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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inflammatory abdominal aortic aneurysm is an uncommon disorder characterized by marked thickening and extensive inflammatory changes of the aneurysmal wall. The appearances of an inflammatory abdominal aortic aneurysm on dynamic Gd-DTPA enhanced magnetic resonance imaging are described and the value of this modality in achieving a pre-operative diagnosis is emphasized.
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PMID:Case report: inflammatory abdominal aortic aneurysm--dynamic Gd-DTPA enhanced magnetic resonance imaging features. 773 76

Inflammatory abdominal aortic aneurysm (IAAA) is a distinct clinicopathological entity, characterized by: (1) clinical presentation, such as back pain, weight loss, and increased ESR, (2) patchy and/or diffuse lymphoplasmacytic infiltration, and (3) marked periaortic fibrosis resulting in thickening of the aneurysmal wall and occasional retroperitoneal fibrosis. Its pathogenesis is unknown, but some authors support the theory that IAAA is a subtype of atherosclerotic abdominal aortic aneurysm because of close relationship between IAAA and atherosclerotic change. In this article, we describe clinical and histological features of IAAA on the basis of the literature and our review of 6 cases of IAAA, emphasizing the similarity and difference between IAAA and atherosclerotic abdominal aortic aneurysm. Our review supports that marked lamellar fibrosis completely replacing the media and adventitia, patchy lymphocytic infiltration (mostly B cells) and endarteritis obliterans are characteristic features of IAAA.
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PMID:[Inflammatory abdominal aortic aneurysm]. 793 2

Ruptured abdominal aortic aneurysm is the major surgical emergency in the retroperitoneal compartment. Rupture of an abdominal aortic aneurysm is always fatal without urgent operative repair. Computed tomography is the reference standard for the diagnosis of ruptured abdominal aortic aneurysm in hemodynamically stable patients. At CT, the diagnosis is based on the combination of abdominal aortic aneurysm and extraluminal retroperitoneal blood. Retroperitoneal hemorrhage usually demonstrates both isodense and hyperdense areas. In most cases hemorrhage is located in psoas compartments and perirenal space. In the case of ruptured abdominal aortic aneurysm other findings may be demonstrated such as focal interruption of the aortic wall and active extravasation of contrast media in the retroperitoneal compartments. Inflammatory abdominal aortic aneurysm, that may present as acute abdominal pain, should be recognized and differentiated from ruptured abdominal aortic aneurysm. Inflammatory abdominal aortic aneurysm is characterized by a fibrotic process around the abdominal aorta that may entrap adjacent structures such as ureters, duodenum and inferior vena cava. Aortic dissection, mycotic aneurysm, and inferior vena cava thrombosis are less common. Complications occurring after emergency aneurysm replacement are also considered.
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PMID:[Retroperitoneal vascular emergencies]. 879 70

Inflammatory abdominal aortic aneurysm is an uncommon variant of abdominal aortic aneurysms. Thorough preoperative imaging of the extent of the aneurysm and inflammation and the associated complications are crucial in the management of this condition. We report a case of inflammatory abdominal aortic aneurysm where, after the initial contrast-enhanced CT, gadolinium-enhanced MR imaging was used to define the true extent of the inflammation and differentiate inflammation from mural thrombus at the iliac extension of the aneurysm. The imaging appearances are presented and the impact of MR imaging on further surgical management options including endovascular repair are discussed.
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PMID:The role of gadolinium-enhanced MR imaging in the preoperative evaluation of inflammatory abdominal aortic aneurysm. 1252 39

Inflammatory abdominal aortic aneurysm (AAA) is an aortic aneurysm of unknown etiology characterized by a thickened aneurysmal wall, perianeurysmal and retroperitoneal fibrosis, and adhesions to adjacent organs. We encountered a case of inflammatory AAA, which developed from an ordinary atherosclerotic AAA over a period of 14 months, with a rapid increase of 48 mm in the maximum diameter of the aneurysm over 12 days. This report describes the evaluation of the serial change by 16-channel multidetector-row computed tomographic (MDCT) angiography.
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PMID:Serial assessment of the development of inflammatory abdominal aortic aneurysm from ordinary atherosclerotic abdominal aortic aneurysm using multidetector-row computed tomographic angiography. 1715 25

Inflammatory abdominal aortic aneurysm (AAA) accounts for 5% to 10% of all cases of AAA and differs from typical atherosclerotic AAA in many important ways. Although both inflammatory and atherosclerotic AAA most commonly affect the infrarenal portion of the abdominal aorta, patients with the inflammatory variant are younger and usually symptomatic, chiefly from back or abdominal pain. Unlike patients with atherosclerotic AAA, most with the inflammatory variant have an elevated erythrocyte sedimentation rate or abnormalities of other serum inflammatory markers. Computed tomography and magnetic resonance imaging are both sensitive for demonstrating the cuff of soft tissue inflammation surrounding the aneurysm that is characteristic of inflammatory AAA. In contrast to atherosclerotic AAA, the inflammatory variant is characterized pathologically by marked thickening of the aneurysm wall, fibrosis of the adjacent retroperitoneum, and rigid adherence of the adjacent structures to the anterior aneurysm wall. An extraordinary expansion of the adventitia due to inflammation also distinguishes inflammatory from atherosclerotic AAA. Although the pathogenesis of inflammatory AAA appears to involve an immune response localized to the vessel wall, the etiology of the inflammatory reaction is unknown. Inflammatory AAA is almost never associated with inflammation of other arteries. Male sex and smoking, the main risk factors for atherosclerotic AAA, are even stronger risk factors for the inflammatory variant. Smoking cessation is the first step of medical therapy. Corticosteroids or immunosuppressive therapies may also have roles. Although inflammatory AAA appears less likely to rupture than atherosclerotic AAA, surgical intervention appears prudent once the diameter of the aneurysm exceeds 5.5 cm. Knowing the features of inflammatory AAA should allow physicians to distinguish it from atherosclerotic AAA or from systemic vasculitis and to treat it with the appropriate combination of medical and surgical therapies.
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PMID:Inflammatory abdominal aortic aneurysm. 1724 36

Inflammatory abdominal aortic aneurysm is a rare cause of abdominal pain in young adults that may be difficult to diagnose in the Emergency Department. This case highlights the significance of this condition as a possible diagnosis in young patients presenting with abdominal symptoms. A 32-year old woman presented with lower abdominal and back pain. She had four previous visits to the Emergency Department and one hospital admission with similar symptoms and had been discharged without a definite diagnosis. Her vascular risk factors included hypercholesterolemia and smoking. A computed tomography (CT) scan showed a non-leaking infrarenal saccular abdominal aortic aneurysm and para-aortic lymphadenopathy. A transthoracic echocardiogram excluded endocarditis. There was no evidence of bacterial, viral, or fungal infection on blood and serum assays, and her autoimmune screen was negative. She underwent urgent open repair using a synthetic graft. The aneurysmal wall and para-aortic lymph node histology confirmed the diagnosis of inflammatory aneurysm with periaortitis. She remained asymptomatic at 8 months after surgery with no evidence of additional aneurysmal disease. Inflammatory abdominal aortic aneurysm is an unusual cause of abdominal pain in young adults. It is more likely in patients with persistent or recurrent abdominal symptoms.
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PMID:Inflammatory infrarenal abdominal aortic aneurysm in a young woman. 1802 83

Inflammatory abdominal aortic aneurysm (AAA) is a member of a family of disorders referred to as "chronic periaortitis" together with retroperitoneal fibrosis. Retroperitoneal fibrosis is included in IgG4-related disease, which is characterized by numerous infiltrating IgG4-positive plasma cells and high serum IgG4 concentrations. However, the relationship between IgG4-related disease and inflammatory AAA has not been documented. In this study, we examined the clinicopathologic characteristics of inflammatory (10 cases) and atherosclerotic (22 cases) AAAs, based on the hypothesis that inflammatory AAA might be related to IgG4-related disease. Cases of inflammatory AAA could be classified into 2 groups based on immunostaining of IgG4. Four patients showed diffuse infiltration of abundant IgG4-positive plasma cells (IgG4-related cases), whereas the remaining 6 cases of inflammatory AAA and all cases of atherosclerotic AAA had only a few IgG4-positive plasma cells (non-IgG4-related cases). IgG4-related inflammatory AAA was pathologically characterized by the frequent infiltration of eosinophils, lymph follicle formation, perineural inflammatory extension, and inconspicuous infiltration of neutrophils compared with non-IgG4-related inflammatory AAA. Obliterative phlebitis, which is venous occlusion with inflammatory cell infiltration, is observed in all IgG4-related cases. In addition, serum IgG4 concentrations were significantly higher in IgG4-related inflammatory AAA (109 to 559 mg/dL, normal range: 4 to 110 mg/dL) than non-IgG4-related inflammatory AAA (32 to 59 mg/dL) and all atherosclerotic AAA (12 to 83 mg/dL). In conclusion, inflammatory AAAs might be classified into 2 groups: IgG4-related or nonrelated. The former might be one of the IgG4-related diseases, and could be included in IgG4-related periaortitis together with retroperitoneal fibrosis.
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PMID:Inflammatory abdominal aortic aneurysm: close relationship to IgG4-related periaortitis. 1822 21

Inflammatory abdominal aortic aneurysm (IAA) is associated with autoimmune disease. However, the precise mechanism of IAA remains unclear. There is increasing evidence that IgG4 is involved in the autoimmune mechanism of various idiopathic sclerosing lesions, including sclerosing pancreatitis and retroperitoneal fibrosis. The present study investigated the hypothesis that the IgG4-related autoimmune reaction is involved in the formation of IAA. The study group consisted of 11 cases of IAA (69.2 +/- 8.59y) and 12 age-matched cases of atherosclerotic abdominal aortic aneurysm (AAA, 69.6 +/- 5.94y), which were used in the previous report. A clinicopathologic examination of these lesions was performed, including histology and immunohistochemistry, in relation to the involvement of IgG4-positive plasma cells in the formation of IAA. No difference in the incidence of risk factors for atherosclerosis was observed between the patients with IAA and AAA. Autoimmune diseases were diagnosed in 2 patients with IAA, including rheumatoid arthritis and polyarteritis nodosa. A patient with IAA had pulmonary fibrosis. In contrast, autoimmune diseases were absent in patients with AAA. However, there was no significant difference in the incidence of autoimmune diseases between the patients with IAA and AAA. Lymphocyte and plasma cell infiltration and fibrosis were significantly more intense and extensive in IAA than in AAA. In addition, lymph follicle formation and vasculitis of small veins and arteries were frequently found in the affected lesions of IAA. Immunohistochemically, IAA showed a significant increase in the number of infiltrating IgG4-positive plasma cells and the incidence of a disrupted follicular dendritic cell network in lymph follicles, in comparison with AAA. These findings suggest that IAA may be an aortic lesion reflecting the presence of IgG4-related sclerosing disease, and not a simple inflammatory aneurysm of the aorta.
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PMID:IgG4-positive plasma cells in inflammatory abdominal aortic aneurysm: the possibility of an aortic manifestation of IgG4-related sclerosing disease. 1830 Jul 98