Corticosteroid Treatment for Acute Respiratory Distress Syndrome

The acute respiratory distress syndrome (ARDS) is caused by an inflammatory injury to the lung that is characterized clinically by acute hypoxemic respiratory failure. Pathologically complex changes in the lung are manifested by an early, exudative phase followed by proliferative and fibrotic phases. Persistent ARDS is characterized by ongoing inflammation, parenchymal-cell proliferation, and disordered deposition of collagen, all of which may be responsive to corticosteroid therapy. Systemic corticosteroids have been considered a potentially beneficial therapy. However, several studies have failed to provide convincing evidence to prove the efficacy of corticosteroids in decreasing the mortality of ARDS. For the secondary outcomes, such as oxygenation improvement and reduction of the duration of mechanical ventilation, have shown consistent findings in favor of corticosteroid therapy. However, the underlying mechanisms that account for the anti-inflammatory actions of corticosteroid in ARDS patients have not yet to be elucidated, and the activities do not appear to be controlled by a single mechanism. Interleukin-18 (IL-18), along with interleukin-1b (IL-1b), is produced by inflammasomes when activated by a number of pathogen, environmental or host-derived danger signals. Inflammasomes are innate immune regulatory protein complexes which seem to play a key role in the host immune response of patients with ARDS. The aim of this study is to determine the role of steroid on IL-18 levels in serum of patients with ARDS and its effect on prognosis.