During phase 2 of SARS, when there is progression of pneumonia and hypoxemia, IV pulse MP (0.5 g daily) has been given to prevent immunopathologic lung injury,1,7,10,12,18–19 with the rationale that progression of the pulmonary disease may be mediated by the host inflammatory response.7 The use of pulse MP during clinical progression was associated with favorable clinical improvement with resolution of fever and lung opacities within 2 weeks.1,10,19 Corticosteroids have been used as therapy because CT scans of the thorax have revealed radiologic features of bronchiolitis obliterans organizing pneumonia,1,10,18–19,29which is a steroid-responsive condition the presence of which is suggestive of an immunologic phenomenon.30 The pulmonary pathologic features were dominated by diffuse alveolar damage,1,31 with the presence of multinucleated pneumocytes, but bronchiolitis obliterans organizing pneumonia-like lesions in subpleural locations were also seen.31 The use of high-dose pulse MP therapy aims to suppress the cytokine-induced lung injury in phase 2 of SARS.1,7,10,12,18–19 Wong et al32 have demonstrated a marked elevation of T helper type 1 cytokine interferon (IFN)-γ, inflammatory cytokines interleukin (IL)-1, IL-6, and IL-12 for at least 2 weeks after SARS onset. The chemokine profile demonstrated a significant elevation of IL-8, monocyte chemoattractant protein-1, and IFN-γ inducible protein-10. Corticosteroids significantly reduced IL-8, monocyte chemoattractant protein-1, and inducible protein-10 concentrations from 5 to 8 days after treatment. The data confirmed the T helper type 1 cell-mediated immunity and hyperinnate inflammatory response in patients with SARS through the accumulation of monocytes/macrophages and neutrophils.32In addition, in patients with fatal SARS, macrophages are the prominent leukocytes present in the alveoli, with evidence of hemophagocytosis in the lungs.33Hemophagocytosis has been attributed to cytokine dysregulation,34and intervention with steroids might modulate this cytokine response and prevent a fatal outcome, as has been proposed for other causes of ARDS.35However, a retrospective analysis36showed that the use of pulsed corticosteroids was associated with an increased risk of 30-day mortality, but the study could not establish whether a causal relationship exists between the use of pulsed corticosteroids and increased risk of death. Nevertheless, prolonged corticosteroid therapy could increase the risk of complications such as disseminated fungal disease37 and avascular necrosis of bones. The optimal dose, timing, and duration of corticosteroid administration require further investigation.