Abstract-Abdominal aortic aneurysm (AAA) is histologically characterized by medial degeneration and various degrees of chronic adventitial inflammation, although the mechanisms for progression of aneurysm are poorly understood. In the present study, we carried out histological study of AAA tissues of patients, and interventional animal and cell culture experiments to investigate a role of mast cells in the pathogenesis of AAA. The number of mast cells was found to increase in the outer media or adventitia of human AAA, showing a positive correlation between the cell number and the AAA diameter. Aneurysmal dilatation of the aorta was seen in the control (ϩ/ϩ) rats following periaortic application of calcium chloride (CaCl 2 ) treatment but not in the mast cell-deficient mutant Ws/Ws rats. The AAA formation was accompanied by accumulation of mast cells, T lymphocytes and by activated matrix metalloproteinase 9, reduced elastin levels and augmented angiogenesis in the aortic tissue, but these changes were much less in the Ws/Ws rats than in the controls. Similarly, mast cells were accumulated and activated at the adventitia of aneurysmal aorta in the apolipoprotein E-deficient mice. The pharmacological intervention with the tranilast, an inhibitor of mast cell degranulation, attenuated AAA development in these rodent models. In the cell culture experiment, a mast cell directly augmented matrix metalloproteinase 9 activity produced by the monocyte/macrophage. Collectively, these data suggest that adventitial mast cells play a critical role in the progression of AAA. Key Words: adventitia Ⅲ inflammation Ⅲ mast cell Ⅲ matrix metalloproteinase Ⅲ aneurysm A bdominal aortic aneurysm (AAA), a relatively common disorder among elderly people, is pathologically characterized by atherosclerosis of the intima and disruption or attenuation of the elastic media with various degrees of adventitial inflammatory infiltration. 1,2 Because approximately 4% of adults older than 65 years harbor AAA, it is among the leading 15 causes of death in elderly persons in the United States. 3 Although substantial efforts have been made to clarify the mechanism of development of AAA, there is currently no effective method to inhibit enlargement of AAA. Repair surgery is necessary to prevent rupture in patients with progressively enlarging AAA, whereas the operative risk is often relatively high because of the other complications resulting from aging.Recent reports suggest that chronic inflammation of the aortic wall and progressive degradation of extracellular matrix proteins are involved in the development, progression, or rupture of AAA. 2,4 -8 As a component of the immune system, mast cells play a critical role in defending hosts against pathogens by releasing a number of immunoregulatory mediators. 9 These cells have also been shown to initiate the inflammatory response by releasing proinflammatory cytokines, growth factors, angiogenic mediators, and proteases, 10 as well as by recruiting other inflammatory cells, such as neutrophils, macrop...
A 70-year-old womanwith type lib therapy-refractory hyperlipidemia was diagnosed as having IgA kappa type multiple myeloma. She had neither a family history nor any other disease known to accompany hyperlipidemia. The serum IgA concentration fell from 3.42 g/dl to 1.24 g/ dl following chemotherapy with melphalan and prednisolone, and a concomitant decrease in both the serumcholesterol and triglyceride levels wasobserved. These serumlipids were positively correlated with the serum IgA concentration (p<0.001) during the three cycles of chemotherapy. These findings suggest the involvement of the monoclonal protein of IgA in the development of hyperlipidemia in the present case.
A 68-year-old woman was found to have atypical coarctation of the aorta, accompanied by systolic hypertension of the upper extremities despite administration of five types of antihypertensive drugs. Since the systolic hypertension was resistant to the conventional antihypertensive therapy, axilloiliac artery bypass grafting with a subcutaneous tunnel was performed to alleviate the pressure gradient. Systolic blood pressure was successfully reduced and hypertension was controlled after surgery.(Hypertens Res 2000; 23: 247-249)
A 36-yr-old male was found to have renovascular hypertension due to an occluded right renal artery and 70% stenosis in the left renal artery, caused by fibromuscular dysplasia. The right kidney was supplied by collateral blood flow, and secreted more renin than the left kidney. Two differential therapeutic approaches were taken: autotransplantation for the right kidney and percutaneous transluminal renal angioplasty followed by stent implantation for the left. The renovascular hypertension was treated with these therapies, preserving renal function in this patient. (Hypertens Res 1999; 22: 141-143) Key Words: renovascular hypertension, fibromuscular dysplasia, autotransplantation, angioplasty, stentThree therapeutic options are currently available for patients with renovascular hypertension; medical antihypertensive therapy, surgical revascularization, and transluminal angioplasty including stent implantation. Percutaneous transluminal renal angioplasty (PTRA) has been widely used for renovascular hypertensive patients (1, 2), and more recently, intravascular stenting is reported to be potentially beneficial in improving the patency of dilated renal arteries (3, 4). In the meantime, surgical revascularization should be considered when these interventions cannot be used. We report here on a patient with bilateral renal arterial stenoses due to fibromuscular dysplasia (FMD), whose renovascular hypertension was treated with autotransplantation for the right kidney and PTRA followed by stent implantation for the left.Case Report A 36-yr-old male was referred to our hospital for elevated blood pressure accompanied by increased plasma renin activity (PRA) to 56 ng/ h/ ml. High blood pressure ranging from 160 to 170 mmHg at systole had been documented since the age of 20, but antihypertensive medicine was not administered until recently. Neither first-nor second-degree relatives had any similar diseases. On physical examination, his blood pressure was 164/110 mmHg with no difference between the two arms, despite antihypertensive treatment with 80 mg nifedipine and 20 mg arotinolol. The chest was clear of percussion and auscultation, and no bruit was audible in the abdomen.There were no abnormal findings in urinary or hematological examinations, and the blood chemistry data were all within normal limits, except for a reduced serum potassium concentration (3.1 mmol/ 1). The serum creatinine level was 0.7 mg/ dl and creatinine clearance was calculated at 65 ml/min. PRA was elevated to 15.1 ng/h/ml, and it further increased by 1,119% 1 h after 25 mg captopril administration, accompanied by reduction of mean blood pressure from 150 to 129 mmHg. Nothing remarkable was found by chest X ray, while SV1 + RV5 was 8.3 mV by electrocardiogram, suggesting left ventricular hypertrophy. A renogram showed a delayed peak of radioisotope uptake by the right kidney, whereas the pattern of the left was within normal limits ( Fig. 1-A). As shown in Fig. 2, abdominal aortography revealed total occlusion of the right renal artery and 70%...
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