Vera JA, García-León SJ, Centeno-Hurtado KT. Actualización en sepsis y choque séptico en adultos. Medunab. 2019 Jul 1,;22(2):213-27.spa
dc.relation.references32. Keeley A, Hine P, Nsutebu E. The recognition and management of sepsis and septic shock: a guide for non-intensivists. Postgraduate Medical Journal. 2017 Oct;93(1104):626-34.spa
dc.relation.references33. Niño-Mantilla ME, Hormiga-Sánchez CM, Ordoñez IT, Villarreal-Ibarra VP, Ardila-Acuña L, Torres-Dueñas D. Mortalidad por sepsis e infecciones complicadas en el departamento de Santander, Colombia. Universidad y Salud. 2014 Dec 1,;16(2):139-49.spa
dc.relation.references34. Huttunen R, Aittoniemi J. New concepts in the pathogenesis, diagnosis and treatment of bacteremia and sepsis. Journal of Infection. 2011;63(6):407-19.spa
dc.relation.references35. Andersson U, Tracey KJ. Reflex Principles of Immunological Homeostasis. Annual Review of Immunology. 2012 Apr 23,;30(1):313-35.spa
dc.relation.references36. Angus DC, van der Poll T. Severe Sepsis and Septic Shock. The New England Journal of Medicine. 2013 Aug 29,;369(9):840-51.spa
dc.relation.references37. Hamlin SK, Parmley CL, Hanneman SK. Microcirculatory Alterations in Shock States. Critical Care Nursing Clinics of North America. 2014 Sep;26(3):399-412.spa
dc.relation.references38. Ince C. The microcirculation is the motor of sepsis. Critical care (London, England). 2005;9(Suppl. 4):S13-9.spa
dc.relation.references39. De Backer D, Donadello K, Taccone F, Ospina-Tascon G, Salgado D, Vincent J. Microcirculatory alterations: potential mechanisms and implications for therapy. Ann Intensive Care. 2011 Dec;1(1):1-8.spa
dc.relation.references40. Andersson U, Tracey KJ. Reflex Principles of Immunological Homeostasis. Annual Review of Immunology. 2012 Apr 23,;30(1):313-35.spa
dc.relation.references41. Vanasco V, Saez T, Magnani ND, Pereyra L, Marchini T, Corach A, et al. Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery. Free Radical Biology and Medicine. 2014 Dec;77:1-9.spa
dc.relation.references42. Cimolai MC, Alvarez S, Bode C, Bugger H. Mitochondrial Mechanisms in Septic Cardiomyopathy. International journal of molecular sciences. 2015 Aug 3,;16(8):17763-78.spa
dc.relation.references43. Francisco J. Romero-Bermejo, Manuel Ruiz-Bailen, Julian Gil-Cebrian, Maria J. Huertos-Ranchal. Sepsis-induced Cardiomyopathy. Current Cardiology Reviews. 2011 Aug;7(3):163-83.spa
dc.relation.references44. Alvarez S, Vico T, Vanasco V. Cardiac dysfunction, mitochondrial architecture, energy production, and inflammatory pathways: Interrelated aspects in endotoxemia and sepsis. International Journal of Biochemistry and Cell Biology. 2016 Dec;81(Pt B):307-14.spa
dc.relation.references45. Thiemermann C, Vane J. Inhibition of nitric oxide synthesis reduces the hypotension induced by bacterial lipopolysaccharides in the rat in vivo. European Journal of Pharmacology. 1990;182(3):591-5.spa
dc.relation.references46. Southey A, Tanaka S, Murakami T, Miyoshi H, Ishizuka T, Sugiura M, et al. Pathophysiological role of nitric oxide in rat experimental colitis. International journal of immunopharmacology. 1997 Nov;19(11-12):669.spa
dc.relation.references47. Coppo JA. Acuaporinas. Revista Veterinaria. 2008 Jul 1,;19(2):167.spa
dc.relation.references48. De Acha Torrez R, Dolz Tejerina H, Dolz Tejerina V. Acuaporinas, implicaciones en modelos patológicos, de tratamiento y rol clínico. Revista Científica Ciencia Médica. 2015;18(2):38-42.spa
dc.relation.references49. Verkman AS, Anderson MO, Papadopoulos MC. Aquaporins: important but elusive drug targets. Nature reviews. Drug discovery. 2014 Apr;13(4):259-77.spa
dc.relation.references50. Papadopoulos M, Papadopoulos M, Saadoun S, Saadoun S, Verkman A, Verkman A. Aquaporins and cell migration. Pflugers Arch - Eur J Physiol. 2008 Jul;456(4):693-700.spa
dc.relation.references51. Karlsson T, Glogauer M, Ellen RP, Loitto V, Magnusson K, Magalhaes MA. Aquaporin 9 phosphorylation mediates membrane localization and neutrophil polarization. Journal of Leukocyte Biology. 2011 Jan 1,;90(5):963-73.spa
dc.relation.references52. Moon C, Rousseau R, Soria J, Hoque MO, Lee J, Jang SJ, et al. Aquaporin expression in human lymphocytes and dendritic cells. American Journal of Hematology. 2004 Mar;75(3):128-33.spa
dc.relation.references53. Hara‐Chikuma M, Sugiyama Y, Kabashima K, Sohara E, Uchida S, Sasaki S, et al. Involvement of aquaporin‐7 in the cutaneous primary immune response through modulation of antigen uptake and migration in dendritic cells. The FASEB Journal. 2012 Jan;26(1):211-8.spa
dc.relation.references54. Rump K, Unterberg M, Bergmann L, Bankfalvi A, Menon A, Schäfer S, et al. AQP5-1364A/C polymorphism and the AQP5 expression influence sepsis survival and immune cell migration: a prospective laboratory and patient study. Journal of translational medicine. 2016 Nov 21,;14(1):321-11.spa
dc.relation.references55. Vieillard-Baron A, Caille V, Charron C, Belliard G, Page B, Jardin F. Actual incidence of global left ventricular hypokinesia in adult septic shock. Critical Care Medicine. 2008 Jun;36(6):1701-6.spa
dc.relation.references56. Heyndrickx GR, Millard RW, McRitchie RJ, Maroko PR, Vatner SF. Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. The Journal of clinical investigation. 1975 Oct;56(4):978-85.spa
dc.relation.references57. Weisel, R. D., Vito, L., Dennis, R. C., Valeri, C. R., & Hechtman, H. B. Myocardial depression during sepsis. The American Journal of Surgery. 1977:512- 21.spa
dc.relation.references58. Vieillard-Baron A. Septic cardiomyopathy. Ann Intensive Care. 2011 Dec;1(1):1-7.spa
dc.relation.references59. Ayuela Azcarate JM, Clau Terré F, Ochagavia A, Vicho Pereira R. Papel de la ecocardiografía en la monitorización hemodinámica de los pacientes críticos. Medicina Intensiva. 2011;36(3):220-32.spa
dc.relation.references60. Cunnion RE, Schaer GL, Parker MM, Natanson C, Parrillo JE. The coronary circulation in human septic shock. Circulation. 1986 Apr;73(4):637-44.spa
dc.relation.references61. Antonucci E, MD, Fiaccadori E, MD, Donadello K, MD, Taccone FS, MD, Franchi F, MD, Scolletta S, MD. Myocardial depression in sepsis: From pathogenesis to clinical manifestations and treatment. Journal of Critical Care. 2014;29(4):500-11.spa
dc.relation.references62. Blanco J, Muriel-Bombín A, Sagredo V, Taboada F, Gandía F, Tamayo L, et al. Incidence, organ dysfunction and mortality in severe sepsis: a Spanish multicentre study. Critical Care. 2008 Dec 1,;12(6):R158.spa
dc.relation.references63. McDonough KH, Virag JI. Sepsis-induced myocardial dysfunction and myocardial protection from ischemia/reperfusion injury. Frontiers in bioscience : a journal and virtual library. 2006 Jan 1,;11(1):23.spa
dc.relation.references64. Smeding L, Plotz FB, Groeneveld ABJ, Kneijber MCJ. Structural Changes of the Heart During Severe Sepsis Or Septic Shock. Shock. 2012;37(5):449-56.spa
dc.relation.references65. Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, et al. Inhibition of Mitochondrial Permeability Transition Prevents Sepsis-Induced Myocardial Dysfunction and Mortality. Journal of the American College of Cardiology. 2006 Jul 18,;48(2):377-85.spa
dc.relation.references66. Levy R, Piel D, Acton P, Zhou R, Ferrari V, Karp J, et al. Evidence of myocardial hibernation in the septic heart. Critical Care Medicine. 2005 Dec;33(12):2752-6.spa
dc.relation.references67. Piantadosi CA, Suliman HB. Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes. BBA - General Subjects. 2012 Apr;1820(4):532-41.spa
dc.relation.references68. Dos Santos CC, Gattas DJ, Tsoporis JN, Smeding L, Kabir G, Masoom H, et al. Sepsis-induced myocardial depression is associated with transcriptional changes in energy metabolism and contractile related genes: A physiological and gene expression-based approach. Critical Care Medicine. 2010;38(3):894-902.spa
dc.relation.references69. Stengl M, Bartak F, Sykora R, Chvojka J, Benes J, Krouzecky A, et al. Reduced L-type calcium current in ventricular myocytes from pigs with hyperdynamic septic shock. Critical Care Medicine. 2010 Feb;38(2):579-87.spa
dc.relation.references70. Hochstadt A, MD, Meroz Y, MD, Landesberg, Giora, MD, DSc, MBA. Myocardial Dysfunction in Severe Sepsis and Septic Shock: More Questions Than Answers? Journal of Cardiothoracic and Vascular Anesthesia. 2011;25(3):526-35.spa
dc.relation.references71. Repessé X, Charron C, Vieillard-Baron A. Evaluation of left ventricular systolic function revisited in septic shock. Critical care (London, England). 2013 Jul 4,;17(4):164.spa
dc.relation.references72. Pulido JN, MD, Afessa B, MD, Masaki, Mitsuru, MD, PhD, Yuasa, Toshinori, MD, PhD, Gillespie S, DO, Herasevich, Vitaly, MD, PhD, et al. Clinical Spectrum, Frequency, and Significance of Myocardial Dysfunction in Severe Sepsis and Septic Shock. Mayo Clinic Proceedings. 2012;87(7):620-8.spa
dc.relation.references73. Vieillard-Baron A, Caille V, Charron C, Belliard G, Page B, Jardin F. Actual incidence of global left ventricular hypokinesia in adult septic shock. Critical Care Medicine. 2008 Jun;36(6):1701-6.spa
dc.relation.references74. Parker MM, Shelhamer JH, Bacharach SL, Green MV, Natanson C, Frederick TM, et al. Profound but Reversible Myocardial Depression in Patients with Septic Shock. Annals of internal medicine. 1984 Apr;100(4):483.spa
dc.relation.references75. Guarracino F, Baldassarri R, Pinsky MR. Ventriculo-arterial decoupling in acutely altered hemodynamic states. Critical care (London, England). 2013 Mar 19,;17(2):213.spa
dc.relation.references76. Jardin F, Fourme T, Page B, Loubières Y, Vieillard-Baron A, Beauchet A, et al. Persistent preload defect in severe sepsis despite fluid loading: A longitudinal echocardiographic study in patients with septic shock. Chest. 1999 Nov;116(5):1354.spa
dc.relation.references77. Poelaert J, Declerck C, Vogelaers D, Colardyn F, Visser CA. Left ventricular systolic and diastolic function in septic shock. Intensive Care Med. 1997;23(5):553- 60.spa
dc.relation.references78. Rajaram SS, Desai NK, Kalra A, Gajera M, Cavanaugh SK, Brampton W, et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database of Systematic Reviews. 2013 Feb 28,;2018(12):CD003408.spa
dc.relation.references79. Sandham JD, Douglas R, Hull D. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. ACC Current Journal Review. 2003;12(2):17.spa
dc.relation.references80. The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Pulmonary-Artery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury. The New England Journal of Medicine. 2006 May 25,;354(21):2213-24.spa
dc.relation.references81. Phua J, Lim T, Lee K. B-type natriuretic peptide: Issues for the intensivist and pulmonologist. Critical Care Medicine. 2005 Sep;33(9):2094-13.spa
dc.relation.references82. Wang F, Wu Y, Tang L, Zhu W, Chen F, Xu T, et al. Brain natriuretic peptide for prediction of mortality in patients with sepsis: a systematic review and meta- analysis. Critical care (London, England). 2012 May 6,;16(3):R74.spa
dc.relation.references83. Brett J, Gerlach H, Nawroth P, Steinberg S, Godman G, Stern D. Tumor necrosis factor/cachectin increases permeability of endothelial cell monolayers by a mechanism involving regulatory G proteins. The Journal of experimental medicine. 1989 Jun 1,;169(6):1977-91.spa
dc.relation.references84. Bessière F, Khenifer S, Dubourg J, Durieu I, Lega J. Prognostic value of troponins in sepsis: a meta-analysis. Intensive Care Med. 2013 Jul;39(7):1181-9.spa
dc.relation.references85. ver Elst KM, Spapen HD, Nguyen DN, Garbar C, Huyghens LP, Gorus FK. Cardiac Troponins I and T Are Biological Markers of Left Ventricular Dysfunction in Septic Shock. Clinical Chemistry. 2000 May 1,;46(5):650-7.spa
dc.relation.references86. Mehta NJ, Khan IA, Gupta V, Jani K, Gowda RM, Smith PR. Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock. International Journal of Cardiology. 2004;95(1):13-7.spa
dc.relation.references87. Arlati S, Brenna S, Prencipe L, Marocchi A, Casella GP, Lanzani M, et al. Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study. Intensive Care Med. 2000 Jan;26(1):31-7.spa
dc.relation.references88. Turner A, Tsamitros M, Bellomo R. Myocardial cell injury in septic shock. Crit Care Med. 1775 1999;27(9):-80.spa
dc.relation.references89. Landesberg G, Jaffe A, Gilon D, Levin P, Goodman S, Abu-Baih A, et al. Troponin Elevation in Severe Sepsis and Septic Shock: The Role of Left Ventricular Diastolic Dysfunction and Right Ventricular Dilatation. Critical Care Medicine. 2014 Apr;42(4):790-800.spa
dc.relation.references90. Landesberg G, Gilon D, Meroz Y, Georgieva M, Levin PD, Goodman S, et al. Diastolic dysfunction and mortality in severe sepsis and septic shock. European heart journal. 2012 Apr;33(7):895-903.spa
dc.relation.references91. Hestenes S, Halvorsen P, Skulstad H, Remme E, Espinoza A, Hyler S, et al. Advantages of Strain Echocardiography in Assessment of Myocardial Function in Severe Sepsis: An Experimental Study. Critical Care Medicine. 2014 Jun;42(6):e432-40.spa
dc.relation.references92. Werdan K, Oelke A, Hettwer S, Nuding S, Bubel S, Hoke R, et al. Septic cardiomyopathy: hemodynamic quantification, occurrence, and prognostic implications. Clin Res Cardiol. 2011 Aug;100(8):661-8.spa
dc.relation.references93. Brown S, Pittman J, Hirshberg E, Jones J, Lanspa M, Kuttler K, et al. Diastolic dysfunction and mortality in early severe sepsis and septic shock: a prospective, observational echocardiography study. Crit Ultrasound J. 2012 Dec;4(1):1-9.spa
dc.relation.references94. Bouhemad B, Nicolas-Robin A, Benois A, Lemaire S, Goarin J, Rouby J. Echocardiographic Doppler Assessment of Pulmonary Capillary Wedge Pressure in Surgical Patients with Postoperative Circulatory Shock and Acute Lung Injury. Anesthesiology. 2003 May;98(5):1091-100.spa
dc.relation.references95. Laski ME. Structure-Function Relationships in Aquaporins. Seminars in Nephrology. 2006;26(3):189-99.spa
dc.relation.references96. Cardiac aquaporin expression in humans, rats, and mice. American journal of physiology. Heart and circulatory physiology. 2006 Aug 1,;291(2):H705-13.spa
dc.relation.references97. Mehlhorn U, Geissler HJ, Laine GA, Allen SJ. Myocardial fluid balance. Eur J Cardiothorac Surg. 2001 Dec;20(6):1220-30.spa
dc.relation.references98. Hasler U, Vinciguerra M, Vandewalle A, Martin P, Féraille E. Dual Effects of Hypertonicity on Aquaporin-2 Expression in Cultured Renal Collecting Duct Principal Cells. Journal of the American Society of Nephrology : JASN. 2005 Jun;16(6):1571-82.spa
dc.relation.references99. Wright AR, Rees SA. Cardiac Cell Volume: Crystal Clear or Murky Waters? A Comparison with Other Cell Types. Pharmacology and Therapeutics. 1998;80(1):89-121.spa
dc.relation.references100. Chapter J. Homeostasis hídrica: vasopresina y acuaporinas.spa
dc.relation.references101. Bergmann L, Nowak H, Siffert W, Peters J, Adamzik M, Koos B, et al. Major Adverse Kidney Events Are Associated with the Aquaporin 5 -1364A/C Promoter Polymorphism in Sepsis: A Prospective Validation Study. Cells. 2020 Apr 7,;9(4):904.spa
dc.relation.references102. Article S. Biotipos genotipos y genotipos ¿De qué tipos somos?spa
dc.relation.references103. Niño-Mantilla ME, Hormiga-Sánchez CM, Ordoñez IT, Villarreal-Ibarra VP, Ardila-Acuña L, Torres-Dueñas D. Mortalidad por sepsis e infecciones complicadas en el departamento de Santander, Colombia. Universidad y Salud. 2014 Dec 1,;16(2):139-49.spa
dc.relation.references104. Rudd KE, Johnson SC, Agesa KM, Shackelford KA, Tsoi D, Kievlan DR, et al. Global, regional, and national sepsis incidence and mortality, 1990–2017: analysis for the Global Burden of Disease Study. The Lancet. 2020 Jan 18,;395(10219):200-11.spa
dc.relation.references105. Sinapidis D, Kosmas V, Vittoros V, Koutelidakis IM, Pantazi A, Stefos A, et al. Progression into sepsis: an individualized process varying by the interaction of comorbidities with the underlying infection. BMC infectious diseases. 2018 May 29,;18(1):242.spa
dc.relation.references106. Vincent J, Sakr Y, Sprung C, Ranieri V, Reinhart K, Gerlach H, et al. Sepsis in European intensive care units: Results of the SOAP study. Critical Care Medicine. 2006 Feb;34(2):344-53.spa
dc.relation.references107. Vieillard-Baron A, Cecconi M. Understanding cardiac failure in sepsis. Intensive Care Med. 2014 Oct;40(10):1560-3.spa
dc.relation.references108. Kakoullis L, Giannopoulou E, Papachristodoulou E, Pantzaris N, Karamouzos V, Kounis NG, et al. The utility of brain natriuretic peptides in septic shock as markers for mortality and cardiac dysfunction: A systematic review. International Journal of Clinical Practice. 2019 Jul;73(7):e13374,n/a.spa
dc.relation.references109. Castillo JR, Zagler A, Carrillo-Jimenez R, Hennekens CH. Brain natriuretic peptide: a potential marker for mortality in septic shock. International Journal of Infectious Diseases. 2004;8(5):271-4.spa
dc.relation.references110. Papanikolaou J, Makris D, Mpaka M, Palli E, Zygoulis P, Zakynthinos E. New insights into the mechanisms involved in B-type natriuretic peptide elevation and its prognostic value in septic patients. Critical care (London, England). 2014 May 9,;18(3):R94.spa
dc.relation.references111. Turner, Krista L., MD, FACS, Moore, Laura J., MD, FACS, Todd, S. Rob, MD, FACS, Sucher, Joseph F., MD, FACS, Jones SA, MD, McKinley BA, PhD, et al. Identification of Cardiac Dysfunction in Sepsis with B-Type Natriuretic Peptide. Journal of the American College of Surgeons. 2011;213(1):139-46.spa
dc.relation.references112. Landesberg G, Gilon D, Meroz Y, Georgieva M, Levin PD, Goodman S, et al. Diastolic dysfunction and mortality in severe sepsis and septic shock. European heart journal. 2012 Apr;33(7):895-903.spa
dc.relation.references113. Rump K, Unterberg M, Dahlke A, Nowak H, Koos B, Bergmann L, et al. DNA methylation of a NF-κB binding site in the aquaporin 5 promoter impacts on mortality in sepsis. Scientific reports. 2019 Dec 6,;9(1):18511-11.spa
dc.relation.references114. Nomura J, Hisatsune A, Miyata T, Isohama Y. The role of CpG methylation in cell type-specific expression of the aquaporin-5 gene. Biochemical and Biophysical Research Communications. 2007;353(4):1017-22.spa
dc.contributor.cvlachttps://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0000066885*
dc.contributor.cvlachttps://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0001692834*
dc.contributor.cvlachttps://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0000898465*
dc.contributor.orcidhttps://orcid.org/0000-0002-8006-7461*
dc.contributor.orcidhttps://orcid.org/0000-0003-2622-9412*
dc.contributor.orcidhttps://orcid.org/0000-0002-4552-3388*
dc.contributor.scopushttps://www.scopus.com/authid/detail.uri?authorId=24282065800*
dc.contributor.scopushttps://www.scopus.com/authid/detail.uri?authorId=36987156500*
dc.contributor.researchgatehttps://www.researchgate.net/scientific-contributions/29124133_David_Fernando_Correa_Gomez*
dc.contributor.researchgatehttps://www.researchgate.net/profile/Miguel_Ochoa7*
dc.subject.lembMedicina internaspa
dc.subject.lembMedicinaspa
dc.subject.lembCiencias médicasspa
dc.subject.lembInfeccionesspa
dc.subject.lembHematologíaspa
dc.subject.lembCorazónspa
dc.identifier.repourlrepourl:https://repository.unab.edu.cospa
dc.description.abstractenglishBackground: Cardiovascular dysfunction associated with sepsis plays a fundamental role at a diagnostic and prognostic level. Various cardiac biomarkers have been studied to identify the cardiovascular dysfunction in sepsis such as troponin, natriuretic peptides and echocardiographic parameters. Molecules have been found such as aquaporins and its polymorphism AQP-5 SNP-136A/C that have been associated to the pathophysiology of sepsis that impact mortality. Objective: An association was determined between polymorphism of the AQP-5 SNP-1364A/C molecule with cardiovascular dysfunction in adult patients with sepsis Methods: Analytic study in a transversal cut added to the cohort of study “Prognostic value of polymorphisms of Extracellular Matrix Metalloproteinase-9 (MMP-9: SNP- 1562C / T), its endogenous tissue inhibitor (TIMP-1: SNP-372T / C), MMP-2 (- 1575 A / G ) and Aquaporin 5 (AQP5: SNP-1364 A / C) in septic patients.” An association was calculated of the NT pro BNP, troponin I dysfunction systolic/diastolic measurements through echocardiographic variables with the polymorphism AQP-5-SNP1364A/C in patients with sepsis. Results: 540 charts were reviewed. The average age of the patients was 59 years with a range of age between 45-74 years. The average NT-pro BNP was 762 (RIQ: 215.5-3284), and the average of troponin I was 0.1 (RIQ: 0.1- 0.1). The most frequent origin of sepsis was via the urinary tract (34.4%). 14.63% of patients expired. Systolic dysfunction was present in 29.64% and diastolic dysfunction was 66.1%. 76.67% were managed in the intensive care unit, 22.04% presented with septic shock. The association between polymorphism of AQP-5 SNP-1364A/C with systolic dysfunction (RP:0.94; IC 95%= 0.64- 1.3; P Value: 0.4503), diastolic dysfunction, (RP: 0.93; IC 95%= 0 .75- 1.14; P value: 0.2909), Troponin I (RP: 1.2; IC 95%= 0 .75- 2.1; P Value: 0.2006) and NT-proBNP (RP: 1.0; IC 95%= 0 .90- 1.15;P Value: 0.4169). Conclusions: There was not a stadistically significant association found between polymorphism AQP-5 SNP-136A/C with the biomarkers of myocardial injury and echocardiographic variables in patients with sepsis. As a result of these findings, the methodology of analysis and evidence is necessary to reorient the strategies of research surrounding the relation between AQP-5 -SNP1364A/C with cardiovascular dysfunction including more patients to assess their association.eng
dc.subject.proposalCiencias de la saludspa
dc.subject.proposalSepsisspa
dc.subject.proposalTroponina Ispa
dc.subject.proposalNT pro BNPspa
dc.subject.proposalMortalidadspa
dc.subject.proposalInsuficiencia cardíaca sistólicaspa
dc.subject.proposalInsuficiencia cardiaca diastólicaspa
dc.subject.proposalDisfunción ventricularspa
dc.subject.proposalChoque sépticospa
dc.subject.proposalAcuaporina 5spa
dc.type.redcolhttp://purl.org/redcol/resource_type/TMspa
dc.rights.creativecommonsAtribución-NoComercial-SinDerivadas 2.5 Colombia*
dc.coverage.campusUNAB Campus Bucaramangaspa
dc.description.learningmodalityModalidad Presencialspa


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