***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Abdominal aortic aneurysm is a multifactorial disorder in which inflammation is an important pathophysiological feature . In explant culture , aneurysm biopsies secrete large amounts of interleukin-6 ( IL-6 ) , and among aneurysm patients , the circulating concentration of IL-6 appears to be increased . Methods and Results We investigated , in 19 patients , whether aneurysm wall was an important source of circulating IL-6 . We also tested the hypotheses , in 466 patients with a small aneurysm , that ( 1 ) high concentrations of circulating IL-6 signaled rapid aneurysm growth and ( 2 ) the −174 G→C polymorphism in the IL-6 promoter predicted survival . For 19 patients with large or inflammatory aneurysms , the concentration of IL-6 was higher in the iliac arteries than the brachial arteries ( median difference 26.5 pg/mL , this difference increasing with aneurysm diameter , P = 0.01 ) . In 466 patients with small aneurysms , the frequency of the −174 C allele ( 0.40 ) was similar to that in a normal healthy population . Patients of GG genotype had lower plasma concentrations of IL-6 than patients of GC and CC genotypes ( medians 1.9 , 4.8 , and 15.6 pg/mL , respectively , Kruskal-Wallis P = 0.047 ) . Cardiovascular and all-cause mortalities were lower for patients of GG genotype than for patients of GC and CC genotype : hazard ratios 0.32 ( 95 % CI 0.12 to 0.93 ) , P = 0.036 , and 0.51 ( 95 % CI 0.25 to 1.00 ) , P = 0.05 , respectively . There was no association between plasma IL-6 or IL-6 genotype and aneurysm growth . Conclusions Aortic aneurysms appear to be an important source of circulating IL-6 , the concentration being influenced by genotype . For patients with small aneurysms , the −174 G→C IL-6 genotype predicts future cardiovascular mortality The native fibrin gel structure formed in vitro from plasma sample s was examined by liquid permeation of hydrated fibrin gel networks in 38 unselected men who had suffered a myocardial infa rct ion before the age of 45 years and in 88 age-matched population -based control men . Both the fibrin gel porosity ( permeability coefficient , Ks ) and the calculated fiber mass-length ratio varied considerably within the two groups , but were generally lower in the patients . Ks was 8.3 + /- 5.2 cm2 x 10(9 ) ( mean + /- SD ) in the patient group and 12.5 + /- 5.7 cm2 x 10(9 ) among controls ( p < 0.001 ) . The corresponding figures for fiber mass-length ratio were 13.1 + /- 7.7 and 16.5 + /- 7.5 Dalton/ cm x 10(-13 ) , respectively ( p < 0.01 ) . Around 50 % of the patients had Ks values below the 10th percentile of the control group . A strong inverse correlation was seen between plasma plasminogen activator inhibitor-1 ( PAI-1 ) activity and Ks ( r = -0.603 , p < 0.001 ) or fiber mass-length ratio ( r = -0.565 , p < 0.001 ) in the patient group . Corresponding weaker associations of PAI-1 with fibrin gel properties were also present in the control group . In addition , inverse relationships of very low density lipoprotein ( VLDL ) triglyceride concentrations to Ks ( r = -0.362 , p < 0.001 ) and fiber mass-length ratio ( r = -0.283 , p < 0.01 ) were found among the controls . Proneness to formation of tight and rigid fibrin gel networks with abnormal architecture in vitro is in vivo associated with myocardial infa rct ion at a young age . Impaired fibrinolytic function secondary to a raised plasma PAI-1 activity level is associated with abnormal fibrin gel structure Abdominal aortic aneurysms have traditionally been thought to be a consequence of severe atherosclerosis of the arterial wall . To date , the role of haemostatic factors in aneurysmal disease has not been extensively research ed . The aim of this study was to see if such factors were independently related to the occurrence of aortic aneurysm . Furthermore , were the associations maintained after taking into account the presence of underlying atherosclerotic disease ? Using data from the Edinburgh Artery Study , a nested case-control design was used involving 40 cases of aortic aneurysm , each being matched to five controls by sex and within a 5-year age b and . After adjustment for age and sex , both fibrinogen ( P × 0.01 ) and fibrin D-dimer ( P × 0.001 ) were each associated with a significant increased risk of aneurysm . Further adjustment for packyears , history of cardiovascular disease and the ankle brachial pressure index result ed in odds ratios of 1.51 ( 95 % CI 1.05 to 2.16 , P × 0.05 ) for fibrinogen and 3.75 ( 95 % CI 1.80 to 7.82 , P × 0.001 ) for fibrin D-dimer . These associations probably arise as a consequence of fibrin deposition and turnover within the aneurysmal sac , although further prospect i ve studies are needed before thrombotic factors can be used in the identification of a group who are at high risk of developing an abdominal aortic aneurysm OBJECTIVE To assess the incidence of lupus anticoagulant ( LAC ) in patients with peripheral vascular disease . DESIGN Prospect i ve clinical study . SETTING University Hospital . MATERIAL S 20 patients with claudication ( group 2 ) , 20 patients with critical ischaemia ( group 3 ) and 20 patients prior to elective abdominal aortic aneurysm surgery ( group 4 ) were compared to 20 general surgical controls ( group 1 ) . CHIEF OUTCOME MEASURES Venous blood sample s for coagulation assay . MAIN RESULTS Positive results for LAC by the Dilute Russell 's viper venom time ( DRVVT ) with the platelet neutralisation procedure were present in 26 out of 60 vascular patients compared with none of the 20 general surgical controls . The three vascular groups showed a similar prevalence of LAC and this differed significantly from that in the control group ( chi 2 = 10.94 , p = 0.0009 ) . Of the 26 positive results only three were associated with an abnormal activated partial thromboplastin time ( APTT ) , which has previously been used as a marker for the presence of LAC activity . Fibrinogen levels were raised in seven of 20 patients in group 2 but were normal in the remaining vascular groups ( p = 0.001 ) . The mean factor VII level ( 124.1 units dl-1 ) in group 2 was higher than the mean of the remaining vascular patients ( 109.3 units dl-1 , p < 0.05 ) . CONCLUSIONS The high prevalence of LAC in patients with peripheral vascular disease and the associated increased risk of early graft thrombosis may justify routine testing by DRVVT prior to reconstructive vascular surgery . Treatment of these patients with antiplatelet agents or formal anticoagulation perioperatively should be considered BACKGROUND A ruptured abdominal aortic aneurysm ( AAA ) is associated with high mortality . Postoperative complications such as hemorrhage , multiple organ failure , myocardial infa rct ion , and thromboembolism are common . An active and balanced hemostatic system is essential to avoid bleeding as well as thrombosis . When these activities are not properly regulated the patient is at risk of developing either excessive bleeding or thrombosis-related complications . Previous studies have shown a state of activated coagulation in patients with ruptured AAA . However , there are conflicting results regarding the fibrinolytic response . OBJECTIVES The aim of the present study was to investigate the fibrinolytic state pre-operatively in patients with ruptured and non-ruptured AAA in relation to the clinical outcome with special regard to the influence of shock . METHODS A prospect i ve study was performed on 95 patients who underwent surgery for a ruptured AAA with shock ( n = 43 ) , a ruptured AAA without shock ( n = 12 ) , and a non-ruptured AAA ( n = 40 ) . Forty-one controls without an aneurysm were matched to the AAA patients according to age , gender and smoking habits . Plasma levels of tissue plasminogen activator antigen ( tPAag ) , and plasminogen activator inhibitor type-1 ( PAI-1 ) were measured as markers of fibrinolytic activity . D-dimer , a marker of fibrin turnover , was also measured . RESULTS D-dimer was significantly higher in patients with a non-ruptured AAA compared with controls without AAA . There were significantly higher levels of D-dimer , tPAag , and PAI-1 in patients operated for ruptured compared with non-ruptured AAA . tPAag was also significantly higher in ruptured AAA patients with shock compared with without shock . No deaths occurred in patients operated on for a non-ruptured AAA or ruptured AAA without shock . There were 12 deaths after repair of a ruptured AAA with shock , of which two patients died from bleeding and the remaining 10 from multiple organ failure and cardiac failure . CONCLUSION Our results indicate a state of activated coagulation in patients with a non-ruptured AAA , the state being intensified by rupture . The present data show normal fibrinolytic activities in patients with a non-ruptured AAA , but increased systemic fibrinolysis , as demonstrated by elevated tPAag level , in patients with a ruptured AAA . The elevated PAI-1 level indicates a simultaneous inhibition of the systemic fibrinolysis . Furthermore , the hyperfibrinolytic state was reinforced by shock in this study . However , the clinical outcome , with a relatively high incidence of thrombosis-related deaths , indicate a prothrombotic state instead of a hyperfibrinolytic state as a major point of attention in patients with shock as a result of a ruptured AAA OBJECTIVES the aim of the study was to determine the effects of infrarenal asymptomatic abdominal aortic aneurysm ( AAA ) on platelet count and activation . DESIGN prospect i ve clinical study in a University Department of Vascular Surgery . PATIENTS one hundred and five patients with AAA . Thirty-two control patients with symptomatic carotid artery stenoses . METHODS  platelet count ( PC ) , plasma glycocalicin levels , prothrombin ratio ( PTR ) , activated partial thromboplastin time ( APPT ) , fibrinogen and D-dimer  were measured in 23 patients with AAA and 16 control patients with symptomatic carotid artery stenoses .  PC alone  was measured in a further 84 patients with AAA and 16 with carotid artery stenoses . RESULTS PC was below the normal range in 8/105 patients and mean PC ( 215x10(9)/l , S.D. 47.5 ) was significantly lower than that of a control population ( 242x10(9)/l , S.D. 16.8 ) and patients with carotid disease ( 269x10(9)/l , S.D. 57 ) . Glycocalicin level was above the normal range in 7/23 patients and the median level ( 28 fg/plt ) was significantly higher than that of a normal population ( 21.6 fg/plt ) and patients with carotid disease ( 12.3 fg/plt ) . Fibrinogen levels , PTR and APPT were all within the normal range . One patient had a minimally elevated level of D-dimer . CONCLUSIONS the combination of low PC and high glycocalicin levels suggests that there is increased platelet destruction , most likely due to activation within the aneurysm sac 
    Output:
    
We found that plasma fibrinogen and D-dimer concentrations are likely to be higher in cases with AAA than control subjects .
Higher plasma fibrinogen and D-dimer concentrations may be associated with the presence of AAA