Variable serotonin release assay pattern and specificity of PF4-specific antibodies in HIT, and clinical relevance.
Variable serotonin release assay pattern and specificity of PF4-specific antibodies in HIT, and clinical relevance.
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DOI：
10.1111/jth.15848
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发表时间：
2022-11
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肝素诱导的血小板减少症(HIT)的诊断需要功能分析，以证明血小板因子4(PF4)特异性抗体激活血小板，通常在检测治疗性肝素(H)浓度时(“经典”模式)。一些HIT样本也可以在没有肝素的情况下激活血小板(“非典型”模式)，但临床意义尚不清楚。我们的目的是评估血小板活化模式和PF4特异性抗体的某些特征是否与HIT的严重程度相关。本文分析了81例HIT患者的5-羟色胺释放试验(SRA)模式，并与其临床和生物学资料进行了比较，其中47例抗PF4/H免疫球蛋白G(Ig G)和抗Pf4-Ig G。抗Pf4/HIg G滴度在具有“非典型”SRA的患者中被检测到(光密度为2.52vs.1.94在具有“典型”模式的患者，p <； .001)。两组患者的血小板计数(PC)最低点和恢复时间相似，但SRA不典型的患者更容易发生血栓事件(69%对34%，P=10.037)。两组患者血清抗PF4抗体阳性率分别为38%和61%。与单纯抗PF4/H 患者相比，抗Pf4抗体阳性患者的PC最低值(35vs.53 G/Ig/Ig，p=0.006)和PC恢复时间(6vs.3 pg/Ig G，p=0.015)明显降低。抗PF4/H抗体滴度升高的非典型SRA模式似乎与HIT中血栓形成的风险增加有关。抗天然PF4的抗体可能导致更严重和更持久的血小板减少症，其检测可能有助于临床实践。
The diagnosis of heparin‐induced thrombocytopenia (HIT) requires functional assays to demonstrate that platelet factor 4 (PF4)‐specific antibodies activate platelets, typically when therapeutic heparin (H) concentrations are tested (“classical” pattern). Some HIT samples also activate platelets without heparin (“atypical” pattern), but with unclear clinical significance. We aimed to assess whether platelet activation pattern and some characteristics of PF4‐specific antibodies were associated with the severity of HIT. Serotonin release assay (SRA) pattern of 81 HIT patients were analyzed and compared with their clinical and biological data, including levels of anti‐PF4/H immunoglobulin G (IgG) and anti‐PF4 IgG in 47 of them. Higher anti‐PF4/H IgG titers were measured in patients with an “atypical” SRA (optical density 2.52 vs. 1.94 in those with a “classical” pattern, p < .001). Patients of both groups had similar platelet count (PC) nadir and time to recovery, but those with an “atypical” SRA more frequently developed thrombotic events (69% vs. 34%, p = .037). Significant levels of anti‐PF4 IgG were detected in both groups (38% and 61%, respectively). Whatever the SRA pattern, a lower PC nadir (35 vs. 53 G/L, p = .006) and a longer PC recovery time (6 vs. 3 days, p = .015) were evidenced in patients with anti‐PF4 antibodies, compared with those with anti‐PF4/H IgG only. An atypical SRA pattern with elevated anti‐PF4/H IgG titers seems associated with an increased risk of thrombosis in HIT. IgG antibodies to native PF4 may contribute to more severe and persistent thrombocytopenia, and their detection could be useful in clinical practice.
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