Kawasaki disease: basic and pathological findings

Springer Science and Business Media LLC - Tập 17 - Trang 690-693 - 2012
Kei Takahashi1, Toshiaki Oharaseki1, Yuki Yokouchi1, Shiro Naoe2, Tsutomu Saji3
1Department of Pathology, Toho University Ohashi Medical Center, Tokyo, Japan
2Biomedical Engineering Center, Toin University of Yokohama, Yokohama, Japan
3Department of Pediatrics, Toho University Omori Medical Center, Tokyo, Japan

Tóm tắt

Kawasaki disease (KD) is considered to be a kind of systemic vasculitis syndrome. It most frequently affects infants and young children and primarily invades medium-sized muscular arteries, including the coronary arteries. The etiology of KD is unknown, but epidemiological data suggest involvement of infectious agents, such as bacteria and viruses, in the onset of KD. In addition, host genetics underlie the disease’s pathogenesis. Histologically, coronary arteritis begins 6–8 days after KD onset, and inflammation of all layers of the artery rapidly ensues. The inflammation spreads completely around the artery, resulting in severe damage to structural components. Then, the artery begins to dilate. KD arteritis is characterized by inflammation consisting of marked accumulation of monocytes/macrophages. Aberrant activation of monocytes/macrophages is thought to be involved in the formation of vascular lesions. Inflammatory-cell infiltration persists until about the 25th day of the disease, after which the inflammatory cells gradually decrease in number. Lesions in all arteries are relatively synchronous, as they evolve from acute to chronic injury. If a giant aneurysm remains or vessel recanalization occurs after thrombotic occlusion of an aneurysm, remodeling of the vascular structure, sometimes including even reocclusion, continues even in the remote stage.

Tài liệu tham khảo

Abe J, Kotzin BL, Jujo K, et al. Selective expansion of T cells expressing T-cell receptor variable regions V beta 2 and V beta 8 in Kawasaki disease. Proc Natl Acad Sci USA. 1992;89:4066–70.

Abe J, Kotzin BL, Meissner C, et al. Characterization of T cell repertoire changes in acute Kawasaki disease. J Exp Med. 1993;177:791–6.

Curtis N, Zheng R, Lamb JR, Levin M. Evidence for a superantigen mediated process in Kawasaki disease. Arch Dis Child. 1995;72:308–11.

Rowley AH, Shulman ST, Mask CA, et al. IgA plasma cell infiltration of proximal respiratory tract, pancreas, kidney, and coronary artery in acute Kawasaki disease. J Infect Dis. 2000;182:1183–91.

Brown TJ, Crawford SE, Cornwall ML, et al. CD8 T lymphocytes and macrophages infiltrate coronary artery aneurysms in acute Kawasaki disease. J Infect Dis. 2001;184:940–3.

Rowley AH, Shulman ST, Spike BT, et al. Oligoclonal IgA response in the vascular wall in acute Kawasaki disease. J Immunol. 2001;166:1334–43.

Rowley AH, Baker SC, Shulman ST, et al. Detection of antigen in bronchial epithelium and macrophages in acute Kawasaki disease by use of synthetic antibody. J Infect Dis. 2004;190:856–65.

Rowley AH, Baker SC, Shulman ST, et al. Cytoplasmic inclusion bodies are detected by synthetic antibody in ciliated bronchial epithelium during acute Kawasaki disease. J Infect Dis. 2005;192:1757–66.

Rowley AH, Baker SC, Shulman ST, et al. RNA-containing cytoplasmic inclusion bodies in ciliated bronchial epithelium months to years after acute Kawasaki disease. PLoS ONE. 2008;3:e1582.

Landing HL, Larson E. Pathological features of Kawasaki disease (mucocutaneous lymph node syndrome). Am J Cardiovasc Pathol. 1987;1:215–29.

Naoe S, Takahashi K, Masuda H, Tanaka N. Kawasaki disease with particular emphasis on arterial lesions. Acta Pathol Jpn. 1991;41:785–97.

Jennette JC, Falk RJ, Andrassy K, et al. Nomenclature of systemic vasculitides: the proposal of an international consensus conference. Arthr Rheum. 1994;37:187–92.

Amano S, Hazawa F, Kubagawa H, et al. General pathology of Kawasaki disease on the morphological alterations corresponding to the clinical manifestations. Acta Pathol Jpn. 1980;30:681–94.

Masuda H, Naoe S, Tanaka N. A pathological study of coronary artery in Kawasaki disease (MCLS)—with special reference to morphogenesis of aneurysm. J Jpn Coll Angiol. 1981;21:899–912.

Takahashi K, Oharaseki T, Yokouchi Y, Yamada H, Shibuya K, Naoe S. A half-century of autopsy results—incidence of pediatric vasculitis syndromes. Especially Kawasaki disease. Circ J. 2012;76:964–70.

Takahashi K, Oharaseki T, Naoe S, et al. Neutrophilic involvement in the damage to coronary arteries in acute stage of Kawasaki disease. Pediatr Int. 2005;47:305–10.

Fujiwara H, Fujiwara T, Kao TC, Ohshio G, Hamashima Y. Pathology of Kawasaki disease in the healed stage; relationship between typical and atypical cases of Kawasaki disease. Acta Pathol Jpn. 1986;36:857–67.

Tanaka N, Naoe S, Masuda H, Ueno T. Pathological study of sequelae of Kawasaki disease (MCLS) with special reference to heart and coronary arterial lesions. Acta Pathol Jpn. 1986;36:1513–27.

Naoe S, Takahashi K. Kawasaki disease with the focus on sequelae. In: Tanabe T, editor. Intractable vasculitis. Sapporo: Syndromes Hokkaido University Press; 1993. p. 93–103.

Sasaguri Y, Kato H. Regression of aneurysms in Kawasaki disease: a pathologic study. J Pediatr. 1982;100:225–31.

Naoe S, Takahashi K, Masuda H, Tanaka N. Coronary findings post Kawasaki disease in children who died of other causes. In: Schulman ST, editor. Kawasaki disease. New York: Liss; 1987. p. 341–6.

Takahashi K, Oharaseki T, Naoe S. Pathological study of postcoronary arteritis in adolescents and young adults, with reference to the relationship between sequelae of Kawasaki disease and atherosclerosis. Pediatr Cardiol. 2001;22:138–42.

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Springer Science and Business Media LLC

Tập 17

690-693

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