Bleomycin-Induced Pneumonitis

Abstract

The cytotoxic agent bleomycin is feared for its induction of sometimes fatal pulmonary toxicity, also known as bleomycin-induced pneumonitis (BIP). The central event in the development of BIP is endothelial damage of the lung vasculature due to bleomycin-induced cytokines and free radicals. Ultimately, BIP can progress in lung fibrosis. The diagnosis is established by a combination of clinical symptoms, radiographic alterations, and pulmonary function test results, while other disorders resembling BIP have to be excluded. Pulmonary function assessments most suitable for detecting BIP are those reflecting lung volumes. The widely used transfer capacity of the lungs for carbon monoxide appeared recently not to be specific when bleomycin is used in a polychemotherapeutic regimen. There are no proven effective treatments for BIP in humans, although corticosteroids are widely applied. When patients survive BIP, they almost always recover completely with normalization of radiographic and pulmonary function abnormalities. This review focuses on BIP, especially on the pathogenesis, risk factors, and its detection.

The antioxidant effect of boric acid and CoQ10 on pulmonary fibrosis in bleomycin induced rats

“…Generation of the ROS in the lung tissue results in DNA injury, lipid peroxidation, alteration in lung prostaglandin synthesis and degradation, and an increase in lung collagen synthesis. As a result of the injury, inflammation and cytokine dysregulation occur after BLM administration, fibroblasts are activated, and collagen production is stimulated, while collagen degradation is inhibited (Sleijfer 2001). In addition, several studies have demonstrated that bleomycin administration in rats decreases the antioxidative capacity, while increasing oxidative stress in the lung tissue (Mata et al 2003).…”

Erythropoietin ameliorates chemotherapy‐induced fibrosis of the lungs in a preclinical murine model

“…3 Specifically, bleomycin is commonly associated with pulmonary toxicity and it is likely that the endothelium is the initial site of damage. 5 This chemotherapeutic drug is a DNA scission agent whose mechanism likely involves intercalation and the release of oxidants that cause damage to the DNA template during replication. This may initiate a cascade of inflammatory events culminating in macrophage infiltration and epithelial injury, characterized by the appearance of dysplastic alveolar epithelial cells.…”

Beyond Conventional Therapy: Role of Pulse Steroids in Bleomycin Induced Lung Injury

“…7 Though the exact mechanism by which bleomycin results in lung injury is unclear, free-radicalinduced oxidation is considered the primary mechanism. 8 The relative deficiency of the bleomycin-inactivating en- Fig. 1.…”