While a mainstay for inflammatory lung disease, corticosteroids are avoided in patients suspected of having infectious lung diseases. Steroid use in fungal lung diseases in particular is concerning for fear of suppressing the host immune response and promoting spread of the pathogen. However, there are case reports of clinical responses to corticosteroid therapy in critically ill patients with invasive fungal lung disease such as histoplasmosis and coccidioidomycosis1,2. We report a case of hypoxemia due to disseminated histoplasmosis, in a patient who was not critically ill, with a dramatic response to steroid therapy.
31-year-old white male with a history of Crohn’s disease, receiving routine infliximab infusions, presents with four weeks of fever, non-productive cough, dyspnea, and abdominal pain. He also reported fatigue and night sweats. He was seen by his primary care physician and started on a seven day course of levofloxacin. His symptoms significantly worsened over two weeks prior to presentation including a 20 pound weight loss, increased dyspnea and development of jaundice. Physical exam: Temperature of 104.6 degrees Fahrenheit, heart rate 96 beats per minute and blood pressure 110/76, SpO2 86% on room air. Lung exam demonstrated bilateral rales, right greater than left, with significant egophony throughout his right lung base. His abdomen was tender to palpation and the liver was palpable approximately 3 cm below his right costal margin. Skin exam revealed jaundice. Laboratory evaluation revealed white blood cell count 4.1, hemoglobin 12.1, platelet count 145, total bilirubin 3.6, direct bilirubin 2.2, alkaline phosphatase 1006, ALT 116, AST 207. Arterial blood gas showed a PaO2 of 54 on two liters of oxygen. Histoplasmosis urinary antigen was strongly positive. PPD was negative. Chest radiograph and CT scan of chest showed bilateral alveolar infiltrates, right greater than left. Bronchoalveolar lavage analysis revealed a profound lymphocytosis (61%) with a lymphocyte helper/suppressor ratio of 0.5. Blood cultures revealed moderate growth of filamentous fungus consistent with Histoplasmosis Capsulatum. Treatment with liposomal amphotericin B was begun. After 4 days of therapy there was minimal improvement in his oxygenation. Prednisone 40 mg once a day was begun and within 24-36 hours his hypoxemia resolved with a SpO2 of 95% on room air, and his liver dysfunction and pancytopenia continued to normalize.
Few patients with acute disseminated pulmonary histoplasmosis with hypoxemia have been prescribed corticosteroids, and all other known reported cases were patients with ARDS.1,3 Experiments have shown that exposure of lymphocytes and alveolar macrophages to H. capsulatum results in T cell proliferation and secretion of pro-inflammatory cytokines which further amplify the inflammatory response. We hypothesize that steroid therapy improved our patient’s hypoxemia by retarding the pulmonary inflammatory response to the histoplasmosis organism in the lung. Steroids have been demonstrated to limit chemotaxis and phagocytosis in pulmonary inflammatory cells, as well as reduce the complement-mediated neutrophil activation and reduce surfactant degradation.
This case demonstrates a dramatic clinical response to corticosteroid therapy in a patient with moderate hypoxemia and disseminated histoplasmosis. While steroids should be used with caution in fungal infections, this case suggests a possible beneficial role of steroids in the treatment of disseminated histoplasmosis with significant lung involvement, particularly in patients with hypoxemia.
J.P. Parsons, None.