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.
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.
Effect estimate: β=5.9 (95% CI 3.1-8.7)
Absolute Event Rate: 34% vs 28%
p-value: p=<0.001
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.
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.