ECTRIMS eLearning

Acute thrombocytopenia during alemtuzumab infusion in a patient with multiple sclerosis
Author(s):
C. Di Carmine
,
C. Di Carmine
Affiliations:
S. Sciamanna
,
S. Sciamanna
Affiliations:
P. Cerrone
,
P. Cerrone
Affiliations:
C. Carrocci
,
C. Carrocci
Affiliations:
C. Marini
,
C. Marini
Affiliations:
A. Carolei
,
A. Carolei
Affiliations:
R. Totaro
R. Totaro
Affiliations:
ECTRIMS Learn. di carmine c. 09/14/16; 145582; EP1487
caterina di carmine
caterina di carmine
Contributions
Abstract

Abstract: EP1487

Type: ePoster

Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression

Background and objective: Alemtuzumab, a humanized monoclonal antibody that targets the CD52 antigen on the surface of B and T lymphocytes, mediates rapid and prolonged lymphocytes depletion resetting lymphocytes population. Adverse events include potentially serious infections and autoimmune mediated conditions. We describe the case of a young woman who developed acute thrombocytopenia during alemtuzumab infusion.

Case presentation: We report the case of a 20-year-old Caucasian female diagnosed with multiple sclerosis starting second-line treatment with alemtuzumab, 12 mg intravenous infusion at the rate of 20ml/h for 5 consecutive days. As per protocol, alemtuzumab was preceded by the intravenous infusion of methylprednisolone 1g. On the second infusion day, a marked decrease of lymphocytes was observed as expected. Furthermore, blood count showed a decrease of platelets from 206 to 133 103/mmc (normal values, 140-4000 103/mmc). On third day, platelets count further decreased to 84 103/mmc. Liver function, anti-RNP antibodies, anti-Sm antibodies, anti-Jo1 antibodies, anti SCL-70 antibodies, antinuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA) and antibodies against platelets were unremarkable. We decided to suspend the third dose. On fourth day, the patient showed an increase of platelet count (118 103/mmc) and the third dose was infused. The day after, platelet count was stationary (113 103/mmc) and the fourth and five doses were infused. During the 6-month follow-up platelet count was within the normal range.

Conclusions: Thus far, this is the first report of transient thrombocytopenia during alemtuzumab infusion. Since typically thrombocytopenia related to alemtuzumab starts months later to infusion as immunomediated mechanism, possible contribution of corticosteroids and other medications cannot be ruled out. However, post-marketing surveillance is warranted to identify rare and potentially serious adverse event following alemtuzumab administration.

Disclosure:

Totaro R. received funding for travel or speaker honoraria from Almirall, Bayer, Biogen, Merck Serono, Novartis, Sanofi-Aventis, and TEVA.

Di Carmine C. nothing to disclose

Sciamanna S.nothing to disclose

Cerrone P. nothing to disclose

Carrocci C. nothing to disclose

Marini C. nothing to disclose

Carolei A. nothing to disclose

Abstract: EP1487

Type: ePoster

Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression

Background and objective: Alemtuzumab, a humanized monoclonal antibody that targets the CD52 antigen on the surface of B and T lymphocytes, mediates rapid and prolonged lymphocytes depletion resetting lymphocytes population. Adverse events include potentially serious infections and autoimmune mediated conditions. We describe the case of a young woman who developed acute thrombocytopenia during alemtuzumab infusion.

Case presentation: We report the case of a 20-year-old Caucasian female diagnosed with multiple sclerosis starting second-line treatment with alemtuzumab, 12 mg intravenous infusion at the rate of 20ml/h for 5 consecutive days. As per protocol, alemtuzumab was preceded by the intravenous infusion of methylprednisolone 1g. On the second infusion day, a marked decrease of lymphocytes was observed as expected. Furthermore, blood count showed a decrease of platelets from 206 to 133 103/mmc (normal values, 140-4000 103/mmc). On third day, platelets count further decreased to 84 103/mmc. Liver function, anti-RNP antibodies, anti-Sm antibodies, anti-Jo1 antibodies, anti SCL-70 antibodies, antinuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA) and antibodies against platelets were unremarkable. We decided to suspend the third dose. On fourth day, the patient showed an increase of platelet count (118 103/mmc) and the third dose was infused. The day after, platelet count was stationary (113 103/mmc) and the fourth and five doses were infused. During the 6-month follow-up platelet count was within the normal range.

Conclusions: Thus far, this is the first report of transient thrombocytopenia during alemtuzumab infusion. Since typically thrombocytopenia related to alemtuzumab starts months later to infusion as immunomediated mechanism, possible contribution of corticosteroids and other medications cannot be ruled out. However, post-marketing surveillance is warranted to identify rare and potentially serious adverse event following alemtuzumab administration.

Disclosure:

Totaro R. received funding for travel or speaker honoraria from Almirall, Bayer, Biogen, Merck Serono, Novartis, Sanofi-Aventis, and TEVA.

Di Carmine C. nothing to disclose

Sciamanna S.nothing to disclose

Cerrone P. nothing to disclose

Carrocci C. nothing to disclose

Marini C. nothing to disclose

Carolei A. nothing to disclose

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