Key result
ADP-induced platelet hypoaggregation is linked to ~21% higher cumulative SOFA scores in septic shock.
Why the study?
Platelet hypoaggregation is recognized in septic shock, but its temporal dynamics and association with organ failure remain poorly understood.
Does ADP-induced platelet hypoaggregation predict progressive organ failure in adult patients with septic shock?
Cohort (n=156)
No
Does ADP-induced platelet hypoaggregation predict progressive organ failure in adult patients with septic shock?
ADP-induced platelet hypoaggregation is independently associated with progressive organ failure and increased mortality in septic shock, particularly in patients with fibrinogen < 2.5 g/L.
Answers are grounded in this paper and cite their sources.
May warrant intensified monitoring in septic shock with ADP hypoaggregation; hypothesis-generating for causality and therapeutic targeting.
Platelet hypoaggregation is increasingly recognized in septic shock; however, its temporal dynamics and association with organ failure remains poorly understood. This study aimed to investigate whether adenosine diphosphate (ADP)-induced platelet hypoaggregation is independently associated with cumulative organ dysfunction in patients with septic shock. In this propensity score-matched retrospective cohort study conducted from 2018 to 2023, 156 patients with septic shock (78 with hyporeactive platelets [ADP-AUC < 30 AU·min] and 78 with normoreactive platelets) were selected from an initial cohort of 264 patients using 1:1 matching. Serial platelet reactivity tests were performed on Days 1, 3, and 5. The primary outcome was the 7-day cumulative SOFA score (excluding the coagulation component). Secondary outcomes included the incidence of acute kidney injury (AKI), duration of mechanical ventilation, and 28-day mortality. Patients in the hyporeactive group exhibited a progressive decline in ADP-induced aggregation (Day 1: 26.5 vs. Day 5: 16.2 AU·min, P < 0.001), whereas platelet reactivity remained stable in the normoreactive group. Hypoaggregation was associated with a 21.4% higher cumulative SOFA score (34 vs. 28, β=5.9, 95% CI: 3.1–8.7, P < 0.001), a 2.08-fold increased risk of AKI (51.3% vs. 33.3%, OR = 2.08, 95% CI: 1.21–3.58), prolonged mechanical ventilation (median increase of 25.0 h, 95% CI: 9.8–40.2), and a 15.3-percentage-point absolute increase (39.7% vs. 24.4%) and 89% higher odds of 28-day mortality (HR = 1.89, 95% CI: 1.25–2.86). The association was more pronounced in patients with fibrinogen < 2.5 g/L. ADP-induced platelet hypoaggregation is temporally associated with and provides complementary prognostic information on progressive organ failure in septic shock, particularly in the context of fibrinogen < 2.5 g/L. Together with platelet count and fibrinogen, serial assessment of ADP-induced aggregation may improve risk stratification and warrants prospective validation.
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Zhang et al. (2026) conducted a cohort in Septic shock (n=156). Platelet hypoaggregation (ADP-AUC <30 AU·min) vs. Normoreactive platelets was evaluated on 7-day cumulative SOFA score (excluding the coagulation component) (β=5.9, 95% CI 3.1-8.7, p=<0.001). ADP-induced platelet hypoaggregation was associated with a 21.4% higher 7-day cumulative SOFA score (median 34 vs. 28, β=5.9) compared to normoreactive platelets in patients with septic shock.
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