Home
|
Inbox
|
Search
|
View Abstract
Disseminated Aspergillosis After IL-5 Therapy for Severe Asthma
Description
.abstract img { width:300px !important; height:auto; display:block; text-align:center; margin-top:10px } .abstract { overflow-x:scroll } .abstract table { width:100%; display:block; border:hidden; border-collapse: collapse; margin-top:10px } .abstract td, th { border-top: 1px solid #ddd; padding: 4px 8px; } .abstract tbody tr:nth-child(even) td { background-color: #efefef; } .abstract a { overflow-wrap: break-word; word-wrap: break-word; }
A1262 - Disseminated Aspergillosis After IL-5 Therapy for Severe Asthma
Author Block: C. Wood, Y. Im, M. Millard; Baylor University Medical Center, Dallas, TX, United States.
A 67-year-old man with severe persistent asthma treated with high dose inhaled fluticasone propionate/salmeterol, tiotropium, and montelukast continued to suffer multiple steroid requiring asthma exacerbations. His past medical history included allergic bronchopulmonary aspergillosis (ABPA), fully treated Mycobacteria kansasii lung infection, grave’s disease, and hyperlipidemia. He was a never smoker. Previous treatment of his ABPA with 3 months of voriconazole was discontinued due to financial reasons. Prior to anti-interlukin-5 (IL-5) treatment, his serum eosinophil count varied between 370/microL and 590/microL. After two doses of an anti-IL-5 antibody, reslizumab, he presented with multiple 2-4 mm palpable subcutaneous tender and non-tender nodules on his anterior chest, abdomen, right arm, and back. Needle aspiration of a nodule produced purulent material which stained positive for fungus and subsequently grew aspergillus species. Voriconazole was restarted with resolution of his nodules over one month. Anti-IL-5 therapy was continued with improvement in asthma control. Eosinophils are key cellular players in modulating and maintaining airway inflammation in eosinophilic asthma. Reslizumab binds to and interferes with IL-5, reducing eosinophil production, recruitment, and survival. Reslizumab has been shown to reduce asthma exacerbations by 50%, improve asthma symptoms and FEV1 in patients with severe persistent asthma accompanied by serum eosinophil counts more then 400/microL. It is generally well tolerated; helminth infection has been reported as an adverse reaction. Neutralization of IL-5 also inhibits macrophages, T and B lymphocytes. Moreover, eosinophils participate in the inflammatory response to fungal infection in humans. Cytotoxic granule proteins from eosinophils directly bind to the cell wall of fungi and cause direct killing. Our case suggests that while suppressing eosinophil production and survival by anti-IL-5 therapy could improve Th2 driven inflammatory response in eosinophilic asthma, at the same time it could allow for aspergillus dissemination in patients who have history of ABPA. While ABPA is often associated with severe persistent asthma, the use of anti-IL-5 monoclonal antibodies should be undertaken with great caution in such patients.
Author Block: C. Wood, Y. Im, M. Millard; Baylor University Medical Center, Dallas, TX, United States.
A 67-year-old man with severe persistent asthma treated with high dose inhaled fluticasone propionate/salmeterol, tiotropium, and montelukast continued to suffer multiple steroid requiring asthma exacerbations. His past medical history included allergic bronchopulmonary aspergillosis (ABPA), fully treated Mycobacteria kansasii lung infection, grave’s disease, and hyperlipidemia. He was a never smoker. Previous treatment of his ABPA with 3 months of voriconazole was discontinued due to financial reasons. Prior to anti-interlukin-5 (IL-5) treatment, his serum eosinophil count varied between 370/microL and 590/microL. After two doses of an anti-IL-5 antibody, reslizumab, he presented with multiple 2-4 mm palpable subcutaneous tender and non-tender nodules on his anterior chest, abdomen, right arm, and back. Needle aspiration of a nodule produced purulent material which stained positive for fungus and subsequently grew aspergillus species. Voriconazole was restarted with resolution of his nodules over one month. Anti-IL-5 therapy was continued with improvement in asthma control. Eosinophils are key cellular players in modulating and maintaining airway inflammation in eosinophilic asthma. Reslizumab binds to and interferes with IL-5, reducing eosinophil production, recruitment, and survival. Reslizumab has been shown to reduce asthma exacerbations by 50%, improve asthma symptoms and FEV1 in patients with severe persistent asthma accompanied by serum eosinophil counts more then 400/microL. It is generally well tolerated; helminth infection has been reported as an adverse reaction. Neutralization of IL-5 also inhibits macrophages, T and B lymphocytes. Moreover, eosinophils participate in the inflammatory response to fungal infection in humans. Cytotoxic granule proteins from eosinophils directly bind to the cell wall of fungi and cause direct killing. Our case suggests that while suppressing eosinophil production and survival by anti-IL-5 therapy could improve Th2 driven inflammatory response in eosinophilic asthma, at the same time it could allow for aspergillus dissemination in patients who have history of ABPA. While ABPA is often associated with severe persistent asthma, the use of anti-IL-5 monoclonal antibodies should be undertaken with great caution in such patients.
|
Home
|
Inbox
|
Search
|