In 2018, dupilumab became the first fully human monoclonal antibody targeting both IL-4 and IL-13 cytokines which initiate type 2 helper T-cell inflammatory pathways behind eosinophilic and allergic diseases. The beneficial effects of dupilumab for treating atopic dermatitis and refractory asthma have been well recognized (1,2), but it has also been associated with adverse events such as transient eosinophilia in clinical trials (3,4) as well as in case studies (5,6,7). CASE PRESENTATION:We describe the case of a 41-year-old Caucasian male with a history of food allergies, atopic dermatitis and allergic rhinitis who developed eosinophilic granulomatosis with polyangiitis (EGPA) after the administration of dupilumab. Remote clinical history included nasal polyposis, treated with functional endoscopic sinus surgery. Given persistent symptoms of asthma and intolerance to treatment with high dose corticosteroids, he started add-on dupilumab every 2 weeks. His baseline absolute eosinophil count (AEC) was normal at 10 cells/mm3 at the start of therapy. However, within 3 months of treatment, he developed symptoms of chest pain with deep breathing, continued shortness of breath, and numbness in his hands and feet. Six months after starting dupilumab, the AEC rose to 1250 cells/mm3. An extensive workup including FISH sequencing for FIP1L1-PDGFRA, flow cytometry, vitamin B12, and antibodies to Strongyloides stercoralis was negative. CT chest demonstrated ground glass opacities in the left upper lobe that resolved with steroids. With the new onset eosinophilia, polyneuropathy and transient pulmonary opacities, he met the 1990 ACR criteria for and was diagnosed anti-neutrophil cytoplasmic antibody (ANCA) negative eosinophilic granulomatosis with polyangiitis (EGPA). Dupilumab was discontinued and he began treatment with an anti-IL-5 monoclonal antibody, mepolizumab, with improvement of his AEC to 0.3 cells/mm3. Respiratory and neurological symptoms improved.
Malignant central airway obstruction (MCAO) is a debilitating and life-limiting complication that occurs in an unfortunately large number of individuals with advanced intrathoracic cancer. Although the management of MCAO is multimodal and interdisciplinary, the task of providing patients with prompt palliation falls increasingly on the shoulders of interventional pulmonologists. While a variety of tools and techniques are available for the management of malignant obstructive lesions, advancements and evolution in this therapeutic venue have been somewhat sluggish and limited when compared with other branches of interventional pulmonary medicine (e.g., the early diagnosis of peripheral lung nodules). Indeed, one pragmatic, albeit somewhat uncharitable, reading of this article's title might suggest a wry smile and shug of the shoulders as to imply that relatively little has changed in recent years. That said, the spectrum of interventions for MCAO continues to expand, even if at a less impressive clip. Herein, we present on MCAO and its endoscopic and nonendoscopic management-that which is old, that which is new, and that which is still on the horizon.
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