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 「Acquired dysfibrinogenemia: monoclonal λ-type IgA binding to fibrinogen caused lower functional plasma fibrinogen level and abnormal clot formation」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。
リケラボ

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

Acquired dysfibrinogenemia: monoclonal λ-type IgA binding to fibrinogen caused lower functional plasma fibrinogen level and abnormal clot formation

Arai, Shinpei Kamijo, Tomu Takezawa, Yuka Sugano, Mitsutoshi Nakazawa, Hideyuki Ynagisawa, Ryu Uehara, Takeshi Honda, Takayuki Okumura, Nobuo 信州大学 DOI:32253663

2022.01.04

概要

Background: We reported a case of acquired dysfibrinogenemia with monoclonal gammopathy of undetermined significance presenting λ-type IgA M protein. The patient showed lower functional (0.38 g/dL) and normal immunological fibrinogen (3.24 g/dL). To examine the cause of the false lower value of fibrinogen, we performed experiments using the patient’s purified fibrinogen and IgA.

Methods: Fibrinogen was purified from the patient’s plasma, and IgA was purified from patient’s plasma or serum by immunoaffinity chromatography. We performed thrombincatalyzed fibrin polymerization, scanning electron microscopy (SEM), immunoblotting analysis, and enzyme-linked immunosorbent assays (ELISAs).

Results: Fibrin polymerization in the patient’s plasma was markedly reduced, and SEM showed no fiber bundles or sponge-like structures. Purified IgA did not influence polymerization, whereas immunoprecipitated plasma with an anti-IgA (α-chain) antibody indicated normalization of polymerization and clot structure. Western blotting analysis revealed the presence of monoclonal λ-type IgA-bound fibrinogen, and the proportion was significantly higher than normal control plasma using ELISA.

Conclusion: Our results suggested that IgA M protein-bound fibrinogen is not normally converted into fibrin, and instead finally forms an aberrantly structured fragile clot. The 3 patient’s reduced plasma fibrinogen level was caused by the presence of IgA M proteinbound fibrinogen and not by IgA M protein alone.

論文の公開元へ

この論文で使われている画像

関連論文

関連論文をもっと見る

参考文献

[1] Mosesson MW. Fibrinogen and fibrin structure and functions. J. Thromb. Haemost. 2005; 3:1894–904.

[2] Lord ST. Fibrinogen and fibrin: scaffold proteins in hemostasis. Curr. Opin. Hematol. 2007; 14:236–41.

[3] De Moerloose P, Casini A, Neerman-Arbez M. Congenital fibrinogen disorders: an update. Semin. Thromb. Hemost. 2013; 39:585–95.

[4] Casini A, Neerman-Arbez M, Ariëns RA, De Moerloose P. Dysfibrinogenemia: from molecular anomalies to clinical manifestations and management. J. Thromb. Haemost. 2015; 13:909–19.

[5] Regañón E, Vila V, Aznar J, Garrido G, Estellés A, Berenguer J. Study of the formation of fibrin clot in cirrhotic patients. An approach to study of acquired dysfibrinogenemia. Thromb. Res. 1987; 46:705–14.

[6] Francis JL, Armstrong DJ. Acquired dysfibrinogenaemia in liver disease. J. Clin. Pathol. 1982; 35: 667–72.

[7] Martinez J, Keane PM, Gilman PB, Palascak JE, The abnormal carbohydrate composition of the dysfibrinogenemia associated with liver disease. Ann. NY Acad. Sci. 1983; 408:388–396.

[8] Levy J, Pettei MJ, Weitz JI. Dysfibrinogenemia in obstructive liver disease. J. Pediatr. Gastroenterol. Nutr. 1987; 6:967–70.

[9] Carr ME Jr, Zekert SL. Abnormal clot retraction, altered fibrin structure, and normal platelet function in multiple myeloma. Am J Physiol. 1994; 266:1195–201.

[10] Shigekiyo T, Kosaka M, Shintani Y, Azuma H, Iishi Y, Saito S. Inhibition of fibrin monomer polymerization by Bence Jones protein in a patient with primary amyloidosis. Acta Haematol. 1989; 81:160–5.

[11] Dawson NA, Barr CF, Alving BM. Acquired dysfibrinogenemia. Paraneoplastic syndrome in renal cell carcinoma. Am. J. Med. 1985; 78:682–6.

[12] Zitomersky NL, Verhave M, Trenor CC3rd. Thrombosis and inflammatory bowel disease: a call for improved awareness and prevention. Inflamm. Bowel Dis. 2011; 17: 458–70.

[13] Ruiz-Arguelles A. Spontaneous reversal of acquired autoimmune dysfibrinogenemia probably due to an antiidiotypic antibody directed to an interspecies cross-reactive idiotype expressed on antifibrinogen antibodies. J. Clin. Invest. 1988; 82: 958–63.

[14] Galanakis DK, Ginzler EM, Fikrig SM. Monoclonal IgG anticoagulants delaying fibrin aggregation in two patients with systemic lupus erythematosus (SLE). Blood. 1978; 52:1037–46.

[15] Ozaki Y, Kagawa H, Yasuzawa M, Yoshimura C, Shimizu T, Nomura S, et al. Antifibrinogen antibody detected in a patient with systemic lupus erythematosus and disseminated intravascular coagulation. Rinsho Ketsueki. 1998; 39:436–41.

[16] Ashby MA, Lazarchick J. Acquired dysfibrinogenemia secondary to mithramycin toxicity. Am. J. Med. Sci. 1986; 292:53–5.

[17] Sugai S. IgA pyroglobulin, hyperviscosity syndrome and coagulation abnormality in a patient with multiple myeloma. Blood. 1972; 39:224–37.

[18] O'Kane MJ, Wisdom GB, Desai ZR, Archbold GP. Inhibition of fibrin monomer polymerisation by myeloma immunoglobulin. J. Clin. Pathol. 1994; 47:266–8.

[19] Kotlín R, Sobotková A, Riedel T, Salaj P, Suttnar J, Reicheltová Z, et al. Acquired dysfibrinogenemia secondary to multiple myeloma. Acta Haematol. 2008; 120:75–81.

[20] Dear A, Brennan SO, Sheat MJ, Faed JM, George PM. Acquired dysfibrinogenemia caused by monoclonal production of immunoglobulin lambda light chain. Haematologica. 2007; 92:111–7.

[21] Arai S, Kamijo T, Takezawa Y, Sugano M, Uehara T, Honda T, et al. Analysis of a false low value for fibrinogen activity and abnormal clot waveform in a patient with IgA M-protein. Rinsho Byori. 2019; 67:449–56.

[22] Rajkumar SV, Dimopoulos MA, Palumbo A, Blade J, Merlini G, Mateos MV, et al. International Myeloma Working Group updated criteria for the diagnosis of multiple myeloma, Lancet Oncol. 2014; 15: e538–48.

[23] Mukai S, Nagata K, Ikeda M, Arai S, Sugano M, Honda T, et al. Genetic analyses of novel compound heterozygous hypodysfibrinogenemia, Tsukuba I: FGG c.1129+62_65 del AATA and FGG c.1299+4 del A. Thromb. Res. 2016; 148:111–7.

[24] Terasawa F, Okumura N, Kitano K, Hayashida N, Shimosaka M, Okazaki M, 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; 94:4122–31.

[25] Takebe M, Soe G, Kohno I, Sugo T, Matsuda M. Calcium ion-dependent monoclonal antibody against human fibrinogen: preparation, characterization, and application to fibrinogen purification. Thromb. Haemost. 1995; 73:662–7.

[26] Ikeda M, Kobayashi T, Arai S, Mukai S, Takezawa Y, Terasawa F, et al. Recombinant γT305A fibrinogen indicates severely impaired fibrin polymerization due to the aberrant function of hole 'A' and calcium binding sites. Thromb. Res. 2014; 134: 518–25.

[27] Kamijyo Y, Hirota-Kawadobora M, Yamauchi K, Terasawa F, Honda T, Ikeya M, et al. Analysis of plasmin generation and clot lysis of plasma fibrinogen purified from a heterozygous dysfibrinogenemia, BbetaGly15Cys (Hamamatsu II). Blood Coagul. Fibrinolysis. 2009; 20:726–32.

[28] 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; 135:710–7.

[29] Doolittle RF. Fibrinogen and fibrin. Sci. Amer. 1981; 245:126–35.

参考文献をもっと見る

全国の大学の
卒論・修論・学位論文
を
一発検索！

この論文の関連論文を見る