Volume 51, Issue 4 pp. 448-452

Neutropenia in the acute phase of Kawasaki disease and prevention of coronary artery aneurysm

Zenshiro Onouchi

Corresponding Author

Zenshiro Onouchi

Department of Pediatric Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine and

Zenshiro Onouchi, MD, PhD, Department of Pediatric Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 2-1-119 Hatoyama, Uji City, Kyoto 611-0012, Japan. Email: [email protected]Search for more papers by this author
Kenji Hamaoka

Kenji Hamaoka

Department of Pediatric Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine and

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Seiichiro Ozawa

Seiichiro Ozawa

Department of Pediatric Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine and

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Koichi Sakata

Koichi Sakata

Department of Pediatric Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine and

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Nobuyuki Kiyosawa

Nobuyuki Kiyosawa

Department of Pediatrics, Second Kyoto Red Cross Hospital, Kyoto, Japan

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Hisato Ito

Hisato Ito

Department of Pediatrics, Second Kyoto Red Cross Hospital, Kyoto, Japan

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First published: 23 July 2009
Citations: 4

Abstract

Background: The significance of neutropenia in Kawasaki disease (KD) has not been fully elucidated as yet.

Methods: Subjects were retrospectively sampled from two clinical trials. These patients treated with aspirin alone (ASA) and PolyglobinN-Bayel (PolyN) given as i.v. immunoglobulin were categorized as ASA-early (n = 0), ASA-late (n = 8), PolyN-early (n = 18), or PolyN-late (n = 27) based on the therapy administered and the incidence of neutropenia before the 10th day of illness (DI) and after 11 DI. Data regarding the time of onset of neutropenia, and incidence of coronary artery lesion (CAL) formation were obtained. P < 0.05 was considered statistically significant.

Results: No patients in the ASA group exhibited neutropenia within 10 DI. The time of onset of neutropenia in the PolyN-early group was 8 ± 1.3 DI. That in the PolyN-late group (19.8 ± 8 DI) was earlier than in the ASA-late group (26.6 ± 14 DI; P < 0.025). PolyN-early patients had a lower incidence of CAL formation than ASA-non patients (patients without neutropenia in the ASA group; P = 0.00019) and ASA-late patients (P = 0.04). That in the PolyN-early group tended to be lower than in the PolyN-late group (P < 0.1).

Conclusion: Early neutropenia indicated that circulating neutrophils within 10 DI may play an indispensable role in the following sequence to CAL formation in KD.

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