scholarly journals N‐glycan profiling alterations of serum and immunoglobulin G in immune thrombocytopenia

Author(s):  
Wei Wang ◽  
Xuewen Xu ◽  
Chenjun Huang ◽  
Chunfang Gao

2020 ◽  
pp. 1-6
Author(s):  
Masuho Saburi ◽  
Masao Ogata ◽  
Yasuhiro Soga ◽  
Takako Satou ◽  
Kazuhito Itani ◽  
...  

<b><i>Objective:</i></b> Platelet-associated immunoglobulin G (PA-IgG) refers to IgG attached to the surface of platelets, while the immature platelet fraction (IPF) reflects the state of platelet production in bone marrow. Since PA-IgG and IPF are increased in patients with immune thrombocytopenia (ITP), reflecting amounts of platelet antibodies and compensatory platelet production, respectively, we hypothesized that these laboratory findings may provide useful markers for predicting treatment response in patients with ITP. We therefore retrospectively investigated associations between levels of these markers at diagnosis and response to first-line therapy in patients with ITP. <b><i>Methods:</i></b> Forty-three patients diagnosed with ITP at Oita Kouseiren Tsurumi Hospital between May 2010 and November 2018 were included. Patients were divided into 2 groups based on response to corticosteroid as first-line therapy. Laboratory findings were compared between responders and nonresponders. <b><i>Results:</i></b> Median PA-IgG was 285 ng/10<sup>7</sup> cells (range, 45.5–18,200 ng/10<sup>7</sup> cells), and median IPF was 15.5% (range, 5.4–62.1%). Median levels were higher than the respective upper limits of normal range (PA-IgG, 0–46 ng/10<sup>7</sup> cells; IPF, 1.1–9.5%). First-line therapy was performed using standard-dose prednisolone (0.5–1.0 mg/kg/day) in 32 patients and high-dose dexamethasone (40 mg/day, 4 days) or methylprednisolone (125–1,000 mg/day, 3–4 days) in 11 patients. Twenty-four patients (55.8%) responded to first-line therapy. In univariate analysis, type of corticosteroid (<i>p</i> = 0.17) tended to differ between groups but did not differ significantly, and no difference in IPF level was apparent between responders (15.35%; range, 5.4–41.5%) and nonresponders (16.7%; range, 6.3–62.1%; <i>p</i> = 0.15). PA-IgG was significantly higher among nonresponders (430 ng/10<sup>7</sup> cells; range, 101–18,200 ng/10<sup>7</sup> cells) than among responders (254.5 ng/10<sup>7</sup> cells; range, 45.5–470 ng/10<sup>7</sup> cells; <i>p</i> = 0.004). Multivariate analysis revealed PA-IgG was independently associated with response to first-line therapy (odds ratio, 1.000; 95% confidence interval, 1.000–1.010; <i>p</i> = 0.029). <b><i>Conclusion:</i></b> Our data suggested that PA-IgG at diagnosis could offer a useful predictor of response to first-line corticosteroid therapy for ITP.



Blood ◽  
2010 ◽  
Vol 116 (18) ◽  
pp. 3660-3668 ◽  
Author(s):  
Pingguo Chen ◽  
Conglei Li ◽  
Sean Lang ◽  
Guangheng Zhu ◽  
Adili Reheman ◽  
...  

Abstract Fetal and neonatal immune thrombocytopenia (FNIT) is a severe bleeding disorder in which maternal antibodies cross the placenta and destroy fetal/neonatal platelets. It has been demonstrated that the neonatal Fc receptor (FcRn) regulates immunoglobulin G (IgG) homeostasis and plays an important role in transplacental IgG transport. However, the role of FcRn in the pathogenesis and therapy of FNIT has not been studied. Here, we developed an animal model of FNIT using combined β3 integrin–deficient and FcRn-deficient (β3−/−FcRn−/−) mice. We found that β3−/−FcRn−/− mice are immunoresponsive to β3+/+FcRn−/− platelets. The generated antibodies were β3 integrin specific and were maintained at levels that efficiently induced thrombocytopenia in adult β3+/+FcRn−/− mice. FNIT was observed when immunized β3−/−FcRn+/+ females were bred with β3+/+FcRn+/+ males, while no FNIT occurred in β3−/−FcRn−/− females bred with β3+/+FcRn−/− males, suggesting that FcRn is indispensable for the induction of FNIT. We further demonstrated that fetal FcRn was responsible for the transplacental transport of various IgG isotypes. We found that anti-FcRn antibody and intravenous IgG prevented FNIT, and that intravenous IgG ameliorated FNIT through both FcRn-dependent and -independent pathways. Our data suggest that targeting FcRn may be a potential therapy for human FNIT as well as other maternal pathogenic antibody-mediated diseases.



2011 ◽  
Vol 29 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Kristel Kodar ◽  
Johannes Stadlmann ◽  
Kersti Klaamas ◽  
Boris Sergeyev ◽  
Oleg Kurtenkov


PLoS ONE ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. e21246 ◽  
Author(s):  
Theresa Guhr ◽  
Judith Bloem ◽  
Ninotska I. L. Derksen ◽  
Manfred Wuhrer ◽  
Anky H. L. Koenderman ◽  
...  




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