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BRIEF REPORT |
Department of Internal Medicine, Tri-Service General Hospital (J.-C.L., S.-C.W., F.-Y.C.), Taipei 114, Taiwan, Republic of China; Divisions of Clinical Research (L.K.S.), Biostatistics (H.-H.T.), and Biotechnology and Pharmaceutical Research (C.-T.C.), National Health Research Institutes, Taipei 114, Taiwan, Republic of China; Department of Medicine, Taipei Veterans General Hospital and National Yang-Ming University (C.-P.F.), Taipei 112, Taiwan, Republic of China; and Fu-Jen Catholic University (J.-J.W.), Taipei 248, Taiwan, Republic of China
Address all correspondence and requests for reprints to: Feng-Yee Chang, Department of Internal Medicine, Tri-Service General Hospital, 325, Section 2, Cheng-Kung Road, Neihu, Taipei 114, Taiwan, Republic of China. E-mail: fychang{at}ndmctsgh.edu.tw.
Context: Diabetes mellitus (DM) and capsular serotypes K1 and K2 Klebsiella pneumoniae have been identified as risk factors for liver abscess and complicated endophthalmitis.
Objective: The objective of this study was to determine whether poor glycemic control contributes to the development of capsular serotype K1 or K2 K. pneumoniae liver abscess.
Design and Setting: Neutrophil phagocytosis in patients with type 2 DM and nondiabetic controls was compared with isolates from liver abscess. Phagocytic rates of 18 K1/K2 and nine non-K1/K2 K. pneumoniae strains were evaluated by flow cytometry and electron microscopy.
Patients or Study Participants: Forty patients with type 2 diabetes, 14 with good glycemic control, 26 with poor glycemic control, and 13 age-matched healthy normal subjects, were studied.
Main Outcome Measures: Phagocytic rate of K. pneumoniae was measured.
Results: Phagocytosis of serotype K1/K2 isolates by neutrophils from diabetics was significantly less than normal controls (P < 0.01). Further analysis revealed that, in type 2 DM patients with poor glycemic control, phagocytosis of K1/K2 was remarkably impaired at 10 min (25.2 ± 1.7 vs. 42.4 ± 1.8%) and persisted until 60 min (51 ± 1.2 vs. 59.4 ± 1.4%; P < 0.01), but in type 2 DM patients with good glycemic control were similar at 10 min (38.2 ± 1.7% vs. 42.4 ± 1.8%) and at 60 min (57 ± 0.3% vs. 59.4 ± 1.4%; P = 0.2). No significant difference in the phagocytosis of non-K1/K2 K. pneumoniae among all subjects was observed.
Conclusions: Poor glycemic control plays a role in impairing neutrophil phagocytosis of K1/K2 K. pneumoniae, but does not significantly affect the phagocytosis of non-K1/K2 K. pneumoniae. This study identifies poor glycemic control as a risk factor for susceptibility to serotype K1/K2 K. pneumoniae liver abscess and complicated endophthalmitis.
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