Histopathology of the lung after bone marrow transplantation

• Published in: Journal of clinical pathology Vol. 36; no. 5; pp. 546 - 554
• Main Authors: Sloane, J P, Depledge, M H, Powles, R L, Morgenstern, G R, Trickey, B S, Dady, P J
• Format: Journal Article
• Language: English
• Published: England BMJ Publishing Group Ltd and Association of Clinical Pathologists 01.05.1983; BMJ Publishing Group LTD
• Subjects: Adolescent; Adult; Bone Marrow Transplantation; Child; Female; Graft Rejection; Humans; Leukemia - therapy; Lung - blood supply; Lung - pathology; Lung Diseases - etiology; Lung Diseases - pathology; Male; Middle Aged; Pulmonary Edema - etiology; Pulmonary Edema - pathology; Pulmonary Fibrosis - etiology; Pulmonary Fibrosis - pathology; Vascular Diseases - etiology; Vascular Diseases - pathology
• ISSN: 0021-9746; 1472-4146
• DOI: 10.1136/jcp.36.5.546

The histopathological changes in the lungs of 32 patients who died after bone marrow transplantation for leukaemia have been studied and compared with those found in 21 patients treated by conventional chemotherapy. The transplanted patients exhibited a higher incidence of interstitial pneumonitis, vascular lesions and viral infections, particularly cytomegalovirus (CMV), although bacterial and fungal diseases were commoner in the non-grafted subjects. The pathogenesis of interstitial pneumonitis is discussed with specific reference to the possible roles of irradiation, chemotherapy, viruses and the immunosuppressive drug cyclosporin A. Ten patients died of a syndrome characterised clinically by fever, skin rash, fluid retention, uraemia, low serum albumin concentrations, low central venous pressure and acute pulmonary oedema. These patients exhibited intra-alveolar haemorrhagic fibrinous exudation with or without interstitial changes. The aetiology of this syndrome is not known but it occurs more frequently in recipients of mismatched grafts and evidence is presented suggesting that viruses may play a significant causative role. No lesion was identified that could be directly attributed to Graft-versus-Host disease.