Introduction: 

Drug-induced interstitial lung disease (DI-ILD) encompasses a broad spectrum of adverse effects secondary to multiple drugs, including chemotherapeutic agents. It is characterised by non-specific clinical, radiological, and histological manifestations, secondary to inflammation and/or fibrosis of the pulmonary parenchyma [1]. Its diagnosis presents a considerable challenge, as the patterns of clinical, radiological, and histopathological presentation can vary significantly from one drug to another, and even among patients on the same drug [2]. 

The incidence of DI-ILD is increasing due to the growing use of novel therapeutic agents, including checkpoint inhibitors and molecular-targeted agents [3]. Numerous drugs have been associated with the development of DI-ILD; however, others have only occasionally been linked to such alterations, and new agents potentially causing interstitial disease continue to be identified. The website www.pneumotox.com can be very useful as it provides an international database for consulting various patterns and drugs.

Aetiopathogenesis:

The exact lesion mechanism is not fully understood; it is multifactorial and depends on the causative agent. Several hypotheses have been proposed, including cytotoxic damage to the endothelial cells of the alveolar capillaries, immune-mediated reactions, oxidative stress, and others [1,4].

Clinical presentation: 

The clinical presentation patterns are broad and can range from mild involvement with symptoms such as dyspnoea, cough, or wheezing to severe manifestations that pose a life-threatening risk to the patient, such as adult respiratory distress syndrome [4,5]. 

An acute presentation may occur with pneumonitis, where the clinical spectrum includes symptoms like fever, dyspnoea, and sometimes peripheral blood eosinophilia, or even alveolar haemorrhage. In cases of a more insidious clinical presentation, the predominant symptoms are typically dyspnoea and reduced functional capacity, with dry crackles on auscultation [3,4]. 

Diagnosis is one of exclusion, with high-resolution CT (HRCT) playing a fundamental role. Establishing a temporal relationship with the administration of the causative agent is crucial. Generally, the onset of these alterations is related to the initiation of a new medication, although they can develop from days to even years after the start of treatment. Clinical context correlation is also essential to determine whether the pulmonary involvement could be due to other causes such as infection, haemorrhage, carcinomatous lymphangitis, or cardiogenic pulmonary oedema. 

Bronchoscopy also plays an important role in the diagnosis of patients with suspected DI-ILD, especially in ruling out alternative diagnoses, such as infectious origin or malignancy [3,4]. 

The treatment for pulmonary toxicity involves discontinuation of the causative drug and administration of corticosteroids.