Relationship between Hemostatic Markers and Circulating Biochemical Markers of Collagen Metabolism in Patients with Aortic Aneurysm
Akihiro IharaToshiharu KawamotoKengo MatsumotoJun KawamotoAkira KatayamaMasao YoshitatsuHironori IzutaniKatsuhiko Ihara
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Abstract:
Our objective was to determine the relationship between plasma levels of hemostatic molecular markers – D-dimer and thrombin-antithrombin III complex (TAT) – and circulating biochemical markers of collagen metabolism – aminoterminal propeptide of type III procollagen (PIIIP) and carboxyterminal propeptide of type I procollagen (PICP) – in patients with aortic aneurysm. The subjects were 43 patients with aortic aneurysm (AA; mean age 71 years) and 26 age-matched controls (mean age 75 years). The mean D-dimer, TAT and PIIIP levels were higher in the patients than in the controls (p < 0.0001, 0.0001 and 0.012, respectively), while the mean PICP level was similar to that in the controls. Increased D-dimer had a significant correlation with PIIIP (r = 0.412, p = 0.006) and PICP (r = 0.342, p = 0.0246), while TAT correlated with PIIIP (r = 0.3194, p = 0.0374), but not with PICP. There was also a significant correlation (r = 0.306, p = 0.0463) between PIIIP and PICP. As shown by the significant positive correlations among D-dimer, TAT and PIIIP, accelerated fibrinolysis and thrombogenesis induce an increase of collagen degradation and procollagen synthesis in atherosclerotic lesions. These findings show that D-dimer and TAT, especially the former, may be useful markers to monitor the progression and predict the prognosis of AA.Keywords:
Procollagen peptidase
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Objective To study the changes of serum endothelin (ET) and D-dimer in the infants with pneumonia and heart failure (HF) and to explore the changes of blood coagulation,fibrinolysis,and endothelial cell function.Methods 80 infants with pneumonia and different degrees of HF and 20 controls were studied.Serum ET,D-dimer were measured.Results ET,D-dimer in two groups were different.The more severe the HF was, the more increased ET,D-dimer were.There were positive relationship between ET and D-dimer(r=0.42,P0.01).Conclusions The dysfunction of endothelial cell, the activation of coagulation and fibrinolysis system appears in the infants with pneumonia and HF.
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The influence of several methods of anaesthesia on the fibrinolysis was observed. Results obtained were summarized as follows : The rate of fibrinolysis was parallel to the degree of the surgical invasion, and in animal experiments, fibrinolysis was inhibited by the administration of rabonal, In human cases Anaesthesia, especially general anesthesis by ether inhibited remarkablly the rate of fibrinolysis at the surgical operation.
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Abstract In clinical practice, occasionally some patients show dissociated values of fibrinogen / fibrin degradation products (FDP) and D‐dimer (cross‐linked fibrin degradation products). In an attempt to assess the frequency, clinical backgrounds, and hemostatic states of these cases, FDP and D‐dimer were simultaneously measured together with other hemostatic parameters in 371 samples from patients with various diseases. As a whole, FDP values were positively correlated with D‐dimer values (r = 0.871, P < 0.0001), and both were elevated in parallel with the progress of activation of blood coagulation and fibrinolysis. However, in patients with elevated FDP and/or D‐dimer, 11.5% of samples showed relatively lower D‐dimer values than those expected from FDP levels, and these were regarded as an apparently dissociated group. In the dissociated group, activation of coagulation and fibrinolysis occurred to a lesser extent than others. Analysis of these samples suggested that the possible reasons for the dissociation bet ween FDP and D‐dimer values were accelerated fibrinogenolysis with or without secondary fibrinolysis, accelerated fibrinogenolysis by non‐plasmic proteinases, elevated soluble fibrin, and possibly false‐positive FDP levels due to unclottable fibrinogen remaining in the serum samples. In practice, simultaneous measurements of FDP and D‐dimer are useful for more accurate estimation of hyperfibrinolytic states. ©1995 Wiley‐Liss, Inc.
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서론: 폐색전증 진단에 있어서 D-dimer의 역학은 잘 알려져 있으나 일정기간 항응고제 치료 뒤 항응고제 중단후에 폐색전증 재발여부를 의심하기 위한 선별검사검사로서 D-dimer 추적검사는 유용할 수 있다. 저자들은 특이소견 없는 무증상환자에서 D-dimer 추적검사를 통해 재발성 폐색전증을 의심하여 진단한 환자를 경험하였기에 보고한다. 증례: 83세 여자로 수일 전부터 지속된 발열, 기침 및 호흡곤란을 주소로 내원하였다. 과거력상 4년전 요추압박골절로 본원정형외과에 입원 중 발생한 폐색전증 및 심부정맥혈전증으로 항응고제 투여받았고, 이후 타병원에서 지속적인 와파린 투여받고 있었고 3년 전 관상동맥 조영술 및 아세틸콜린 유발검사상 좌전하행 동맥내 혈관연축 확인되어 변이형 협심증 진단하에 약물치료 중이었다. 이학적 소견상 우측 폐야에서 호흡음 감소되어 있었으며 단순흉부촬영상 대량의 우측 흉수소견 관찰되었다. 흉수천자상 LDH 797 IU/L, Total protein 4.7 g/dL로 삼출액 소견 보이고 있었고 AFB 염색 및 배양 검사상 음성 소견이었으나 ADA 127U/L로 증가되어 결핵성 늑막염 진단하에 항결핵제 투여 시작하였다. 입원시 시행한 흉부전산화단층촬영상 더 이상 폐색전증 관찰되지 않았고 D-dimer 음성소견이었기에 와파린 중단키로 하고 통원치료하였다. 2달 뒤 전신쇠약을 주소로 재입원하여 시행한 흉부단순촬영상 흉수는 호전되었으나 추적검사로 시행한 D-dimer 5,120 ng/ml로 상승된 소견 관찰되었고 이어 시행한 흉부전산화단층촬영상 우측 폐동맥내 혈전소견관찰되어 재발성 폐색전증 진단하에 현재 항응고제 다시 투여중이다. 고찰: 원인 미상의 심부정맥혈전증의 경우 D-dimer 추적검사가 재발 및 치료 시기 결정에 있어서 도움이 될 수 있는 것으로 알려져 있으나 가역적 원인을 가진 심부정맥혈전증 및 폐색전증의 경우 항응고제치료 중단 후 D-dimer 추적검사의 유용성은 잘 알려지지 않았다. 이에 본 저자들은 특이소견 없는 무증상환자에서 D-dimer 추적검사를 통해 재발성 폐색전증을 의심하여 진단한 환자를 경험하였기에 보고한다.
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Summary The term “D-dimer assay” suggests, that these assays report the concentrations of the end-stage degradation product of crosslinked fibrin. This hardly occurs in patients. Degradation products of crosslinked fibrin rather occur with a wide range of molecular weights, and comprise various numbers of the D-dimer motif. Moreover, the numerical values obtained with different “D-dimer” assays vary widely. The variations are probably due to differences in reactivity of the various monoclonal antibodies used with the various D-dimer containing degradation products as they occur in patients; and to the various calibrators with a value assigned by the manufacturers. For the reasons indicated above a calibrator in the strict sense (e.g. pure D-dimer) is not feasible. This study shows that: it appears feasible to generate a conversion factor for each of the “D-dimer” assays studied, which will make the widely varying results obtained with these kits comparable; that the conversion factors can be based on a pool of real patient samples; and that the conversion factors are pool-independent. The next and final step in this study is to prepare and make available an international reference material for use by manufacturers and others facing a comparison problem. This is being carried out, in collaboration with the NIBSC (Dr. P. Gaffney), and the material is expected to be available in early 1997.
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It has been suggested that a sensitive assay of D-dimer, a fragment found in plasmin-mediated crosslinked fibrin digests, might contribute to our understanding of natural and induced fibrinolysis in man (P.J. Gaffney, Lancet (1972) ii, 1422). Towards this end, further characterisation of the heterogeneity of the D-dimer complex was attempted using gel electrophoretic techniques, while some attempts to raise rabbit antisera to D-dimer were also assessed. It was confirmed that D-dimer, following plasmin-mediated release from crosslinked fibrin, was non-covalently linked to fragment E. The E fragment was released from the D-dimer/E complex during progressive digestion. The earliest digests examined showed that more than 50% of the total E fragment (immunologically measured) was complexed with D-dimer while some E remained in the complexed form even after intensive digestion. During examination of various timed digests it was observed that the electrophoretic properties of the various D-dimer complexes changed while the detergent gel patterns remained consistent. Antisera raised in rabbits to the D-dimer/E complex, following absorption with fragments D and E, reacted with purified fibrinogen and suggests that these antibodies may be recognising the dimeric D structure in fibrinogen. It was concluded that studies of the immunological properties of the D-dimer/E complex, this being the earliest form of soluble crosslinked fibrin fragments, might be the most useful in eventually establishing an assay which would further our understanding of natural and induced fibrinolysis.
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