“…Por último, haremos notar que el uso del CT y el CCA está al alcance de una gran proporción de los centros de atención hospitalaria, pero son menos los que cuentan con los recursos para utilizar la escala de APACHE II y otros marcadores de severidad de PA, como la proteína C reactiva, la interleucina 6, el TMX o la procalcitonina 6,[12][13][14] . El calcio sérico y la albúmina para el cálculo de CCA son marcadores bioquí-micos simples, que se llevan a cabo de manera rutinaria en la mayoría de los centros hospitalarios.…”
Section: Discussionunclassified
“…Los marcadores bioquímicos también han resultado predictores útiles. Algunos ejemplos de ellos son la proteína C reactiva, la procalcitonina, la interleucina-6, la tioredoxina-1 y la elastasa de polimorfonucleares, entre otros 6,[12][13][14] .…”
TC and ACC, measured within the first 24hours, are useful severity predictors in acute pancreatitis, with sensitivity and predictive values comparable or superior to those of the conventional prognostic scales.
“…Por último, haremos notar que el uso del CT y el CCA está al alcance de una gran proporción de los centros de atención hospitalaria, pero son menos los que cuentan con los recursos para utilizar la escala de APACHE II y otros marcadores de severidad de PA, como la proteína C reactiva, la interleucina 6, el TMX o la procalcitonina 6,[12][13][14] . El calcio sérico y la albúmina para el cálculo de CCA son marcadores bioquí-micos simples, que se llevan a cabo de manera rutinaria en la mayoría de los centros hospitalarios.…”
Section: Discussionunclassified
“…Los marcadores bioquímicos también han resultado predictores útiles. Algunos ejemplos de ellos son la proteína C reactiva, la procalcitonina, la interleucina-6, la tioredoxina-1 y la elastasa de polimorfonucleares, entre otros 6,[12][13][14] .…”
TC and ACC, measured within the first 24hours, are useful severity predictors in acute pancreatitis, with sensitivity and predictive values comparable or superior to those of the conventional prognostic scales.
“…1 The most severe form of the disease is present in up to 30% of the cases. The mortality rates vary from 1% in the mild form to 20-30% in the severe form 2 , corresponding to the 14 th main cause of death of gastrointestinal origin 3 .…”
The PANC 3 criteria are applicable to define the severity and the prognosis of acute pancreatitis, and are not a substitute method, but rather a method to be associated with the Ranson criteria, mainly due to its high accuracy, positive predictive value and specificity.
“…Apelin expression is most likely amplified by another mechanism. Pancreatic production of proinflammatory cytokines increases during pancreatitis (21,27,34,42), and proinflammatory cytokines will stimulate apelin transcription via a putative Stat3 binding site in the apelin promoter (14).…”
Pancreatitis is classified into acute pancreatitis (AP) and chronic pancreatitis (CP). Apelin, a small regulatory peptide, is the endogenous ligand for the APJ receptor. Apelin and APJ are expressed in the pancreas. The aims of this study were to examine whether apelin influences the inflammatory and fibrosis responses to pancreatitis in mice and to identify mechanisms behind apelin's activities. Supramaximal cerulein induction of AP or CP caused significant ( P < 0.05) elevations in pancreatic apelin and APJ expression. Levels declined during the recovery phases. In apelin gene-knockout mice with pancreatitis, pancreatic neutrophil invasion and myeloperoxidase activity were enhanced significantly, and apelin treatment suppressed both. Apelin exposure reduced CP-induced elevations of extracellular matrix-associated proteins. Apelin inhibited PDGF-simulated connective tissue growth factor production and proliferation of pancreatic stellate cells (PSCs). Serum granulocyte colony-stimulating factor and keratinocyte cytokine levels were higher in apelin gene-knockout than wild-type mice with pancreatitis. Apelin reduced AP- and CP-induced elevations in pancreatic NF-κB activation. Together, these findings imply that the pancreatic apelin-APJ system functions to curb the inflammatory and fibrosis responses during pancreatitis. Furthermore, findings suggest that apelin reduces inflammation and fibrosis by reducing neutrophil recruitment and PSC activity. Inhibition of neutrophil invasion may be mediated by reduced keratinocyte cytokine and granulocyte colony-stimulating factor secretion. Apelin-induced reductions in PSC proliferation and connective tissue growth factor production are putative mechanisms underlying apelin's inhibition of extracellular matrix production. The apelin-associated changes in NF-κB binding may be linked to apelin's regulation of pancreatic inflammatory and fibrosis responses during pancreatitis.
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