viernes, 14 de julio de 2017

Diabetes y UCI / ICU and diabetic patients

Julio 12, 2017. No. 2747





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El efecto de la administración de insulina sobre el péptido c en el diabético tipo 2 grave
The effect of insulin administration on c-peptide in critically ill patients with type 2 diabetes.
Ann Intensive Care. 2017 Dec;7(1):50. doi: 10.1186/s13613-017-0274-5. Epub 2017 May 12.
Abstract
BACKGROUND: In critically ill patients with permissive hyperglycemia, it is uncertain whether exogenous insulin administration suppresses or enhances c-peptide secretion (a marker of pancreatic beta-cell response). We aimed to explore this effect in patients with type 2 diabetes. METHODS: We prospectively enrolled a cohort of 45 critically ill patients with type 2 diabetes managed according to a liberal glucose protocol (target blood glucose 10-14 mmol/l). We recorded the administration of insulin and oral hypoglycemic agents and measured plasma c-peptide as surrogate marker of endogenous insulin secretion on the first two consecutive days in ICU. RESULTS: Overall, 20 (44.4%) patients required insulin to achieve target blood glucose. Insulin-treated patients had higher glycated hemoglobin A1c, more premorbid insulin-requiring type 2 diabetes, and greater blood glucose levels but lower c-peptide levels on admission. Premorbid insulin-requiring diabetes was independently associated with lower admission c-peptide, whereas greater plasma creatinine was independently associated with higher levels. Increases in c-peptide were positively correlated with an increase in blood glucose both in patients who did (r = 0.54, P = 0.01) and did not (r = 0.56, P = 0.004) receive insulin. However, insulin administration was independently associated with a greater increase in c-peptide (P = 0.04). This association was not modified by the use of oral insulin secretagogues. CONCLUSIONS: C-peptide, a marker of beta-cell response, responds to and is influenced by glycemia and renal function in critically ill patients with type 2 diabetes. In addition, in our cohort, exogenous insulin administration was associated with a greater increase in c-peptide in response to hyperglycemia. Trial Registration Australian New Zealand Clinical Trials Registry (ACTRN12615000216516).
KEYWORDS: Blood glucose; C-peptide; Critical care, beta-cell; Diabetes mellitus; Insulin

Hiperglicemia inducida por estrés y el riesgo subsecuente de DM2 en sobrevivientes de UCI
Stress Induced Hyperglycemia and the Subsequent Risk of Type 2 Diabetes in Survivors of Critical Illness.
PLoS One. 2016 Nov 8;11(11):e0165923. doi: 10.1371/journal.pone.0165923. eCollection 2016.
Abstract
OBJECTIVE: Stress induced hyperglycemia occurs in critically ill patients who have normal glucose tolerance following resolution of their acute illness. The objective was to evaluate the association between stress induced hyperglycemia and incident diabetes in survivors of critical illness. DESIGN: Retrospective cohort study. SETTING: All adult patients surviving admission to a public hospital intensive care unit (ICU) in South Australia between 2004 and 2011. PATIENTS:
Stress induced hyperglycemia was defined as a blood glucose ≥ 11.1 mmol/L (200 mg/dL) within 24 hours of ICU admission. Prevalent diabetes was identified through ICD-10 coding or prior registration with the Australian National Diabetes Service Scheme (NDSS). Incident diabetes was identified as NDSS registration beyond 30 days after hospital discharge until July 2015. The predicted risk of developing diabetes was described as sub-hazard ratios using competing risk regression. Survival was assessed using Cox proportional hazards regression. MAIN RESULTS: Stress induced hyperglycemia was identified in 2,883 (17%) of 17,074 patients without diabetes. The incidence of type 2 diabetes following critical illness was 4.8% (821 of 17,074). The risk of diabetes in patients with stress induced hyperglycemia was approximately double that of those without (HR 1.91 (95% CI 1.62, 2.26), p<0.001) and was sustained regardless of age or severity of illness. CONCLUSIONS: Stress induced hyperglycemia identifies patients at subsequent risk of incident diabetes.

Revisión de la evidencia para los protocolos de manejo de cetoacidosis diabética en adultos.
Review of Evidence for Adult Diabetic Ketoacidosis Management Protocols.
Front Endocrinol (Lausanne). 2017 Jun 13;8:106. doi: 10.3389/fendo.2017.00106. eCollection 2017.
Abstract
BACKGROUND: Diabetic ketoacidosis (DKA) is an endocrine emergency with associated risk of morbidity and mortality. Despite this, DKA management lacks strong evidence due to the absence of large randomised controlled trials (RCTs). OBJECTIVE: To review existing studies investigating inpatient DKA management in adults, focusing on intravenous (IV) fluids; insulin administration; potassium, bicarbonate, and phosphate replacement; and DKA management protocols and impact of DKA resolution rates on outcomes.
CONCLUSION: There are major deficiencies in evidence for optimal management of DKA. Current practice is guided by weak evidence and consensus opinion. All aspects of DKA management require RCTs to affirm or redirect management and formulate consensus evidence-based practice to improve patient outcomes.
KEYWORDS: diabetes; diabetic ketoacidosis; hypoglycemia; hypokalemia; insulin; metabolic acidosis; protocol; rehydration

XIV Congreso Virtual Mexicano de Anestesiología 2017
Octubre 1-Diciembre 31, 2017
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Diabetes y corazon / Heart and diabetes

Julio 13, 2017. No. 2748






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Disfunción cardiaca relacionada a la diabetes
Diabetes-Related Cardiac Dysfunction.
Endocrinol Metab (Seoul). 2017 Jun;32(2):171-179. doi: 10.3803/EnM.2017.32.2.171.
Abstract
The proposal that diabetes plays a role in the development of heart failure is supported by the increased risk associated with this disease, even after correcting for all other known risk factors. However, the precise mechanisms contributing to the condition referred to as diabetic cardiomyopathy have remained elusive, as does defining the disease itself. Decades of study have defined numerous potential factors that each contribute to disease susceptibility, progression, and severity. Many recent detailed reviews have been published on mechanisms involving insulin resistance, dysregulation of microRNAs, and increased reactive oxygen species, as well as causes including both modifiable and non-modifiable risk factors. As such, the focus of the current review is to highlight aspects of each of these topics and to provide specific examples of recent advances in each area.
KEYWORDS: Diabetic cardiomyopathies; Energy metabolism; Heart failure; Metabolic diseases; Mitochondria, heart; Stress, physiological
La diabetes mellitus y la cardioprotección
Dr. Pastor Luna, Dr. Gustavo Pastelín, Dr. Martín Martínez
Revista Mexicana de Anestesiología, Vol. 34. No. 2 Abril-Junio 2011 pp 111-125
RESUMEN
La diabetes mellitus (DM) es una enfermedad metabólica que constituye un poderoso factor de riesgo para las enfermedades cardiovasculares (ECV). El 80% aproximadamente de estos pacientes mueren de ECV y cerca del 75% corresponden a muertes por enfermedad arterial coronaria (EAC). En la DM existen diversas alteraciones que hacen más susceptible al corazón al daño por isquemia-reperfusión (I/R). Por otra parte, la cardioprotección constituye todas las intervenciones o estrategias que evitan o disminuyen el daño por I/R. Una de estas estrategias es el precondicionamiento por isquemia (PCI) el cual consiste en breves períodos de isquemia seguidos de un período isquémico prolongado, el cual también se puede inducir por fármacos. La cardioprotección inducida por el PCI es inhibida en condiciones de DM. En esta revisión se describen las alteraciones del metabolismo de los principales sustratos energéticos (ácidos grasos y glucosa) que se presentan en condiciones de DM. Además se estudia la influencia que ejerce el fenómeno de la memoria metabólica en el curso de la DM y constituye en la actualidad uno de los principales factores que favorecen la susceptibilidad del paciente diabético para desarrollar ECV, ya que induce complicaciones micro y macrovasculares; se describen también los mecanismos propuestos para la instalación de la memoria metabólica y cómo este fenómeno inhibe el PCI en animales de experimentación. Finalmente se presentan las estrategias para proteger al corazón diabético de los efectos deletéreos de la memoria metabólica. Se resalta la importancia de un diagnóstico temprano de la enfermedad y del control de la glucemia. Palabras clave: Diabetes mellitus, memoria metabólica, cardioprotección.

XIV Congreso Virtual Mexicano de Anestesiología 2017
Octubre 1-Diciembre 31, 2017
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Cardiomiopatia diabetica / Diabetic cardiomyopathy

Julio 14, 2017. No. 2749







Factores de estrés metabólico y bioquímico en cardiomiopatía metabólica
Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy.
Front Cardiovasc Med. 2017 May 31;4:31. doi: 10.3389/fcvm.2017.00031. eCollection 2017.
Abstract
Diabetic cardiomyopathy (DCM) or diabetes-induced cardiac dysfunction is a direct consequence of uncontrolled metabolic syndrome and is widespread in US population and worldwide. Despite of the heterogeneous and distinct features of DCM, the clinical relevance of DCM is now becoming established. DCM progresses to pathological cardiac remodeling with the higher risk of heart attack and subsequent heart failure in diabetic patients. In this review, we emphasize lipid substrate quality and the phenotypic, metabolic, and biochemical stressors of DCM in the rodent and human pathophysiology. We discuss lipoxygenase signaling in the inflammatory pathway with multiple contributing and confounding factors leading to DCM. Additionally, emerging biochemical pathways are emphasized to make progress toward therapeutic advancement to treat DCM.
KEYWORDS: cardiac remodeling; cardiomyopathy; diabetes; fatty acids; hypertension; inflammation
Cardiomiopatía diabética: Abordaje actual y metas potenciales de diagnóstico y tratamiento
Diabetic Cardiomyopathy: Current Approach and Potential Diagnostic and Therapeutic Targets.
J Diabetes Res. 2017;2017:1310265. doi: 10.1155/2017/1310265. Epub 2017 Mar 21.
Abstract
Although ischemic heart disease is the major cause of death in diabetic patients, diabetic cardiomyopathy (DCM) is increasingly recognized as a clinically relevant entity. Considering that it comprises a variety of mechanisms and effects on cardiac function, increasing the risk of heart failure and worsening the prognosis of this patient category, DCM represents an important complication of diabetes mellitus, with a silent development in its earlier stages, involving intricate pathophysiological mechanisms, including oxidative stress, defective calcium handling, altered mitochondrial function, remodeling of the extracellular matrix, and consequent deficient cardiomyocyte contractility. While DCM is common in diabetic asymptomatic patients, it is frequently underdiagnosed, due to few diagnostic possibilities in its early stages. Moreover, since a strategy for prevention and treatment in order to improve the prognosis of DCM has not been established, it is important to identify clear pathophysiological landmarks, to pinpoint the available diagnostic possibilities and to spot potential therapeutic targets.

Miocardiopatía diabética: concepto, función cardiaca y patogenia
P. CODINACH HUIX, R. FREIXA PAMIAS
ANALES DE MEDICINA INTERNA Vol. 19, N.º 6, 2002
RESUMEN
La miocardiopatía diabética es una enfermedad producida por la diabetes en si misma, que se caracteriza por la presencia de disfunción ventricular izquierda, la cual puede ser diastólica, sistólica o mixta. Consideramos como causas de la miocardiopatía, por ser éstas consecuencia de la propia diabetes, las siguientes: enfermedad metabólica, fibrosis intersticial e hipertrofia miocelular, enfermedad microvascular y disfunción autonómica. Las enfermedades concomitantes con la diabetes (hipertensión arterial, enfermedad coronaria y nefropatía), puesto que también se dan frecuentemente en ausencia de la misma, deben excluirse como causas de la citada miocardiopatía. No hay evidencia de que la miocardiopatía diabética aislada pueda producir clínica de insuficiencia cardiaca. Sin embargo, se ha objetivado la presencia de disfunción ventricular subclí- nica en diabéticos jóvenes asintomáticos sin otras patologías acompañantes capaces de afectar el músculo cardiaco, en los cuales debe asumirse que dicha afectación miocárdica es exclusivamente debida a la propia diabetes, pero carecemos de estudios sobre su evolución. PALABRAS CLAVE: Miocardiopatía diabética. Disfunción ventricular izquierda. Diabetes juvenil.
PDF 

XIV Congreso Virtual Mexicano de Anestesiología 2017
Octubre 1-Diciembre 31, 2017
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