ECTRIMS eLearning

Acute respiratory distress syndrome following treatment with alemtuzumab for relapsing multiple sclerosis
Author(s):
A. Pace
,
A. Pace
Affiliations:
F. Jackson
,
F. Jackson
Affiliations:
W. Lusher
,
W. Lusher
Affiliations:
T. Mihalova
,
T. Mihalova
Affiliations:
N. Sharaf
,
N. Sharaf
Affiliations:
D. Rog
,
D. Rog
Affiliations:
P. Talbot
P. Talbot
Affiliations:
ECTRIMS Learn. Pace A. 09/15/16; 146505; P665
Adrian Pace
Adrian Pace
Contributions
Abstract

Abstract: P665

Type: Poster

Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression

Background: Alemtuzumab is a highly effective treatment for relapsing remitting multiple sclerosis (RRMS) that induces lysis of lymphocytes and other cells expressing CD52. Despite the resultant transient lymphopaenia, serious opportunistic infections (OI) are not frequently encountered. We describe a case of severe acute respiratory distress syndrome in a pwMS shortly following alemtuzumab therapy.

Case report: A 54 year old woman received a 5-day course of alemtuzumab for RRMS, together with prophylactic acyclovir 400mg BD continued for 28 days after completion of treatment. She was diagnosed with RRMS in 2004 and had previously been on Betaferon, Copaxone and Avonex. Two months earlier she suffered a disabling relapse with left hemiparesis, spasticity and deteriorating mobility. Her last prior relapse had been 13 months earlier.

Five weeks following treatment she presented to hospital with dyspnoea, cough and haemoptysis. On examination she was pyrexial, tachypnoeic, hypotensive and tachycardic. Oxygen saturation dropped to 72% on minimal exertion. Auscultation revealed inspiratory crepitations in both lower lobes, arterial blood gases indicated Type 1 respiratory failure, and chest X-ray showed bibasilar reticulonodular shadowing. CTPA excluded pulmonary embolism but showed patchy consolidation and ground glass opacities throughout both lungs, without lymphadenopathy or pleural effusion

She was treated empirically with IV acyclovir, co-amoxiclav, clarithromycin and Primaquine, and was transferred to ICU for intubation and ventilation on the fourth day of admission. Broncho-alveolar washings confirmed the presence of Pneumocystis jirovecii (PJP) and blood PCR yielded a positive result for CMV (13008 IU/ml), both consistent with active infection. She gradually responded to treatment and was discharged after 25 days on viral and fungal prophylaxis. Despite her severe infection, she did not experience significant deterioration in neurological function.

Conclusions: Serious OI infrequently complicate treatment with alemtuzumab for RRMS, but the potential for morbidity is high. Clinicians administering alemtuzumab should carefully weigh the risks and benefits of alemtuzumab use and be vigilant to possible early infections. It is uncertain if the recommended duration and dose of acyclovir prophylaxis post-treatment is truly protective against Herpetic infections. Standard prescription of PJP prophylaxis following treatment should also be considered.

Disclosure:

Adrian Pace: nothing to disclose

Fran Jackson: nothing to disclose

William Lusher: nothing to disclose

Tatiana Mihalova: nothing to disclose

Nazar Sharaf: nothing to disclose

David Rog: nothing to disclose

Paul Talbot: nothing to disclose

Abstract: P665

Type: Poster

Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression

Background: Alemtuzumab is a highly effective treatment for relapsing remitting multiple sclerosis (RRMS) that induces lysis of lymphocytes and other cells expressing CD52. Despite the resultant transient lymphopaenia, serious opportunistic infections (OI) are not frequently encountered. We describe a case of severe acute respiratory distress syndrome in a pwMS shortly following alemtuzumab therapy.

Case report: A 54 year old woman received a 5-day course of alemtuzumab for RRMS, together with prophylactic acyclovir 400mg BD continued for 28 days after completion of treatment. She was diagnosed with RRMS in 2004 and had previously been on Betaferon, Copaxone and Avonex. Two months earlier she suffered a disabling relapse with left hemiparesis, spasticity and deteriorating mobility. Her last prior relapse had been 13 months earlier.

Five weeks following treatment she presented to hospital with dyspnoea, cough and haemoptysis. On examination she was pyrexial, tachypnoeic, hypotensive and tachycardic. Oxygen saturation dropped to 72% on minimal exertion. Auscultation revealed inspiratory crepitations in both lower lobes, arterial blood gases indicated Type 1 respiratory failure, and chest X-ray showed bibasilar reticulonodular shadowing. CTPA excluded pulmonary embolism but showed patchy consolidation and ground glass opacities throughout both lungs, without lymphadenopathy or pleural effusion

She was treated empirically with IV acyclovir, co-amoxiclav, clarithromycin and Primaquine, and was transferred to ICU for intubation and ventilation on the fourth day of admission. Broncho-alveolar washings confirmed the presence of Pneumocystis jirovecii (PJP) and blood PCR yielded a positive result for CMV (13008 IU/ml), both consistent with active infection. She gradually responded to treatment and was discharged after 25 days on viral and fungal prophylaxis. Despite her severe infection, she did not experience significant deterioration in neurological function.

Conclusions: Serious OI infrequently complicate treatment with alemtuzumab for RRMS, but the potential for morbidity is high. Clinicians administering alemtuzumab should carefully weigh the risks and benefits of alemtuzumab use and be vigilant to possible early infections. It is uncertain if the recommended duration and dose of acyclovir prophylaxis post-treatment is truly protective against Herpetic infections. Standard prescription of PJP prophylaxis following treatment should also be considered.

Disclosure:

Adrian Pace: nothing to disclose

Fran Jackson: nothing to disclose

William Lusher: nothing to disclose

Tatiana Mihalova: nothing to disclose

Nazar Sharaf: nothing to disclose

David Rog: nothing to disclose

Paul Talbot: nothing to disclose

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