INTRAVENOUS, BUT NOT ORAL, STEROID REQUIRED TO CONTROL EOSINOPHILIA IN HYPEREOSINOPHILIC SYNDROME

Abstract

Introduction Hypereosinophilic syndrome (HES) is a condition resulting in peripheral eosinophilia (>1500 cells/μL) with end organ damage. Flares of this disease can be controlled with corticosteroids, although alternate agents are typically used for baseline control. Case Description A 59-year-old woman with HES with pulmonary involvement, presented to the emergency department with hemoptysis, dyspnea, and fever. The patient had been tapering her prednisone dose of 60mg daily and was also taking hydroxyurea 500mg BID. Upon presentation, her eosinophil count was 1670 cells/μL. CT revealed diffuse groundglass opacities throughout the lungs. Bronchoalveolar lavage (BAL) revealed 55% eosinophils. Methylprednisolone 80mg IV every 8 hours was administered for 4 days. The patient clinically improved and her eosinophil count dropped to 370 cells/μL. Alternate steroids were attempted with the goal of switching to an oral route for taper and discharge. Intramuscular triamcinolone, intravenous dexamethasone and oral prednisone were attempted. The patient failed all therapies with rising eosinophilia to peak of 6320 cells/μL. She was administered mepolizumab 300mg subcutaneously for long-term control of eosinophilia and to facilitate tapering of methylprednisolone. She was discharged with a peripherally inserted central catheter for a 4 week taper. Her eosinophil count has since remained zero while on mepolizumab. Discussion This case illustrates a scenario where outpatient therapy with intravenous methylprednisolone was needed to treat eosinophilic lung involvement in HES. Use of intravenous methylprednisolone therapy may be considered as bridge to steroid sparing therapies. Treatment with mepolizumab is very effective for treatment of HES and can spare patients of long-term corticosteroid therapy and associated side effects. Hypereosinophilic syndrome (HES) is a condition resulting in peripheral eosinophilia (>1500 cells/μL) with end organ damage. Flares of this disease can be controlled with corticosteroids, although alternate agents are typically used for baseline control. A 59-year-old woman with HES with pulmonary involvement, presented to the emergency department with hemoptysis, dyspnea, and fever. The patient had been tapering her prednisone dose of 60mg daily and was also taking hydroxyurea 500mg BID. Upon presentation, her eosinophil count was 1670 cells/μL. CT revealed diffuse groundglass opacities throughout the lungs. Bronchoalveolar lavage (BAL) revealed 55% eosinophils. Methylprednisolone 80mg IV every 8 hours was administered for 4 days. The patient clinically improved and her eosinophil count dropped to 370 cells/μL. Alternate steroids were attempted with the goal of switching to an oral route for taper and discharge. Intramuscular triamcinolone, intravenous dexamethasone and oral prednisone were attempted. The patient failed all therapies with rising eosinophilia to peak of 6320 cells/μL. She was administered mepolizumab 300mg subcutaneously for long-term control of eosinophilia and to facilitate tapering of methylprednisolone. She was discharged with a peripherally inserted central catheter for a 4 week taper. Her eosinophil count has since remained zero while on mepolizumab. This case illustrates a scenario where outpatient therapy with intravenous methylprednisolone was needed to treat eosinophilic lung involvement in HES. Use of intravenous methylprednisolone therapy may be considered as bridge to steroid sparing therapies. Treatment with mepolizumab is very effective for treatment of HES and can spare patients of long-term corticosteroid therapy and associated side effects.