LIVING WITH IT WORKING WITH IT TREATING IT
1.Introductiona.A 25 year old Canadian female presents to the ED with cough, hemoptysis, fatigue, and chest discomfort for five days. Chest x-ray showed a large left apical cavitary lesion and cultures were negative for tuberculosis. We explore further infectious and non-infectious causes of fibrocavitary lesions in an otherwise healthy young adult.2.Descriptiona.A 25 year old female cruise line performer presented with submassive hemoptysis, fatigue, and chest discomfort for five days. Her travel history is extensive over four continents over the past four years with visits to Arizona where her family has relocated. She has no significant past medical history and is on no medications. Her family history is significant for ankylosing spondylitis in her father. On exam, she is afebrile, hemodynamically stable and in no acute distress. CT of the thorax revealed a large (3.7x4.1 cm) thin walled pleural based cavity of the left upper lobe. Initial acid fast smears and rapid PCR for mycobacterium tuberculosis and avium were negative. HIV, hepatitis, ANA, and ANCA testing were negative. Bronchoscopy cultures were negative. Coccidioides and aspergillus antigen were negative, however her coccidiodies antibody titer returned positive. HLA-B27 was also positive.3.Discussiona.Fibrocavitary lesions in immunocompetent hosts are a cause of concern and can represent a diagnostic challenge. Our case emphasizes that despite a thorough history and evaluation, the etiology of the patient’s fibrocavitary lesion remains a diagnostic dilemma. It is unclear if her fibrocavitary lesion is related to ankylosing spondylitis or coccidiomycoses. Both etiologies are rare and our patient did not have classic clinical features of either disease. Her cocci antibody titer could represent immunity or active disease. Cavitary lesions can be asymptomatic and self-limiting or progress to chronic fibrocavitary disease. 95% of ankylosing spondylitis patients has HLA-B27 positivity. The association between AS and pulmonary disease was first described in the 1940s. In one review of 2100 patients with AS, less than 3% showed apical fibrocavitary lesions. Exact mechanism of cavitary formation is unknown, but speculated secondary to inflammation and impaired thoracic respiratory mechanics. Patients with fibrocavitary lesions are at increased risk of superinfection with mycobacteria or fungal pathogens. Our case emphasizes the need for a thorough clinical, environmental and occupational history in order to guide further evaluation and management.
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