Contributions
Abstract: EP1741
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Introduction: The Food and Drug Administration recommends prophylaxis against pneumocystis jirovecii pneumonia (PJP) for patients on alemtuzumab for B cell lymphoma, but not for patients on alemtuzumab for multiple sclerosis (MS). We present a case of suspected PJP secondary to alemtuzumab immunosuppression in a patient with MS.
Case report: A 37-year-old male with a history of MS presented to the emergency room 10/8/2016 with new symptoms of fever, weakness, blurry vision, and shortness of breath. The patient's immunotherapy for MS had recently been switched from natalizumab to alemtuzumab. He received his first alemtuzumab infusion 41 days prior to the onset of these new symptoms. There was a five week washout period between alemtuzumab and his last dose of natalizumab.
Initial infectious workup revealed no abnormalities. There was no leukocytosis, blood cultures showed no growth, and all initial standard viral assays were negative. Spinal fluid studies were within normal limits. Chest X-ray was unremarkable, and magnetic resonance imaging brain revealed no new lesions. The patient was admitted, improved with supportive care, and was discharged with a proposed diagnosis of upper respiratory tract infection 10/12/2016. The patient returned to the emergency department on 10/18/2016 with symptoms of fever, shortness of breath, and non-productive cough. He was found to have exertional hypoxia to the 70's and was re-admitted. Lactate dehydrogenase was elevated to 345 U/L, and CD4 was found to be 36 cells/microliter.
Streptococcal culture, respiratory viral panel, and sputum culture were within normal limits. Computed tomography chest revealed bilateral ground glass opacities. Bronchoscopy was unremarkable. (1→3)-β-D-glucan assay was >500 pg/ml, however gomori methenamine silver stain (GMS) was negative. PJP polymerase chain reaction was not sent. Empiric trimethoprim/sulfamethoxazole (TMP-SMX) and oral corticosteroids were started, and the patient quickly improved. He was discharged on TMP-SMX and was seen as outpatient in both infectious disease and neurology clinic where he was observed to do very well.
Conclusion: While GMS was negative in this patient, the clinical picture, elevated (1→3)-β-D-glucan assay, low CD4 count, and improvement with TMP-SMX raise suspicion that this was a case of PJP secondary to alemtuzumab immunosuppression. This case supports the possible need for TMP-SMX prophylaxis in MS patients taking alemtuzumab.
Disclosure: Elizabeth D Verter: Nothing to disclose
Bridget Bagert, MD: Nothing to disclose
Jonathan Hand, MD: Nothing to disclose
Abstract: EP1741
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Introduction: The Food and Drug Administration recommends prophylaxis against pneumocystis jirovecii pneumonia (PJP) for patients on alemtuzumab for B cell lymphoma, but not for patients on alemtuzumab for multiple sclerosis (MS). We present a case of suspected PJP secondary to alemtuzumab immunosuppression in a patient with MS.
Case report: A 37-year-old male with a history of MS presented to the emergency room 10/8/2016 with new symptoms of fever, weakness, blurry vision, and shortness of breath. The patient's immunotherapy for MS had recently been switched from natalizumab to alemtuzumab. He received his first alemtuzumab infusion 41 days prior to the onset of these new symptoms. There was a five week washout period between alemtuzumab and his last dose of natalizumab.
Initial infectious workup revealed no abnormalities. There was no leukocytosis, blood cultures showed no growth, and all initial standard viral assays were negative. Spinal fluid studies were within normal limits. Chest X-ray was unremarkable, and magnetic resonance imaging brain revealed no new lesions. The patient was admitted, improved with supportive care, and was discharged with a proposed diagnosis of upper respiratory tract infection 10/12/2016. The patient returned to the emergency department on 10/18/2016 with symptoms of fever, shortness of breath, and non-productive cough. He was found to have exertional hypoxia to the 70's and was re-admitted. Lactate dehydrogenase was elevated to 345 U/L, and CD4 was found to be 36 cells/microliter.
Streptococcal culture, respiratory viral panel, and sputum culture were within normal limits. Computed tomography chest revealed bilateral ground glass opacities. Bronchoscopy was unremarkable. (1→3)-β-D-glucan assay was >500 pg/ml, however gomori methenamine silver stain (GMS) was negative. PJP polymerase chain reaction was not sent. Empiric trimethoprim/sulfamethoxazole (TMP-SMX) and oral corticosteroids were started, and the patient quickly improved. He was discharged on TMP-SMX and was seen as outpatient in both infectious disease and neurology clinic where he was observed to do very well.
Conclusion: While GMS was negative in this patient, the clinical picture, elevated (1→3)-β-D-glucan assay, low CD4 count, and improvement with TMP-SMX raise suspicion that this was a case of PJP secondary to alemtuzumab immunosuppression. This case supports the possible need for TMP-SMX prophylaxis in MS patients taking alemtuzumab.
Disclosure: Elizabeth D Verter: Nothing to disclose
Bridget Bagert, MD: Nothing to disclose
Jonathan Hand, MD: Nothing to disclose