Successful treatment of vaccine-induced prothrombotic immune thrombocytopenia (VIPIT)

被引：82

作者：

Thaler, Johannes ^{[1
]}

Ay, Cihan ^{[1
]}

Gleixner, Karoline, V ^{[1
]}

Hauswirth, Alexander W. ^{[1
]}

Cacioppo, Filippo ^{[2
]}

Grafeneder, Jurgen ^{[2
]}

Quehenberger, Peter ^{[3
]}

Pabinger, Ingrid ^{[1
]}

Knoebl, Paul ^{[1
]}

机构：

[1] Med Univ Vienna, Dept Med 1, Div Hematol & Hemostaseol, Wahringer Gurtel 18-20, A-1090 Vienna, Austria

[2] Med Univ Vienna, Dept Emergency Med, Vienna, Austria

[3] Med Univ Vienna, Dept Lab Med, Vienna, Austria

来源：

JOURNAL OF THROMBOSIS AND HAEMOSTASIS | 2021年 / 19卷 / 07期

关键词：

COVID-19; ChAdOx1; vaccine; vaccine-induced prothrombotic immune thrombocytopenia; VIPIT; high-dose intravenous immunoglobulins; ANTIBODIES; MEDIATE;

D O I：

10.1111/jth.15346

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Cases of unusual thrombosis and thrombocytopenia after administration of the ChAdOx1 nCoV-19 vaccine (AstraZeneca) have been reported. The term vaccine-induced prothrombotic immune thrombocytopenia (VIPIT) was coined to reflect this new phenomenon. In vitro experiments with VIPIT patient sera indicated that high-dose intravenous immunoglobulins (IVIG) competitively inhibit the platelet-activating properties of ChAdOx1 nCoV-19 vaccine induced antibodies. Here, we report a case of a 62-year-old woman who had received this vaccine and developed VIPIT. She visited the emergency ward because of petechiae and hematomas. In the laboratory work-up, thrombocytopenia, low fibrinogen, elevated D-dimer, and positivity in the platelet factor 4/heparin-enzyme-immunoassay were present. Signs and symptoms of thrombosis were absent. Upon immediate therapy with non-heparin anticoagulation, high-dose IVIG, and prednisolone, laboratory parameters steadily improved and the patient was discharged from hospital without thrombotic complications. We conclude that early initiation of VIPIT treatment results in a swift response without thrombotic complications.

引用

页码：1819 / 1822

页数：4

共 10 条

[1] Polyphosphate/platelet factor 4 complexes can mediate heparin-independent platelet activation in heparin-induced thrombocytopenia [J].