リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。

リケラボ 全国の大学リポジトリにある学位論文・教授論文を一括検索するならリケラボ論文検索大学・研究所にある論文を検索できる

リケラボ 全国の大学リポジトリにある学位論文・教授論文を一括検索するならリケラボ論文検索大学・研究所にある論文を検索できる

大学・研究所にある論文を検索できる 「Screening method for congenital dysfibrinogenemia using clot waveform analysis with the Clauss method」の論文概要。リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。

コピーが完了しました

URLをコピーしました

論文の公開元へ論文の公開元へ
書き出し

Screening method for congenital dysfibrinogenemia using clot waveform analysis with the Clauss method

Arai, Shinpei Kamijo, Tomu Hayashi, Fumiaki Shinohara, Sho Arai, Nobuo Sugano, Mitsutoshi Uehara, Takeshi Honda, Takayuki Okumura, Nobuo 信州大学 DOI:33030793

2022.01.04

概要

Introduction: Congenital fibrinogen disorders (CFD) are classified as afibrinogenemia or hypofibrinogenemia (Hypo), dysfibrinogenemia (Dys), or hypodysfibrinogenemia (Hypodys), according to functional and antigenic fibrinogen concentrations. However, in routine laboratory tests, plasma fibrinogen levels are mostly measured using the functional Clauss method and not as an antigenic level. Therefore, it is difficult to discriminate CFD from acquired hypofibrinogenemia (aHypo). To establish a screening method for CFD, we investigated the parameters of clot waveform analysis (CWA) from the Clauss method.

Methods: We compared fibrinogen concentrations determined using Clauss and prothrombin time (PT)-derived methods for 67 aHypo and CFD cases (19 Dys, 4 Hypodys, and 1 Hypo determined using antigen levels and DNA sequence analysis) with a CS-2400 instrument, and the CWA parameters, dH and Min1, were analyzed automatically with an on-board algorithm. dH and Min1 are the maximum change in transmittance at the end of coagulation and the maximum velocity of transmittance change during coagulation, respectively.

Results: Clauss/PT-derived ratios detected 18 cases of Dys and Hypodys but no Hypo cases, whereas Clauss/dH plus Clauss/Min1 ratios calculated from fibrinogen 3 concentration using the Clauss method and CWA parameters detected 21 cases of Dys and Hypodys and one Hypo cases. Moreover, the Clauss/PT-derived ratio and Clauss/dH plus Clauss/Min1 ratio detected 22 cases of Dys and Hypodys cases and one Hypo cases. Conclusion: This report demonstrates that CWA parameters of the Clauss method, Clauss/dH plus Clauss/Min1 ratio, screened Dys patients with a higher rate, whereas, Clauss/PT-derived ratios did not.

関連論文

参考文献

[1] Mosesson MW. Fibrinogen and fibrin structure and functions. J Thromb Haemost. 2005; 3 (8):1894–1904.

[2] Lord ST. Fibrinogen and fibrin: scaffold proteins in hemostasis. Curr Opin Hematol. 2007; 14 (3):236–241.

[3] de Moerloose P, Casini A, Neerman-Arbez M. Congenital fibrinogen disorders: an update. Semin. Thromb Hemost. 2013; 39 (6):585–595.

[4] Casini A, Neerman-Arbez M, Ariëns RA, de Moerloose P. Dysfibrinogenemia: from molecular anomalies to clinical manifestations and management. J Thromb Haemost. 2015; 13 (6):909–919.

[5] Clauss A. Rapid physiological coagulation method in determination of fibrinogen. Acta Haematol. 1957; 17 (4):237-246.

[6] Miesbach W, Schenk J, Alesci S, Lindhoff-Last E. Comparison of the fibrinogen Clauss assay and the fibrinogen PT derived method in patients with dysfibrinogenemia. Thromb Res. 2010; 126 (6):428-433.

[7] Chitolie A, Mackie I.J, Machin S.J. The type of thromboplastin reagent has important effects on the PT-derived fibrinogen potency. Laboratory Hematology. 1998; 4:149-155.

[8] Chantarangkul V, Tripodi A, Mannucci P.M. Evaluation of a fully automated centrifugal analyzer for performance of hemostasis tests. Clin Chem. 1987; 33 (10):1888- 1890.

[9] Rossi E, Mondonico P, Lombardi A, Preda L. Method for the determination of functional (clottable) fibrinogen by the new family of ACL coagulometers. Thromb Res. 1988; 52 (5):453-468.

[10] Shima M, Thachil J, Nair S.C, Srivastava A. Scientific and Standardization Committee, Towards standardization of clot waveform analysis and recommendations for its clinical applications. J Thromb Haemost. 2013; 11 (7):1417-1420.

[11] Shima M, Matsumoto T, Fukuda K, et al. The utility of activated partial thromboplastin time (aPTT) clot waveform analysis in the investigation of hemophilia A patients with very low levels of factor VIII activity (FVIII:C). Thromb Haemost. 2002; 87 (3):436-441.

[12] Matsumoto T, Shima M, Takeyama M, et al. The measurement of low levels of factor VIII or factor IX in hemophilia A and hemophilia B plasma by clot waveform analysis and thrombin generation assay. J Thromb Haemost. 2006; 4 (2):377-384.

[13] Shima M, Matsumoto T, Ogiwara K. New Assays for Monitoring Haemophilia Treatment. Haemophilia. 2008; 14 (3):83-92.

[14] Braun P.J, Givens T.B, Stead A.G, et al. Properties of Optical Data from Activated Partial Thromboplastin Time and Prothrombin Time Assays. Thromb Haemost. 1997; 78 (3):1079-1087.

[15] Jacquemin M, Vanlinthout I, Van Horenbeeck I, et al. The amplitude of coagulation curves from thrombin time tests allows dysfibrinogenemia caused by the common mutation FGG-Arg301 to be distinguished from hypofibrinogenemia. Int J Lab Hematol. 2017; 39(3):301-307.

[16] Suzuki A, Suzuki N, Kanematsu T, et al. Clot waveform analysis in Clauss fibrinogen assay contributes to classification of fibrinogen disorders. Thromb Res. 2019; 174:98- 103.

[17] Casini A, Undas A, Palla R, Thachil J, de Moerloose P. Subcommittee on Factor XIII and Fibrinogen, Diagnosis and classification of congenital fibrinogen disorders: communication from the SSC of the ISTH. J Thromb Haemost. 2018; 16 (9):1887-1890.

[18] Terasawa F, Okumura N, Kitano K, et al. Hypofibrinogenemia associated with a heterozygous missense mutation gamma153Cys to Arg (Matsumoto IV): in vitro expression demonstrates defective secretion of the variant fibrinogen. Blood. 1999; 94 (12):4122–4131.

[19] Mackie J, Lawrie AS, Kitchen S, et al. A performance evaluation of commercial fibrinogen reference preparations and assays for Clauss and PT-derived fibrinogen. Thromb Haemost. 2002; 87 (6):997-1005.

[20] Xiang L, Luo M, Yan J, et al. Combined use of Clauss and prothrombin time-derived methods for determining fibrinogen concentrations: Screening for congenital dysfibrinogenemia. J Clin Lab Anal. 2018; 32 (4):e22322.

[21] Hirota-Kawadobora M, Terasawa F, Yonekawa O, et al. Fibrinogens Kosai and Ogasa: Bbeta15Gly→Cys (GGT→TGT) substitution associated with impairment of fibrinopeptide B release and lateral aggregation. J Thromb Haemost. 2003; 1 (2):275-283.

[22] Kamijo T, Nagata K, Taira C, Higuchi Y, Arai S, Okumura N. Fibrin monomers derived from thrombogenic dysfibrinogenemia, Naples-type variant (BβAla68Thr), showed almost entirely normal polymerization. Thromb Res. 2018; 172:1-3.

[23] Terasawa F, Okumura N, Higuchi Y, et al. Fibrinogen Matsumoto III: a variant with gamma275 Arg→Cys (CGC→TGC) comparison of fibrin polymerization properties with those of Matsumoto I (gamma364 Asp→His) and Matsumoto II (gamma308 Asn→Lys). Thromb Haemost. 1999; 81 (5):763-766.

[24] Hirota-Kawadobora M, Terasawa F, Suzuki T, Tozuka M, Sano K, Okumura N. Comparison of thrombin-catalyzed fibrin polymerization and factor XIIIa-catalyzed cross-linking of fibrin among three recombinant variant fibrinogens, gamma 275C, gamma 275H, and gamma 275A. J Thromb Haemost. 2004; 2 (8):1359-1367.

[25] Kamijyo Y, Hirota-Kawadobora M, Fujihara N, et al. Functional analysis of heterozygous plasma dysfibrinogens derived from two families of gammaArg275Cys and three families of gammaArg275His, and haplotype analysis for these families. Rinsho Byori. 2009; 57 (7):651-658.

[26] Okumura N, Furihata K, Terasawa F, Ishikawa S, Ueno I, Katsuyama T. Fibrinogen Matsumoto II: gamma 308 Asn→Lys (AAT→AAG) mutation associated with bleeding tendency. Br J Haematol. 1996; 94 (3):526-528.

[27] Okumura N, Terasawa F, Fujita K, Fujihara N, Tozuka M, Koh C.S. Evidence that heterodimers exist in the fibrinogen Matsumoto II (gamma308N-->K) proband and participate in fibrin fiber formation. Thromb Res. 2002; 107 (3-4):157-162.

[28] Weisel J.W, Nagaswami C. Computer modeling of fibrin polymerization kinetics correlated with electron microscope and turbidity observations: clot structure and assembly are kinetically controlled. Biophys J. 1992; 63 (1):111-128.

[29] Hirota-Kawadobora M, Kani S, Terasawa F, et al. Functional analysis of recombinant Bbeta15C and Bbeta15A fibrinogens demonstrates that Bbeta15G residue plays important roles in FPB release and in lateral aggregation of protofibrils. J Thromb Haemost. 2005; 3 (5):983-990.

[30] Ikeda M, Arai S, Mukai S, Takezawa Y, Terasawa F, Okumura N. Novel heterozygous dysfibrinogenemia, Sumida (AαC472S), showed markedly impaired lateral aggregation of protofibrils and mildly lower functional fibrinogen levels. Thromb Res. 2015; 135 (4):710-717.

[31] Okumura N, Furihata K, Terasawa F, Nakagoshi R, Ueno I, Katsuyama T. Fibrinogen Matsumoto I: a gamma 364 Asp→His (GAT→CAT) substitution associated with defective fibrin polymerization. Thromb Haemost. 1996; 75 (6):887-891.

参考文献をもっと見る

全国の大学の
卒論・修論・学位論文

一発検索!

この論文の関連論文を見る