Biochemical Changes in Patients at Risk from the Adult Respiratory Distress Syndrome: Does the Pancreas Play a Role?

Abstract

The adult respiratory distress syndrome (ARDS) is the clinical manifestation of a pathophysiological process of rapid onset, characterized by severe dyspnoea, hypoxaemia, increased lung stiffness and diffuse bilateral pulmonary infiltrates. It results from direct or non-specific pulmonary damage to previously normal lungs. The mechanism of acute lung injury in ARDS remains unknown, but different mediator systems are likely to play a role in the pathogenesis of this syndrome. Two recent papers (Deby-Dupont et al. 1984; Nicod et al. 1985) have pointed to a potential role for pancreatic enzymes in the pathogenesis of ARDS, particularly in patients with sepsis, where highly abnormal plasma levels of immunoreactive trypsin have been found. When liberated into the systemic circulation trypsin is a potent protease which can induce damage in very different organs, as observed in acute pancreatitis. Furthermore, trypsin may activate all the other proenzymes including the kallikrein-kininogen-kinin system (KKK system). This may lead to the generation of kinins, especially bradykinin, one of the supposed mediators of ARDS (Fig. 5.1).