No abstract

Fifty-five patients with 72 aneurysms of the iliac vessels were evaluated retrospectively during a 12-year period (1972 to 1985). Atherosclerotic vascular disease was found in all aneurysms. Marked male predominance (5:1) and advanced age (mean 74.6 years) characterized this population group. Two thirds of them harbored multiple aneurysms and isolated aneurysms were found primarily to involve the internal iliac artery (12 of 18 patients). Although symptomatic presentation varied with anatomic location and presence of rupture, most patients were either asymptomatic (45%) or had such nonspecific complaints (11%) that diagnosis was often delayed or erroneous. A mass detected during abdominal, rectal, or vaginal examination was found in 39 patients (70%). Aneurysm size ranged from 2.5 to 18 cm (mean 5.5 cm) for the entire group. Internal iliac aneurysms tended to be larger (7.7 cm) yet demonstrated no increased risk of rupture, which was encountered in 33% of patients. Elective operative management was undertaken in 26 patients with a mortality rate of 11%. When repair had to be performed as an emergency procedure mortality increased to 33%. Aneurysm ligation, resection, or endoaneurysmorrhaphy coupled with graft interposition when necessary did not seem to influence patient survival. Eleven patients treated nonoperatively demonstrated enlargement in three, rupture in one, and progressive ureteral obstruction in one patient. Iliac aneurysms demonstrate expansile growth with eruptive and erosive complications and therefore should be managed aggressively under elective circumstances.

No abstract

Thrombosis and inflammation are closely related. However, the response of the vein wall to venous thrombosis has been poorly documented. This study examines the hypothesis that venous thrombosis is associated with an inflammatory response in the vein wall. In a rat model of inferior vena caval thrombosis, vein wall was temporally examined for inflammation by assessment of histopathology, leukocyte morphometrics, and cytokine levels. Animals were killed 1 hour and 1, 3, and 6 days after thrombus induction. Our findings demonstrated an early (day 1) neutrophil infiltration into the vein wall followed by a later (days 3 and 6) monocyte/macrophage and lymphocyte response. Cytokines were elevated only under conditions of venous thrombosis. Levels of epithelial neutrophil activating protein-78 (ENA-78), tumor necrosis factor-alpha (TNF), interleukin-6, and JE/monocyte chemoattractant protein-1 (JE/MCP-1) increased over the 6-day period, while macrophage inflammatory protein-1 alpha (MIP-1 alpha) peaked at day 3 after thrombus induction. Additionally, rats were passively immunized with neutralizing antibodies to TNF, ENA-78, MIP-1 alpha, JE/MCP-1, intercellular adhesion molecule-1 (ICAM-1), and CD18 compared with control antibodies. The most effective antibody early after thrombus induction for attenuating vein wall neutrophil extravasation was anti-TNF (P < .01). The monocyte/macrophage extravasation was inhibited most by anti-ICAM-1 followed by anti-TNF (P < .01). These findings demonstrate that venous thrombosis is associated with significant vein wall inflammation that is partially inhibited by neutralizing antibodies to cytokines and adhesion molecules.