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

Chen-Hsiang Lee,1,2 Seng-Kee Chuah,2,3 Wei-Chen Tai,2,3 I-Ling Chen4 1Department of Internal Medicine, Division of Infectious Diseases, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; 2Chang Gung University College of Medicine, Kaohsiung, Taiwan; 3Department of Internal Medicine, Division of Gastroenterology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; 4Department of Pharmacology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan Objective: 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 methods: 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. Results: 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 thrombophlebitis 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