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1.
World J Surg ; 33(11): 2427-32, 2009 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-19641951

RESUMEN

BACKGROUND: Whether pancreatic necrosis is a prerequisite for the development of multiorgan failure (MOF) in severe acute pancreatitis (AP) is not clear and has implications for the rational design of translational therapies. This study was designed to investigate the magnitude of any association between MOF and radiologically evident pancreatic or extrapancreatic complications of AP. METHODS: Data regarding 276 patients with AP were analyzed retrospectively with regard to clinical presentation, MOF severity, computerized tomography (CT) evidence of pancreatic necrosis, and modified CT severity index (MCTSI). RESULTS: Agreement between the presence of necrosis and MOF status was seen in 160 of 276 patient episodes (58%; 95% confidence intervals (CI), 52.1-63.8%). In 116 of 276 episodes, the MCTSI and MOF scores disagreed (42%; 95% CI, 36.2-47.9%). CT evidence of pancreatic necrosis was present in 21 of 104 (20.2%) patients without any evidence of MOF, and there was no evidence of necrosis on CT scan in 95 of 176 (54%) patients with MOF. Full-factorial univariate analysis suggested that extrapancreatic complications seen on CT, in particular intra-abdominal fluid collections (effect size = 0.02; P = 0.016) and abnormal liver enhancement (effect size = 0.035; P = 0.031) were associated with severity of MOF, and exerted an even greater effect when they occurred synchronously. CONCLUSIONS: The discrepancy between the presence of necrosis and the occurrence of MOF favors association but not cause in AP. A complex, systems-based, pleiotropic inflammatory network with a common root, in which the extent of pancreatic necrosis influences the severity of MOF in certain individuals and MOF exacerbates the development of pancreatic necrosis in others, seems more likely.


Asunto(s)
Insuficiencia Multiorgánica/diagnóstico , Páncreas/patología , Pancreatitis Aguda Necrotizante/patología , Humanos , Insuficiencia Multiorgánica/etiología , Necrosis , Páncreas/diagnóstico por imagen , Pancreatitis Aguda Necrotizante/complicaciones , Pancreatitis Aguda Necrotizante/diagnóstico por imagen , Pronóstico , Estudios Retrospectivos , Índice de Severidad de la Enfermedad , Tomografía Computarizada por Rayos X
2.
Am J Med ; 128(5): 493-501.e3, 2015 May.
Artículo en Inglés | MEDLINE | ID: mdl-25436428

RESUMEN

BACKGROUND: Lowering the diagnostic threshold for troponin is controversial because it may disproportionately increase the diagnosis of myocardial infarction in patients without acute coronary syndrome. We assessed the impact of lowering the diagnostic threshold of troponin on the incidence, management, and outcome of patients with type 2 myocardial infarction or myocardial injury. METHODS: Consecutive patients with elevated plasma troponin I concentrations (≥50 ng/L; n = 2929) were classified with type 1 (50%) myocardial infarction, type 2 myocardial infarction or myocardial injury (48%), and type 3 to 5 myocardial infarction (2%) before and after lowering the diagnostic threshold from 200 to 50 ng/L with a sensitive assay. Event-free survival from death and recurrent myocardial infarction was recorded at 1 year. RESULTS: Lowering the threshold increased the diagnosis of type 2 myocardial infarction or myocardial injury more than type 1 myocardial infarction (672 vs 257 additional patients, P < .001). Patients with myocardial injury or type 2 myocardial infarction were at higher risk of death compared with those with type 1 myocardial infarction (37% vs 16%; relative risk [RR], 2.31; 95% confidence interval [CI], 1.98-2.69) but had fewer recurrent myocardial infarctions (4% vs 12%; RR, 0.35; 95% CI, 0.26-0.49). In patients with troponin concentrations 50 to 199 ng/L, lowering the diagnostic threshold was associated with increased healthcare resource use (P < .05) that reduced recurrent myocardial infarction and death for patients with type 1 myocardial infarction (31% vs 20%; RR, 0.64; 95% CI, 0.41-0.99), but not type 2 myocardial infarction or myocardial injury (36% vs 33%; RR, 0.93; 95% CI, 0.75-1.15). CONCLUSIONS: After implementation of a sensitive troponin assay, the incidence of type 2 myocardial infarction or myocardial injury disproportionately increased and is now as frequent as type 1 myocardial infarction. Outcomes of patients with type 2 myocardial infarction or myocardial injury are poor and do not seem to be modifiable after reclassification despite substantial increases in healthcare resource use.


Asunto(s)
Infarto del Miocardio/clasificación , Troponina I/sangre , Anciano , Femenino , Humanos , Incidencia , Tiempo de Internación , Masculino , Persona de Mediana Edad , Infarto del Miocardio/sangre , Infarto del Miocardio/mortalidad , Infarto del Miocardio/terapia
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