Introduction Fibrotic hypersensitivity pneumonitis (HP) represents a more extensive subset of chronic HP that is associated with high morbidity and mortality. The most common causes of HP include exposure to avian antigen, microbial products and chemical compounds in the environment. In our case report, a male patient with colorectal cancer, who received 11 course of chemotherapy with 5-fluorouracil, leucovorin and oxaliplatin (FOLFOX), was diagnosed as having fibrotic HP. Generally, the major side effects of oxaliplatin include gastrointestinal, hematologic and neurologic toxicities. However, there has been little literature on oxaliplatin-induced interstitial lung disease, specifically fibrotic HP.
Case Report A 58-year-old non-smoking male computer engineer presented with a two-week history of dyspnea. Six months before, he underwent surgical resection for colorectal adenocarcinoma with stage T3N2M0. Subsequently, he received 11 cycles of FOLFOX chemotherapy with bi-weekly leucovorin (400 mg/m2), 5-fluorouracil (2400 mg/m2) and oxaliplatin (85 mg/m2). During treatment, no complaints were noticed and he didn’t receive any follow-up chest radiographs. Unfortunately, the 12th cycle of chemotherapy was postponed due to dyspnea. Chest radiograph and computed tomography demonstrated reticulation, traction bronchiectasis and volume loss in upper lobes and perihilar regions (Fig. 1), which were suggestive of fibrotic HP. The serological markers of autoimmune disease were all negative. Transbronchial lung biopsy via the flexible bronchoscope revealed chronic inflammation with increased lymphocytic infiltration and no microorganisms (e.g. bacteria, mycobacteria, fungi, viruses, Pneumocystis jiroveci polymerase chain reaction and aspergillus galactomannan antigen) were detected by bronchoalveolar lavage. With the suspicion of oxaliplatin-induced fibrotic HP, we discontinued FOLFOX chemotherapy and intravenous methylprednisolone (20 mg every 8 hours) was administered. With his symptoms and radiological abnormalities improved after treatment, he was discharged on the 20th admission day.
Discussion Not all patients with HP manifest progressive lung fibrosis and the mechanisms of increased susceptibility of fibrosis are not well-defined. Based on exposure history, radiological and histopathological features, the diagnosis of fibrotic HP is quite challenging, especially when the balance between obtaining adequate tissue and reducing procedural risk is considered. In the meantime, with the development of novel anti-fibrotic therapy for idiopathic pulmonary fibrosis, it is important that preventable fibrotic lung disease-such as fibrotic HP-be well recognized. In our case, no other risk factor causing lung fibrosis is found and the diagnosis is based on exposure history and compatible radiological features. As a possible offending agent, fibrotic HP should be considered in patients receiving oxaliplatin and regular follow-up chest radiography is warranted.
Full conference title:
- ATS 2018