Use of intravenous immunoglobulin G to treat spontaneous heparin-induced thrombocytopenia.
Journal
Transfusion
ISSN: 1537-2995
Titre abrégé: Transfusion
Pays: United States
ID NLM: 0417360
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
01
10
2018
revised:
13
11
2018
accepted:
13
11
2018
pubmed:
18
12
2018
medline:
9
11
2019
entrez:
18
12
2018
Statut:
ppublish
Résumé
Spontaneous heparin-induced thrombocytopenia (HIT) is a rare but serious prothrombotic syndrome characterized by thrombosis, thrombocytopenia, and strong platelet-activating HIT antibodies in the absence of heparin exposure, and is frequently characterized by a suboptimal response to standard therapies. Here, we present the first report of intravenous immunoglobulin G (IVIG) use in a patient with spontaneous HIT. Patient information, including demographic, clinical, and laboratory results, were obtained from the electronic medical record. Laboratory testing was performed in the serotonin release assay, platelet factor 4 (PF4)-dependent P-selectin expression assay, and PF4/polyvinylsulfonate enzyme-linked immunosorbent assay to study the impact of IVIG on HIT antibody-mediated platelet activation. The patient was also genotyped for a polymorphism in the IgG receptor on platelets, FcγRIIa, at amino acid position 131. A 30-year-old man had a thrombotic stroke and thrombocytopenia and strong HIT serologies in the absence of proximate heparin use. Direct thrombin inhibitor therapy was not associated with a prompt response. Due to severity and extent of thrombosis and persistent thrombocytopenia, he was treated with high-dose IVIG. This treatment was associated with rapid and sustained normalization of platelet counts and a gradual improvement in thrombotic complications. Platelet activation induced by HIT antibodies in the PF4-dependent P-selectin expression assay (low PF4) was significantly lower after IVIG treatment, correlating well with platelet rise. Consistent with the severity of thrombosis, the patient was found to possess the 131HR polymorphism in FcγRIIa. These results suggest that IVIG may be a useful adjunctive therapy in spontaneous HIT.
Sections du résumé
BACKGROUND
Spontaneous heparin-induced thrombocytopenia (HIT) is a rare but serious prothrombotic syndrome characterized by thrombosis, thrombocytopenia, and strong platelet-activating HIT antibodies in the absence of heparin exposure, and is frequently characterized by a suboptimal response to standard therapies. Here, we present the first report of intravenous immunoglobulin G (IVIG) use in a patient with spontaneous HIT.
STUDY DESIGN AND METHODS
Patient information, including demographic, clinical, and laboratory results, were obtained from the electronic medical record. Laboratory testing was performed in the serotonin release assay, platelet factor 4 (PF4)-dependent P-selectin expression assay, and PF4/polyvinylsulfonate enzyme-linked immunosorbent assay to study the impact of IVIG on HIT antibody-mediated platelet activation. The patient was also genotyped for a polymorphism in the IgG receptor on platelets, FcγRIIa, at amino acid position 131.
RESULTS
A 30-year-old man had a thrombotic stroke and thrombocytopenia and strong HIT serologies in the absence of proximate heparin use. Direct thrombin inhibitor therapy was not associated with a prompt response. Due to severity and extent of thrombosis and persistent thrombocytopenia, he was treated with high-dose IVIG. This treatment was associated with rapid and sustained normalization of platelet counts and a gradual improvement in thrombotic complications. Platelet activation induced by HIT antibodies in the PF4-dependent P-selectin expression assay (low PF4) was significantly lower after IVIG treatment, correlating well with platelet rise. Consistent with the severity of thrombosis, the patient was found to possess the 131HR polymorphism in FcγRIIa.
CONCLUSION
These results suggest that IVIG may be a useful adjunctive therapy in spontaneous HIT.
Identifiants
pubmed: 30556588
doi: 10.1111/trf.15105
pmc: PMC6402961
mid: NIHMS1000037
doi:
Substances chimiques
Immunoglobulins, Intravenous
0
P-Selectin
0
Heparin
9005-49-6
Types de publication
Case Reports
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
931-934Subventions
Organisme : NHLBI NIH HHS
ID : K08 HL133479
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL013629
Pays : United States
Informations de copyright
© 2018 AABB.
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