Objective: To investigate the characteristics of chest high-resolution computed tomography (HRCT) and pathogenesis of acute graft versus host disease (aGVHD)-induced lung injury after allogenic hematopoietic stem cell transplantation (allo-HSCT).
Methods: Chest HRCT was performed in 47 patients with aGVHD of grade II - IV after allo-HSCT. Twenty-four of the patients underwent different treatment regimens against aGVHD. Before the treatment peripheral blood samples were collected to detect the serum interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). Transbronchial biopsy was performed in 4 patients that failed to recover completely after treatment. Pulmonary function was examined in the patients who survived more than 6 months in every 3 months.
Results: Twenty of the 47 patients showed abnormal images by chest HRCT and 17 of the 20 patients were suspected to be with aGVHD-induced lung injury. The HRCT images were characterized by diffused interstitial infiltrate in 5 cases, diffused interstitial and alveolar infiltrate in 7 cases, and diffused interstitial and segmental lobar alveolar infiltrate in 5 cases. Nine cases had bilateral pleural effusion and hydropericardium, including 4 cases accompanied by myocardial hypertrophy. The levels of serum IFN-gamma and TNF-alpha of the patients with lung injury were (6.9 +/- 1.8) microg/L and (400 +/- 102) microg/L respectively, both not significantly different from those of the patients without lung injury [(6.3 +/- 1.2) microg/L and (428 +/- 83) microg/L respectively, P = 0.202, 0.306]. The histopathology of the lung tissue was characterized by disorganization, epithelial cell damage, interstitial fibroplasia, and interstitial T lymphocyte or macrophage infiltrate. The effective rate of treatment for aGVHD-induced lung injury was positively correlated with that for aGVHD (r = 0.771, P = 0.01). Eleven of the 24 patients who survived more than 6 months had abnormal pulmonary function, including 7 out of the 9 patients with aGVHD-induced lung injury and 4 out the 15 patients without aGVHD-induced lung injury. There was no significant difference in the incidence of abnormal pulmonary function between the patients with and without lung injury (P = 0.033).
Conclusions: Lung is one of the target organs of aGVHD. IFN-gamma and TNF-alpha may play a role in the pathogenesis of aGVHD-induced lung injury. Acute GVHD-induced lung injury may progress to late-onset non-infectious lung injury.