Factores de riesgo en pancreatitis
Páginas: 43 (10516 palabras)
Publicado: 22 de noviembre de 2011
Gastroenterol Clin N Am 36 (2007) 277–296
GASTROENTEROLOGY CLINICS
OF NORTH AMERICA
Risk and Markers of Severe Acute Pancreatitis
Georgios I. Papachristou, MDa,b,*, Gilles Clermont, MD, MScc, Arun Sharma, BAa, Dhiraj Yadav, MD, MPHa, David C. Whitcomb, MD, PhDa
Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA bDivision of Gastroenterology, Pittsburgh VA Health Care System, Pittsburgh, PA, USA c Center for Inflammation and Regenerative Modeling, CRISMA Laboratory and Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
a
A
cute pancreatitis (AP) is a common acute inflammatory process of the pancreas that affects approximately 100,000 individuals in theUnited States annually [1]. The clinical course of AP varies significantly between individuals. In most patients, the condition is mild and self-limiting, but approximately 20% of patients suffer severe attacks associated with prolonged hospitalization, significant morbidity, and mortality ranging between 30% and 50% [2]. The process is initiated by activation of pancreatic zymogens, resulting inpancreatic autodigestion and an inflammatory response mediated by the innate immune system. The inflammatory reaction is initiated at the site of injury and, if marked, can lead to systemic inflammation. The immune response is independent of the event or process that initiates activation of the digestive enzymes and pancreatic injury in AP, but accounts for much of the subsequent damage. Cytokines play acritical role in the pathogenesis of pancreatitis by driving the subsequent inflammatory response. Knowledge of the inflammatory cascade is important in recognizing when the peak response occurs for various cytokines and inflammatory mediators. A number of studies provide information of the profile of inflammatory markers that peak on the day AP occurs, at 24 hours, 48 hours, and later. These studiesalso examine the potential of inflammatory markers to discriminate patients into high-risk and low-risk groups based on their physiologic measurements and clinical outcome. Early prognosis of severity in AP subjects remains unsatisfactory, however, and an extensive
*Corresponding author. GI Administration, Mezzanine Level 2, C Wing, UPMC Presbyterian Hospital, 200 Lothrop Street, Pittsburgh, PA15213. E-mail address: papachristoug@ dom.pitt.edu (G.I. Papachristou).
0889-8553/07/$ – see front matter doi:10.1016/j.gtc.2007.03.003
ª 2007 Elsevier Inc. All rights reserved. gastro.theclinics.com
278
PAPACHRISTOU, CLERMONT, SHARMA, ET AL
search for objective tools that predict severity and outcome at the time of hospital admission remains a major challenge. MULTISYSTEM ORGANFAILURE AND PANCREATIC NECROSIS Eighty percent of patients with AP develop abdominal pain and elevated pancreatic enzyme levels in the blood and urine for a few days. Twenty percent of patients progress to a more severe course with a prolonged hospitalization or death. About 50% of deaths in subjects with severe AP occur within the first week. An exaggerated inflammatory response and the resultantmultisystem organ failure are the primary causes of death when early mortality occurs [3]. The first sign of multisystem organ failure in AP subjects is commonly impaired lung function caused by adult respiratory distress syndrome. Systemic inflammation also affects the cardiovascular system, kidneys, and liver. Severe AP can be defined in several ways. The Atlanta classification system [4] defines severeAP based on organ dysfunction, including systolic blood pressure less than 90 mm Hg, PaO2 less than 60, serum creatinine greater than 2 mg/dL after rehydration, and gastrointestinal bleeding greater than 500 mL/24 hours. Furthermore, severe AP is defined using the Ranson’s criteria with a score greater than or equal to 3 [5] and the Acute Physiology and Chronic Health Evaluation (APACHE)-II...
GASTROENTEROLOGY CLINICS
OF NORTH AMERICA
Risk and Markers of Severe Acute Pancreatitis
Georgios I. Papachristou, MDa,b,*, Gilles Clermont, MD, MScc, Arun Sharma, BAa, Dhiraj Yadav, MD, MPHa, David C. Whitcomb, MD, PhDa
Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA bDivision of Gastroenterology, Pittsburgh VA Health Care System, Pittsburgh, PA, USA c Center for Inflammation and Regenerative Modeling, CRISMA Laboratory and Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
a
A
cute pancreatitis (AP) is a common acute inflammatory process of the pancreas that affects approximately 100,000 individuals in theUnited States annually [1]. The clinical course of AP varies significantly between individuals. In most patients, the condition is mild and self-limiting, but approximately 20% of patients suffer severe attacks associated with prolonged hospitalization, significant morbidity, and mortality ranging between 30% and 50% [2]. The process is initiated by activation of pancreatic zymogens, resulting inpancreatic autodigestion and an inflammatory response mediated by the innate immune system. The inflammatory reaction is initiated at the site of injury and, if marked, can lead to systemic inflammation. The immune response is independent of the event or process that initiates activation of the digestive enzymes and pancreatic injury in AP, but accounts for much of the subsequent damage. Cytokines play acritical role in the pathogenesis of pancreatitis by driving the subsequent inflammatory response. Knowledge of the inflammatory cascade is important in recognizing when the peak response occurs for various cytokines and inflammatory mediators. A number of studies provide information of the profile of inflammatory markers that peak on the day AP occurs, at 24 hours, 48 hours, and later. These studiesalso examine the potential of inflammatory markers to discriminate patients into high-risk and low-risk groups based on their physiologic measurements and clinical outcome. Early prognosis of severity in AP subjects remains unsatisfactory, however, and an extensive
*Corresponding author. GI Administration, Mezzanine Level 2, C Wing, UPMC Presbyterian Hospital, 200 Lothrop Street, Pittsburgh, PA15213. E-mail address: papachristoug@ dom.pitt.edu (G.I. Papachristou).
0889-8553/07/$ – see front matter doi:10.1016/j.gtc.2007.03.003
ª 2007 Elsevier Inc. All rights reserved. gastro.theclinics.com
278
PAPACHRISTOU, CLERMONT, SHARMA, ET AL
search for objective tools that predict severity and outcome at the time of hospital admission remains a major challenge. MULTISYSTEM ORGANFAILURE AND PANCREATIC NECROSIS Eighty percent of patients with AP develop abdominal pain and elevated pancreatic enzyme levels in the blood and urine for a few days. Twenty percent of patients progress to a more severe course with a prolonged hospitalization or death. About 50% of deaths in subjects with severe AP occur within the first week. An exaggerated inflammatory response and the resultantmultisystem organ failure are the primary causes of death when early mortality occurs [3]. The first sign of multisystem organ failure in AP subjects is commonly impaired lung function caused by adult respiratory distress syndrome. Systemic inflammation also affects the cardiovascular system, kidneys, and liver. Severe AP can be defined in several ways. The Atlanta classification system [4] defines severeAP based on organ dysfunction, including systolic blood pressure less than 90 mm Hg, PaO2 less than 60, serum creatinine greater than 2 mg/dL after rehydration, and gastrointestinal bleeding greater than 500 mL/24 hours. Furthermore, severe AP is defined using the Ranson’s criteria with a score greater than or equal to 3 [5] and the Acute Physiology and Chronic Health Evaluation (APACHE)-II...
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