Gutiérrez-Grobe Y

Language: Spanish
References: 16
Page: 170-175
PDF size: 74.97 Kb.

ABSTRACT

In the United States approximately 200,000 new cases of acute pancreatitis are diagnosed each year, and the incidence continues increasing worldwide. The most frequent causes of acute pancreatitis are biliary lithiasis and alcohol excess; however other causes may include dyslipidemia, hipercalcemia, medications, trauma, post-surgical states, infections and post endoscopic retrograde cholangiopancreatography. Almost 20% cases of acute pancreatitis cases are classified as idiopathic because the cause cannot be determined. Around 80% of the pancreatitis is interstitial or edematous type, and the rest correspond to the necrotic type, associated to a higher mortality. The pathophysiology of acute pancreatitis occurs in three phases. In the first stage there is trypsin activation in pancreatic acinus cells. Several mechanisms have been proposed, including the disruption of calcium signaling in acinar cells, cleavage of trypsinogen to trypsin by cathepsin B and reduced activity of intracellular trypsin inhibitor; once the trypsin turns activated, various pancreatic enzymes that cause injury are also activated. The second phase is characterized by intrapancreatic inflammation through various mechanisms and pathways. The third phase is characterized by extrapancreatic inflammation and respiratory distress syndrome. In the latter stages, there are 4 steps mediated by cytokines and other inflammatory mediators: 1. Activation of inflammatory cells. 2. Chemo-attraction of inflammatory cells to the microcirculation. 3. Activation of adhesion molecules, and 4. Migration of activated cells to sites of inflammation. This article presents a case of hypertriglyceridemia- induced acute pancreatitis and its treatment according to the most recent literature.

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