Iatrogenic Lung Diseases

Abstract

Drug-induced interstitial lung diseases present with a variety of tissue reaction, most of them already discussed in previous chapters. A common presentation is diffuse alveolar damage as an acute reaction, often followed by organizing DAD, where hyaline membranes can still be recognized, and finally ending as organizing pneumonia and lung fibrosis. Other drugs induce NSIP-like tissue reactions. The major problem in interpreting drug reaction in the lung is our limited understanding of drug metabolism. Some drugs will induce toxic injury of endothelial cells, thus the blood barrier is leaking, and proteins can enter the interstitium and finally the alveolar lumen. Here these proteins will form complexes and by the action of respiration hyaline membranes will form. In addition the exudate from the capillaries will cause a transient edema and this is followed by hypoxia affecting the pneumocytes. This damage will contribute to DAD development (Fig. 14.1). Later on organizing pneumonia can result. Other drugs act on the immune system, forming immune complexes either because they are immunogenic by themselves or by complexing with endogenous proteins like a hapten. In these cases a NSIP or LIP pattern can result. In these cases scattered eosinophils are regularly found. Rarely granulomas are formed, usually pointing to an underlying immune mechanism. Since our understanding is so limited and no systematic experimental investigation has been performed, we still need to rely on databases, summarizing all described drug reactions in a systematic way (www.pneumotox.com; [1–8]).