Platelet reactivity in diabetic patients with invasive Klebsiella pneumoniae liver abscess syndrome

Diabetic patients with IKLAS demonstrated platelet hyperreactivity, which may be associated with a higher risk for vascular complications.

To determine the relationships of platelet activity in diabetic patients with invasive Klebsiella pneumoniae liver abscess syndrome (IKLAS), a total of 175 diabetic patients with community-acquired Klebsiella pneumoniae (KP) bacteremia were included in this study. We compared the platelet reactivity of 40 patients with IKLAS, 40 patients with non-IKLAS, and eight healthy controls using a whole-blood flow cytometry-based assay.

Platelets catalyze the development of hyperinflammation and microthrombosis and contribute to increases in accumulation of circulating platelet-leukocyte complex, the key event in the development of disseminated infection. Subjects and

Patients who were infected with strains expressing K1/K2 serotype (adjusted odds ratio [AOR], 8.81; 95% CI, 2.18-35.53) and those with HbA1c ≥9% (AOR, 4.97; 95% CI, 1.73-14.23) were more likely to present with IKLAS, whereas those who had recent therapy with aspirin (AOR, 0.17; 95% CI, 0.04-0.79) were less likely to present with IKLAS. Among patients with IKLAS, patients with a poor glycemic control were more likely to present with hepatic venous thrombo-phlebitis than those with suboptimal or good glycemic control (P=0.03). Patients with IKLAS had a higher median fluorescence intensity of the platelet membrane expression of P-selectin than those with non-IKLAS (78.0 vs 28.0, P<0.001) and controls (78.0 vs 22.0, P< 0.001). The IKLAS group also demonstrated a significantly higher platelet-monocyte aggregation and higher plasma levels of PF-4 than the non-IKLAS group (47.0 vs 18.0 and 47.0 vs 4.0, respectively, both P <0.001) and controls (46.0 vs 24.0 and 46.0 vs 13.0, respectively, both P <0.001).