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Pathophysiology of Lung Injury After Hematopoietic Stem Cell Transplantation

  • Kenneth R. Cooke
Chapter
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Part of the Contemporary Hematology book series (CH)

Abstract

Over the last several decades, hematopoietic stem cell transplantation (SCT) has emerged as an important therapeutic option for a number of malignant and nonmalignant conditions. Unfortunately, the utility of this treatment strategy is limited by several side effects, the most serious of which include the development of graft-vs-host disease (GVHD) and pulmonary toxicity. Pulmonary dysfunction, specifically diffuse lung injury, is a major complication of SCT; it occurs in 25–55% of SCT recipients and can account for approximately 50% of transplant-related mortality (1–6). Diffuse lung injury is described as either acute or chronic with respect to both the time of onset after SCT and the tempo of disease progression once the diagnosis has been established. Approximately 50% of the time, an infectious etiology is uncovered, whereas in the remaining 50% of cases, no microbial organisms are identified in the lungs of affected patients (7). In recent years, the judicious use of broad-spectrum antimicrobial prophylaxis has tipped the balance of pulmonary complications after SCT from infectious to noninfectious. In this context, two types of pulmonary dysfunction have been recognized: acute noninfectious lung injury (termed idiopathic pneumonia syndrome [IPS]) and subacute or chronic noninfectious lung injury. Two forms of subacute/chronic lung injury are common in patients over 100 d posttransplant: airflow obstruction and restrictive lung injury (8–16). Each form of noninfectious lung injury is associated with significant morbidity and mortality and, unfortunately, clinical responses to standard therapeutic approaches are limited. This chapter will be devoted to noninfectious lung injury occurring both early and late

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© Springer Science+Business Media New York 2004

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  • Kenneth R. Cooke

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