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1/7. Successful catheter interventional therapy for acute coronary syndrome secondary to kawasaki disease in young adults.

    acute coronary syndrome occurred in 2 young adults who had a history of Kawasaki disease (KD), but few other coronary risk factors. The first patient was a 27-year-old male with acute myocardial infarction without stenosis detected by coronary arteriography 4 years earlier. Emergency coronary arteriography showed occlusion of the right coronary artery. Aspiration-thrombectomy and rescue balloon angioplasty were successfully performed. The second patient was a 32-year-old male with unstable angina. Right coronary arteriography showed total occlusion with severe calcification. Left coronary arteriography showed 99% stenosis at the proximal site of the circumflex artery, and a directional coronary atherectomy was performed. Histological examination of a specimen from this site revealed a lipid core, macrophages, and smooth muscle cells. Restenosis was not observed on follow-up coronary arteriography after 5-6 months in either case. The coronary stenosis in each case was probably caused by accelerated atherosclerosis at the site without aneurysm as it seemed to be 'normal' on arteriography. Conventional catheter intervention was effective treatment. The sequelae of KD should be recognized as independent coronary risk factors.
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2/7. Longstanding obliterative panarteritis in Kawasaki disease: lack of cyclosporin A effect.

    Kawasaki disease is a childhood vasculitis of medium-sized vessels, affecting the coronary arteries in particular. We have treated a therapy-resistant child who met all diagnostic criteria for Kawasaki disease. After the boy was given intravenous immunoglobulins and salicylates, as well as several courses of pulsed methylprednisolone, disease recurred and coronary artery lesions became progressively detectable. Cyclosporin A was started and seemed clinically effective. In contrast to the positive effect on inflammatory parameters, ie, c-reactive protein and white blood cell counts, a novel plasma marker for cytotoxicity (granzyme B) remained elevated. coronary disease progressed to fatal obstruction and myocardial infarction. echocardiography, electrocardiograms, and myocardial creatine phosphokinase did not predict impending death. At autopsy an obliterative panarteritis was observed resulting from massive fibrointimal proliferation, affecting the aorta and several large and medium-sized arteries. Immunophenotypic analysis of the inflammatory infiltrates in arteries revealed mainly granzyme-positive cytotoxic T cells and macrophages in the intima and media, as well as nodular aggregates of T cells, B cells, and plasma cells in the adventitia of affected arteries. These findings further endorse the role of specific cellular and humoral immunity in Kawasaki disease. Unremitting coronary arteritis and excessive smooth muscle hyperplasia resulted in coronary occlusion despite the use of cyclosporin A.
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3/7. Are children with Kawasaki disease and prolonged fever at risk for macrophage activation syndrome?

    Kawasaki disease (KD) patients are known to be at increased risk for coronary artery lesions. We present evidence of another possible complication associated with KD: macrophage activation syndrome (MAS). In this case, a patient with KD and prolonged fever developed MAS. This case is of particular interest because of the late age of onset and recurrent nature of KD as well as the complication of MAS. We also present a review of the literature that supports the inclusion of MAS as an infrequent complication of KD.
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4/7. A fatal case of ruptured giant coronary artery aneurysm.

    A 5-year-old Japanese boy died because of a ruptured left coronary artery aneurysm (CAA). He was diagnosed as having Kawasaki disease (KD) on the 5th day from onset, with all of the principal signs. On the 7th day of illness, bilateral CAAs were already found via echocardiography, and he was treated with intravenous (IV) gamma globulin and oral ASA. However, the fever persisted and the CAA progressed rapidly. echocardiography on the 12th illness day showed a giant (18-mm) left anterior descending (LAD) artery aneurysm. Oral propranolol and nifedipine were administered, in conjunction with warfarin/aspirin anti-coagulation therapy. On the 13th day of illness, cardiac arrest developed abruptly, and, despite cardiopulmonary resuscitation (CPR), the patient remained unresponsive and died one hour later. The final pathological diagnosis was a ruptured LAD artery aneurysm and cardiac tamponade. Microscopic investigation of the ruptured vascular wall revealed marked neutrophilic infiltration, with fewer macrophages and lymphocytes. CAA ruptures are a very rare, but fatal, complication of KD. Based on a review of previous reports on CAA ruptures, we consider it useful to distinguish aneurysms which rapidly dilate and continue to expand beyond a diameter of 10 mm with ongoing vasculitis (these CAAs can be termed "super-giant") from the more common giant CAAs limited to a diameter of 8 or 9 mm, because a decision must be made as to whether to start intensive care or to intervene surgically, in order to ensure the survival of patients with such a potentially critical complication.
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5/7. macrophage activation syndrome as the presenting manifestation of rheumatic diseases in childhood.

    We describe 3 patients who presented with features of macrophage activation syndrome (MAS) at the time of presentation of systemic lupus erythematosus (SLE), systemic juvenile idiopathic arthritis, and Kawasaki disease. Immunohistochemical studies in the patient with SLE demonstrated extensive expression of CD163 on hemophagocytic macrophages, suggesting a possible role as a marker of MAS.
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6/7. Class II major histocompatibility antigen expression on coronary arterial endothelium in a patient with Kawasaki disease.

    To investigate the class II major histocompatibility antigen expression on coronary arterial endothelium of Kawasaki disease and immunophenotypes of the infiltrating cells in the coronary vascular lesions, myocardial sections from a patient who died during the acute stage of Kawasaki disease were studied using an immunoperoxidase technique. The mononuclear cells in the lesions mainly consisted of macrophages and T cells, whereas B cells and NK/K cells were not seen. The majority of T cells reacted with Leu-3a antibodies, and only a few reacted with Leu-2a antibodies. Cells bearing the interleukin-2 receptor, indicative of activated T cells, were also found in the lesions. To determine the distribution of class II antigen, we used anti-HLA-DR antibodies. The massive expression of HLA-DR antigen on mononuclear cells was found in the lesions. In addition, the HLA-DR activation antigen was expressed on the coronary arterial endothelium at the infiltrates in which macrophages and T cells coexisted. In contrast, coronary arterial endothelium did not express hla-dr antigens in the myocardial tissues of controls (n = 4). HLA-DR endothelial cells may play an important role in the development of Kawasaki vasculitis.
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7/7. Kawasaki's disease and infantile polyarteritis nodosa: is pseudomonas infection responsible? Report of a case.

    A nineteen-month-old child presented with a febrile illness, skin rash, painful swelling of the joints, lymphadenopathy and hepatosplenomegaly. pseudomonas was cultured from the blood during life and, subsequently, at autopsy. autopsy revealed a generalized panarteritis involving the coronary, retroperitoneal and pulmonary arteries with thickening of arterial walls and narrowing of the lumina. Thrombi and foci of necrosis and infarcts were found in many organs. Numerous bacilli were present in fresh lesions, but not in the organizing lesions. periodic acid-Schiff-positive deposits were found in occasional macrophages, in walls of affected vessels, in the marginal sinuses of lymph nodes and diffusely in epicardial and retroperitoneal adipose tissue. The findings suggest that some or even all cases of Kawasaki's disease and infantile polyarteritis nodosa may be caused by pseudomonas sepsis. It is also suggested that the vasculitis and paucity of inflammatory reaction in many cases of pseudomonas sepsis might be related to the fact that many strains of pseudomonas produce high-molecular-weight levan (or another polysaccharide). This compound is known to inhibit the inflammatory reaction and to increase bacterial pathogenicity.
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