COVID-19與免疫性血小板減少症的關聯性

Transfusion

. 2021 Jul;61(7):2014-2018. doi: 10.1111/trf.16368. Epub 2021 Mar 16.

Outcomes and management of immune thrombocytopenia secondary to COVID-19: Cleveland clinic experience

Tariq Kewan 1, Tarini N Gunaratne 1, Komal Mushtaq 1, Dina Alayan 1, Hamed Daw 2, Abdo Haddad 2

Affiliations expand

• PMID: 33724474

•  PMCID: PMC8250532

•  DOI: 10.1111/trf.16368

Free PMC article

Abstract

Background: Immune thrombocytopenia (ITP) is an acquired disease characterized by thrombocytopenia secondary to autoantibodies against platelets. Here, we report the clinical characteristics of coronavirus disease 2019 (COVID-19)-induced ITP cases.

Study design and methods: We retrospectively reviewed 3255 COVID-19 patients. COVID-19-induced ITP was diagnosed after excluding possible common causes. Bleeding severity was assessed based on the modified World Health Organization (WHO) bleeding severity score.

Results: We identified 11 (0.34%) patients with COVID-19-induced ITP. Of all patients, 63.6% were males and the median age was 63 years. The median time from COVID-19 diagnosis to the onset of ITP was 10 days. Bleeding observed in 63.6% of the patients. Clinically significant bleeding (WHO Grade 3) occurred in single patient who required blood transfusion. Standard treatment with glucocorticoids and intravenous immunoglobulin (IVIG) was effective in achieving excellent response in most cases. Of all patients, complete response and response to treatment were achieved in 45.5% and 27.3% patients, respectively. The median time to ITP recovery was 4 days. Eltrombopag was used in three patients who relapsed. Four patients required mechanical ventilation, and none of them survived secondary to hypoxic respiratory failure.

Conclusion: ITP secondary to COVID-19 usually presents after the first week of symptoms beginning. Most of our patients had WHO Grade 1-2 bleeding scores. Standard treatment with glucocorticoids and IVIG is effective in achieving an excellent response. The safety of eltrombopag is not very well established in COVID-19 patients, and additional studies are needed for a better safety profile.

Keywords: immune thrombocytopenia; intravenous immunoglobulin.

© 2021 AABB.

EJHaem

. 2023 Oct 5;4(4):1148-1151. doi: 10.1002/jha2.811. eCollection 2023 Nov.

Infant case of severe immune thrombocytopenia caused by COVID-19 infection

Tatsuya Anzai 1 2, Naomi Nakashima 2, Hiroyuki Betsui 1, Yuta Kawahara 1, Yuriko Hayashi 3, Hirokazu Kimura 3, Akira Shimada 1

Affiliations expand

• PMID: 38024599

•  PMCID: PMC10660122

•  DOI: 10.1002/jha2.811

Free PMC article

Abstract

Immune thrombocytopenia (ITP) is a common childhood acute autoimmune bleeding disorder caused by numerous viruses and characterized by isolated thrombocytopenia. Although cases of ITP caused by coronavirus disease 2019 (COVID-19) infection have been reported in adults, pediatric reports are limited. We present the case of a 1-year-old girl who developed COVID-19-infection-related ITP with a very low platelet count (0.0 × 104/μL). We searched for COVID-19-related pediatric ITP cases and found 10 other cases, with the majority having platelet counts of <1.0 × 104/μL. Although pediatric ITP cases caused by COVID-19 infection may be severe, further studies are needed.

Keywords: child; coronavirus disease 2019 (COVID‐19); immune thrombocytopenia (ITP).

© 2023 The Authors. eJHaem published by British Society for Haematology and John Wiley & Sons Ltd.

PubMed Disclaimer

J Thromb Haemost

. 2021 Feb;19(2):370-379. doi: 10.1111/jth.15176. Epub 2021 Jan 3.

Plasma levels of S100A8/A9, histone/DNA complexes, and cell-free DNA predict adverse outcomes of immune thrombotic thrombocytopenic purpura

Jingrui Sui 1, Ruinan Lu 1 2, Konstantine Halkidis 1 3, Nicole K Kocher 1, Wenjing Cao 1 2, Marisa B Marques 1, X Long Zheng 1 2

Affiliations expand

• PMID: 33188723

•  PMCID: PMC8058879

•  DOI: 10.1111/jth.15176

Free PMC article

Abstract

Background: Immune thrombotic thrombocytopenic purpura (iTTP) is a life-threatening blood disorder, primarily resulting from autoantibodies against ADAMTS13. Infection or inflammation often precedes acute iTTP. However, the association of inflammation and inflammatory mediators with disease severity and outcome of acute iTTP is not fully assessed.

Objectives: Here, we determined plasma levels of S100A8/A9, histone/DNA complexes, citrullinated histone H3 (CitH3), and cell-free DNA (cfDNA) in a cohort of 108 acute episodes from 94 unique iTTP patients and healthy controls, and assessed the association of each of these biomarkers with the disease severity and mortality.

Results: All acute iTTP patients had significantly increased plasma levels of S100A8/A9 (median 84.8, interquartile range [IQR] 31.2-157.4 µg/mL), histone/DNA complexes (median 55.7, IQR 35.8-130.8 U/mL), CitH3 (median 3.8, IQR 2.2-6.4 ng/mL), and cfDNA (median 937.7, IQR 781.3-1420.0 ng/mL) on the admission blood samples when compared with healthy controls. An increased plasma level of S100A8/A9, histone/DNA complex and cfDNA was associated with organ damage, coagulopathy, and mortality in iTTP. After being adjusted for age and history of hypertension, Cox proportional hazard regression analysis demonstrated that a hazard ratio (95% confidence interval) for an elevated plasma level of S100A8/A9, histone/DNA complexes, and cfDNA was 11.5 (1.4-90.9) (P = .021), 10.3 (2.7-38.5) (P = .001), and 12.8 (3.9-42.0) (P = .014), respectively.

Conclusion: These results indicate that inflammation or plasma inflammatory mediators such as S100A8/A9 or NETosis markers such as histone/DNA complexes and cfDNA may play a role in pathogenesis of iTTP, which may help stratify patients with a high risk of death during acute iTTP episodes.