Pathophysiology of pulmonary complications of acute pancreatitis

被引:98
作者
Browne, George W. [1 ]
Pitchumoni, C. S. [1 ]
机构
[1] St Peters Univ Hosp, Robert Wood Johnson Med Sch, New Brunswick, NJ 08903 USA
关键词
acute pancreatitis; cytokines; acute respiratory distress syndrome; complications of pancreatitis; pleural effusion; interleukins;
D O I
10.3748/wjg.v12.i44.7087
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Acute pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia, acute respiratory distress syndrome, atelectasis, and pleural effusion. The pathogenesis of some of the above complications is attributed to the production of noxious cytokines. Clinically significant is the early onset of pleural effusion, which heralds a poor outcome of acute pancreatitis. The role of circulating trypsin, phospholipase A2, platelet activating factor, release of free fatty acids, chemoattractants such as tumor necrsosis factor (TNF)alpha, interleukin (IL)-1, IL-6, IL-8, fMet-leu-phe (a bacterial wall product), nitric oxide, substance P, and macrophage inhibitor factor is currently studied. The hope is that future management of acute pancreatitis with a better understanding of the pathogenesis of lung injury will be directed against the production of noxious cytokines. (C) 2006 The WJG Press. All rights reserved.
引用
收藏
页码:7087 / 7096
页数:10
相关论文
共 116 条
[1]  
Agarwal N, 1993, Gastroenterologist, V1, P115
[2]  
[Anonymous], 2000, Stedman's medical dictionary, V27th
[3]   Phospholipase A(2) and acute respiratory distress syndrome [J].
Arbibe, L ;
Vial, D ;
Touqui, L .
PHOSPHOLIPASE A2: BASIC AND CLINICAL ASPECTS IN INFLAMMATORY DISEASES, 1997, 24 :79-87
[4]   Tumor necrosis factor receptor-associated factors (TRAFs) - a family of adaptor proteins that regulates life and death [J].
Arch, RH ;
Gedrich, RW ;
Thompson, CB .
GENES & DEVELOPMENT, 1998, 12 (18) :2821-2830
[5]   The American-European Consensus Conference on ARDS, Part 2 - Ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling [J].
Artigas, A ;
Bernard, GR ;
Carlet, J ;
Dreyfuss, D ;
Gattinoni, L ;
Hudson, L ;
Lamy, M ;
Marini, JJ ;
Matthay, MA ;
Pinsky, MR ;
Spragg, R ;
Suter, PM ;
Blanch, L ;
Burchardi, H ;
Hedenstierna, C ;
Lemaire, F ;
Roussos, C ;
Mancebo, J ;
Morris, A ;
Pesenti, A ;
Rossi, A ;
Van Asbeck, BS ;
Brigham, KL ;
Dhainaut, JF ;
Fowler, AA ;
Hyers, TM ;
Morel, D ;
Rodriguez-Roisin, R ;
Schaller, MD ;
Hemmer, M ;
Torres, A ;
Villar, J ;
Vincent, JL ;
Leeper, K ;
Meyrick, B ;
Oppenheimer, L ;
Reid, L ;
Murray, JF ;
Bihari, D ;
Bosken, C ;
Goris, J ;
Johanson, WJ ;
Lanken, PN ;
Le Gall, JR ;
Morris, AH ;
Rinaldo, J ;
Pattishal, EN .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1998, 157 (04) :1332-1347
[6]  
ASHBAUGH DG, 1967, LANCET, V2, P319
[7]   INTRATHORACIC COMPLICATIONS OF ACUTE-PANCREATITIS [J].
BASRAN, GS ;
RAMASUBRAMANIAN, R ;
VERMA, R .
BRITISH JOURNAL OF DISEASES OF THE CHEST, 1987, 81 (04) :326-331
[8]   Natural course of acute pancreatitis [J].
Beger, HG ;
Rau, B ;
Mayer, J ;
Pralle, U .
WORLD JOURNAL OF SURGERY, 1997, 21 (02) :130-135
[9]   THE AMERICAN-EUROPEAN CONSENSUS CONFERENCE ON ARDS - DEFINITIONS, MECHANISMS, RELEVANT OUTCOMES, AND CLINICAL-TRIAL COORDINATION [J].
BERNARD, GR ;
ARTIGAS, A ;
BRIGHAM, KL ;
CARLET, J ;
FALKE, K ;
HUDSON, L ;
LAMY, M ;
LEGALL, JR ;
MORRIS, A ;
SPRAGG, R ;
COCHIN, B ;
LANKEN, PN ;
LEEPER, KV ;
MARINI, J ;
MURRAY, JF ;
OPPENHEIMER, L ;
PESENTI, A ;
REID, L ;
RINALDO, J ;
VILLAR, J ;
VANASBECK, BS ;
DHAINAUT, JF ;
MANCEBO, J ;
MATTHAY, M ;
MEYRICK, B ;
PAYEN, D ;
PERRET, C ;
FOWLER, AA ;
SCHALLER, MD ;
HUDSON, LD ;
HYERS, T ;
KNAUS, W ;
MATTHAY, R ;
PINSKY, M ;
BONE, RC ;
BOSKEN, C ;
JOHANSON, WG ;
LEWANDOWSKI, K ;
REPINE, J ;
RODRIGUEZROISIN, R ;
ROUSSOS, C ;
ANTONELLI, MA ;
BELOUCIF, S ;
BIHARI, D ;
BURCHARDI, H ;
LEMAIRE, F ;
MONTRAVERS, P ;
PETTY, TL ;
ROBOTHAM, J ;
ZAPOL, W .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 149 (03) :818-824
[10]   MIF IS A PITUITARY-DERIVED CYTOKINE THAT POTENTIATES LETHAL ENDOTOXEMIA [J].
BERNHAGEN, J ;
CALANDRA, T ;
MITCHELL, RA ;
MARTIN, SB ;
TRACEY, KJ ;
VOELTER, W ;
MANOGUE, KR ;
CERAMI, A ;
BUCALA, R .
NATURE, 1993, 365 (6448) :756-759