Persistent monocytosis after intravenous immunoglobulin therapy correlated with the development of coronary artery lesions in patients with Kawasaki disease
Ho-Chang Kuo, Chih-Lu Wang, Chi-Di Liang, Hong-Ren Yu, Hsin-Hsu Chen, Lin Wang, Kuender D. Yang
Division of Allergy, Immunology, and Rheumatology, Department of Pediatrics, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Graduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Kaohsiung; 2Department of Pediatrics, Po-Jen Hospital, Kaohsiung; and 3Division of Pediatric Cardiology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Kaohsiung, Taiwan
Received: June 29, 2006 Revised: August 1, 2006 Accepted: August 30, 2006
Background and purpose:
This study was conducted to investigate whether changes in the complete blood count (CBC)/differential count (DC) and C-reactive protein (CRP) were correlated to Kawasaki disease (KD) with coronary artery lesions (CALs).
A retrospective analysis was performed of all children with KD at Chang Gung Memorial Hospital at Kaohsiung from 2001 to 2006. KD patients were divided into those with and without CALs for testing of correlations with changes in CBC/DC and CRP levels.
A total of 147 patients were enrolled for this analysis. Serial CBC/DC and CRP measurements and echocardiographic data for determination of CAL formation were obtained before and after intravenous immunoglobulin (IVIG) treatment. There were 44 (29%) KD patients having CAL formation (>3 mm in diameter of internal lumen). There was no significant difference in terms of age distribution and major diagnostic criteria between KD patients with and without CALs. Male KD patients, however, had a significantly higher rate of CAL formation (p=0.009). In multivariate logistical regression analysis, persistent monocytosis after IVIG treatment was the only factor significantly correlated to CAL formation (p=0.003).
Of the febrile routine measurements of CBC/DC and CRP in KD, persistent monocytosis after IVIG treatment was correlated to CAL formation. Further studies to clarify the mechanism of monocytosis may help prevent the CALs of KD.
Coronary arteriosclerosis; C-reactive protein; Mucocutaneous lymph node syndrome
J Microbiol Immunol Infect. 2007;40:395-400.