Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ruptured abdominal aortic aneurysm (AAA) contributes largely to aneurysm-related morbidity and mortality. An inflammatory gene, COX-2, was found to be widely expressed in AAA. However, the involvement of COX-2 metabolites and other inflammatory mediators in the disease and particularly in AAA rupture still needs elucidation. The purpose of the present study was to evaluate the secretion of inflammatory mediators and the expression of macrophages in aneurysms and determine their significance in ruptured AAA. Aortic tissue was harvested at time of aortic reconstructive surgery for the group of intact AAA (n=20) and ruptured AAA (n=10) or at time of organ harvest for normal aortic tissue (n=4). Aortic explant cultures were immediately established and the culture medium was collected after 72 h. Specific enzyme-linked immunoassorbent assays were used to quantify COX-2 metabolites and inflammatory cytokines. Inflammatory macrophage cells were also quantified in the corresponding aortic walls immunohistochemically. Differences in the secretory levels of inflammatory metabolites and the macrophage quantity in all groups were assessed. All three explant culture groups secreted detectable levels of studied COX-2 metabolites, including PGE(2), PGF(2alpha), PGI(2) and TxB(2) and inflammatory cytokines, including interleukin (IL)-1beta, IL-6, IL-8 and IL-10. The secretory levels of PGE(2), TXB(2) and IL-6 were highest in the ruptured AAA explant cultures and statistically higher than those in intact AAA cultures (p<0.05). The secretion of those inflammatory mediators and the local expression of macrophages in ruptured aneurysm probably reflects the active inflammatory processes in the aortic lesions. A means of modifying the inflammatory process in the wall of AAAs might play an important role in preventing aneurysm rupture.
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PMID:Differential secretion of prostaglandin E(2), thromboxane A(2) and interleukin-6 in intact and ruptured abdominal aortic aneurysms. 1767 46

The prostaglandin I(2) (PGI(2)) analogue iloprost, a potent vasodilator and inhibitor of platelet activation, has traditionally been utilized in pulmonary hypertension and off-label use for revascularization of chronic critical lower limb ischemia. This study was designed to assess the effect of 72 hr iloprost infusion on systemic ischemia post-open elective abdominal aortic aneurysm (EAAA) surgery. Between January 2000 and 2007, 104 patients undergoing open EAAA were identified: 36 had juxtarenal, 15 had suprarenal, and 53 had infrarenal aneurysms, with a mean maximal diameter of 6.9 cm. The male-to-female ratio was 2.5:1, with a mean age of 71.9 years. No statistically significant difference was seen between the study groups with regard to age, sex, risk factors, American Society of Anesthesiologists (ASA) grade, or diameter of aneurysm repaired. All emergency, urgent, and endovascular procedures for aneurysms were excluded. Fifty-seven patients received iloprost infusion for 72 hr in the immediate postoperative period compared with 47 patients who did not. Patients were monitored for signs of pulmonary, renal, cardiac, systemic ischemia, and postoperative intensive care unit (ICU) morbidity. Statistically significantly increased ventilation rates (p=0.0048), pulmonary complication rates (p=0.0019), and myocardial ischemia (p=0.0446) were noted in those patients not receiving iloprost. These patients also had significantly higher renal indices including estimate glomerular filtration rate changes (p=0.041) and postoperative urea level rises (p=0.0286). Peripheral limb trashing was noted in five patients (11.6%) in the non-iloprost group compared with no patients who received iloprost. Increased rates of transfusion requirements and bowel complications were noted in those who did not receive iloprost, with their ICU stay greater than twice that of iloprost patients. All-cause morbidity affected 67% of patients not receiving iloprost compared to 40% who did. Survival rates were significantly better with iloprost than without in both 30-day (p=0.009) and 5-year cumulative (p=0.0187) survival. Iloprost infusion for 72 hr after open AAA repair was associated with improved systemic perfusion and decreased systemic ischemia. Patients had a significant survival benefit at 30 days and 5 years and significantly improved renal, cardiac, and respiratory function.
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PMID:Six years' experience with prostaglandin I2 infusion in elective open repair of abdominal aortic aneurysm: a parallel group observational study in a tertiary referral vascular center. 1899 65