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Journal articles on the topic 'Dysfibrinogenemie'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Marchi, Rita, Shah Soltan Mirshahi, Claudine Soria, et al. "Thrombotic Dysfibrinogenemia." Thrombosis Research 99, no. 2 (2000): 187–93. http://dx.doi.org/10.1016/s0049-3848(00)00235-8.

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2

Bithell, T. C. "Hereditary dysfibrinogenemia." Clinical Chemistry 31, no. 4 (1985): 509–16. http://dx.doi.org/10.1093/clinchem/31.4.509.

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Abstract Inherited qualitative abnormalities of fibrinogen have been documented in more than 100 families. These dysfibrinogenemias usually are clinically silent, but in some cases are associated with bleeding, thrombosis, or defective wound healing. Abnormalities of the fibrinogen molecule may impair any of the major steps involved in the conversion of fibrinogen into stabilized fibrin; i.e., cleavage of the fibrinopeptides by thrombin, polymerization, and cross-linking of fibrin. Biochemical studies of several abnormal fibrinogens have demonstrated that the functional defects are the result

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3

Martinez, Jose. "Congenital dysfibrinogenemia." Current Opinion in Hematology 4, no. 5 (1997): 357–65. http://dx.doi.org/10.1097/00062752-199704050-00010.

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4

Mosesson, Michael. "Dysfibrinogenemia and Thrombosis." Seminars in Thrombosis and Hemostasis 25, no. 03 (1999): 311–19. http://dx.doi.org/10.1055/s-2007-994933.

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5

Hayes, Timothy. "Dysfibrinogenemia and Thrombosis." Archives of Pathology & Laboratory Medicine 126, no. 11 (2002): 1387–90. http://dx.doi.org/10.5858/2002-126-1387-dat.

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Abstract Objectives.—To review the state of the art relating to congenital dysfibrinogenemia as a potential risk factor for thrombosis, as reflected by the medical literature and the consensus opinion of recognized experts in the field, and to make recommendations for the use of laboratory assays for assessing this thrombotic risk in individual patients. Data Sources.—Review of the medical literature, primarily from the last 10 years. Data Extraction and Synthesis.—After an initial assessment of the literature, key points were identified. Experts were assigned to do an in-depth review of the l

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6

Cunningham, Mark T., John T. Brandt, Michael Laposata, and John D. Olson. "Laboratory Diagnosis of Dysfibrinogenemia." Archives of Pathology & Laboratory Medicine 126, no. 4 (2002): 499–505. http://dx.doi.org/10.5858/2002-126-0499-ldod.

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Abstract Dysfibrinogenemia is a coagulation disorder caused by a variety of structural abnormalities in the fibrinogen molecule that result in abnormal fibrinogen function. It can be inherited or acquired. The inherited form is associated with increased risk of bleeding, thrombosis, or both in the same patient or family. Traditionally, dysfibrinogenemia is diagnosed by abnormal tests of fibrin clot formation; the thrombin time and reptilase time are the screening tests, and the fibrinogen clotting activity–antigen ratio is the confirmatory test. The inherited form is diagnosed by demonstrating

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7

EDWARDS, R. "Dysfibrinogenemia and placental abruption." Obstetrics & Gynecology 95, no. 6 (2000): 1043. http://dx.doi.org/10.1016/s0029-7844(00)00867-x.

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8

Khosrotehrani, Kiarash, Catherine Leroy-Matheron, Claude Mourier, Jean Revuz, and Martine Bagot. "Sneddon Syndrome revealing dysfibrinogenemia." International Journal of Dermatology 42, no. 7 (2003): 561–62. http://dx.doi.org/10.1046/j.1365-4362.2003.01723_1.x.

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9

Oo, Thein H. "Hypofibrinogenemia, dysfibrinogenemia or hypodysfibrinogenemia?" Blood Coagulation & Fibrinolysis 24, no. 3 (2013): 353–54. http://dx.doi.org/10.1097/mbc.0b013e32835e42bd.

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10

Haverkate, F., and M. Samama. "Familial Dysfibrinogenemia and Thrombophilia." Thrombosis and Haemostasis 73, no. 01 (1995): 151–61. http://dx.doi.org/10.1055/s-0038-1653741.

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SummaryApproximately 250 cases of dysfibrinogenemia have been reported; 55% were asymptomatic (detected by chance), 25% had a tendency to bleeding, and 20% were reported to have a tendency to thrombosis.To establish a possible association between familial dysfibrinogenemia and thrombophilia, data on cases with both affections were collected in a study within the framework of the SSC Subcommittee on Fibrinogen of the International Society on Thrombosis and Haemostasis. Registry forms of 51 cases were received. Twenty-six cases fulfilled the (arbitrarily chosen) criteria of familial dysfibrinoge

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11

Edwards, Robert Z., and Asha Rijhsinghani. "DYSFIBRINOGENEMIA AND PLACENTAL ABRUPTION." Obstetrics & Gynecology 95, Supplement (2000): 1043. http://dx.doi.org/10.1097/00006250-200006001-00028.

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12

Principe, Domenico Del, Adriana Menichelli, Massimo Giordani, Carlo M. Colucci, Claudio Colistra, and Stefano Di Giulio. "DYSFIBRINOGENEMIA IN BURNED CHILDREN." Pediatric Research 26, no. 5 (1989): 504. http://dx.doi.org/10.1203/00006450-198911000-00030.

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13

Martini, Francesca, Nadia Cecconi, Aldo Paolicchi, et al. "Interference of Monoclonal Gammopathy with Fibrinogen Assay Producing Spurious Dysfibrinogenemia." TH Open 03, no. 01 (2019): e64-e66. http://dx.doi.org/10.1055/s-0039-1683969.

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AbstractAbnormal coagulation properties indicative of a dysfibrinogenemia were found in the plasma of an asymptomatic 65-year-old male. An immunoglobulin k light chain was found to interfere with Fg functional assay and coagulation tests (activated partial thromboplastin time, prothrombin time, and thrombin time). Steroid therapy reduced the inhibitory effect (after dexamethasone treatment coagulation test and functional Fg value normalized). Spurious dysfibrinogenemia associated with light chain monoclonal gammopathy of undetermined significance was diagnosed.

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14

Mathonnet, Florence, Jean-Yves Peltier, Laurent Roda, et al. "Three New Cases of Dysfibrinogenemia." Thrombosis Research 103, no. 3 (2001): 201–7. http://dx.doi.org/10.1016/s0049-3848(01)00318-8.

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15

Wajima, Takeshi. "Liver Cirrhosis Manifested by Dysfibrinogenemia." Clinical and Applied Thrombosis/Hemostasis 3, no. 2 (1997): 102–3. http://dx.doi.org/10.1177/107602969700300206.

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We report a case in which liver cirrhosis was manifested by dysfibrinogenemia before the diagnosis of liver cirrhosis was made. A patient developed gastrointestinal bleeding and hepatic encephalopathy although liver function tests, prothrombin time (PT), activated partial thromboplastin time (aPTT), bleeding time, fibrin (ogen) degradation products (FDP), and platelet counts were normal. However, thrombin time (TT) was prolonged. The gastrointestinal bleeding (GI bleeding) was successfully treated with cryoprecipitate and fresh frozen plasma (FFP). Key Words: Dysfibrinogenemia—Liver disease—Th

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16

Matsuo, T., S. Okuno, T. Mukaida, S. Ueshima, K. Okada, and O. Matsuo. "A Hereditary Dysfibrinogenemia: Fibrinogen Awaji." Pathophysiology of Haemostasis and Thrombosis 17, no. 1-2 (1987): 89–97. http://dx.doi.org/10.1159/000215563.

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17

Levy, Joseph, Michael J. Pettei, and Jeffrey I. Weitz. "Dysfibrinogenemia in Obstructive Liver Disease." Journal of Pediatric Gastroenterology and Nutrition 6, no. 6 (1987): 967–70. http://dx.doi.org/10.1097/00005176-198711000-00025.

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18

Galanakis, Dennis K., Miriam Rafailovich, and Liudi Zhang. "Hemorrhagic Dysfibrinogenemia Undetectable By Clinical Coagulation Tests and Identified By Isolated Fibrinogen Investigations (Crypto-Dysfibrinogenemia)." Blood 122, no. 21 (2013): 3608. http://dx.doi.org/10.1182/blood.v122.21.3608.3608.

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Abstract A pilot study of isolated 7μM fibrinogen (fg) from 17 probands, with typical clinical coagulation test results and different (heterozygous) missense mutations, yielded acceleration of visually determined clot lysis (CL), which was induced by recombinant tissue plasminogen activator (rtPA,190 nM) in15% afibrinogenemic plasma, pH 7.4. Mean CL time was 44 minutes, control 190 minutes. The diagnosis in a few probands was suspected by mildly abnormal clinical laboratory test results suggesting that normal clinical test results can mask the presence of dysfibrinogenemia. To test this hypoth

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19

Kotlín, Roman, Alžběta Sobotková, Tomáš Riedel, et al. "Acquired Dysfibrinogenemia Secondary to Multiple Myeloma." Acta Haematologica 120, no. 2 (2008): 75–81. http://dx.doi.org/10.1159/000160182.

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20

Kotlin, Roman, Ondrej Pastva, Jaromir Novak, et al. "Two Cases of Dysfibrinogenemia in Childhood." Blood 124, no. 21 (2014): 5066. http://dx.doi.org/10.1182/blood.v124.21.5066.5066.

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Abstract Introduction Hemostasis in childhood differs from that of adults; and the hemostatic system is still developing during childhood. These differences offer a protective advantage to children with hemorrhagic and thrombotic complications. Plasma levels of coagulation factors (except for fibrinogen, factor V and factor VIII), as well as plasma levels of protein C, protein S and antithrombin are reduced. Hereditary dysfibrinogenemia is a rare disorder wherein an inherited abnormality in fibrinogen structure may result in defective fibrin function and/or structure. Clinical symptoms may var

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21

Patil, Rucha, Alfiya Mukaddam, Kanjaksha Ghosh, and Shrimati Shetty. "Management of pregnancy in dysfibrinogenemia cases." Blood Coagulation & Fibrinolysis 28, no. 1 (2017): 91–93. http://dx.doi.org/10.1097/mbc.0000000000000514.

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22

Undas, Anetta. "Acquired dysfibrinogenemia in atherosclerotic vascular disease." Polish Archives of Internal Medicine 121, no. 9 (2011): 310–19. http://dx.doi.org/10.20452/pamw.1083.

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23

Zhou, Rong-Fu, Zhou Na, and OuYang Jian. "Studies on the Genetic Mutations of Hereditary Fibrinogen Disorder." Blood 128, no. 22 (2016): 4954. http://dx.doi.org/10.1182/blood.v128.22.4954.4954.

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Abstract Hereditary fibrinogen disorder is a rare kind of bleeding disease, which divided into two types. Type I is a kind of quantity disorder, including afibrinogenemia and hypofibrinogenemia. Type II is a kind of quality disorder, including dysfibrinogenemia. Fibrinogen is a kind of hexameric glycoprotein and consists of two pairs of three chains, which are Aα, Bβ and γchain. FGA、FGB and FGG code for the relevant glycoprotein. The mutations on these genes are responsible for this disorder. In this study, the levels of fibrinogen antigen of 12 cases with low fibrinogen activity were firstly

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24

Fish, Richard J., Cristina Freire, Corinne Di Sanza, and Marguerite Neerman-Arbez. "Venous Thrombosis and Thrombocyte Activity in Zebrafish Models of Quantitative and Qualitative Fibrinogen Disorders." International Journal of Molecular Sciences 22, no. 2 (2021): 655. http://dx.doi.org/10.3390/ijms22020655.

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Venous thrombosis occurs in patients with quantitative and qualitative fibrinogen disorders. Injury-induced thrombosis in zebrafish larvae has been used to model human coagulopathies. We aimed to determine whether zebrafish models of afibrinogenemia and dysfibrinogenemia have different thrombotic phenotypes. Laser injuries were used to induce venous thrombosis and the time-to-occlusion (TTO) and the binding and aggregation of fluorescent Tg(itga2b:EGFP) thrombocytes measured. The fga−/− larvae failed to support occlusive venous thrombosis and showed reduced thrombocyte binding and aggregation

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25

Fish, Richard J., Cristina Freire, Corinne Di Sanza, and Marguerite Neerman-Arbez. "Venous Thrombosis and Thrombocyte Activity in Zebrafish Models of Quantitative and Qualitative Fibrinogen Disorders." International Journal of Molecular Sciences 22, no. 2 (2021): 655. http://dx.doi.org/10.3390/ijms22020655.

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Venous thrombosis occurs in patients with quantitative and qualitative fibrinogen disorders. Injury-induced thrombosis in zebrafish larvae has been used to model human coagulopathies. We aimed to determine whether zebrafish models of afibrinogenemia and dysfibrinogenemia have different thrombotic phenotypes. Laser injuries were used to induce venous thrombosis and the time-to-occlusion (TTO) and the binding and aggregation of fluorescent Tg(itga2b:EGFP) thrombocytes measured. The fga−/− larvae failed to support occlusive venous thrombosis and showed reduced thrombocyte binding and aggregation

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26

Casini, Alessandro, Marc Blondon, Aurélien Lebreton, et al. "Natural history of patients with congenital dysfibrinogenemia." Blood 125, no. 3 (2015): 553–61. http://dx.doi.org/10.1182/blood-2014-06-582866.

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Key Points Major bleeding, thrombosis, and postpartum hemorrhage are frequent in propositi and relatives with congenital dysfibrinogenemia. Hotspot mutations were not predictive of either phenotype or outcome.

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27

Lebowa, Weronika, Jakub Kenig, and Joanna Zdziarska. "Congenital dysfibrinogenemia as a rare cause of recurrent gastrointestinal bleeding." Polish Journal of Surgery 92, no. 5 (2020): 1–5. http://dx.doi.org/10.5604/01.3001.0014.0948.

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<b>Introduction: </b>Gastrointestinal bleeding is a common disease that surgeons encounter in everyday clinical practice. It is most often easy to diagnose and treat. However, rare causes of bleeding can lead to delayed diagnosis and ineffective treatment. Dysfibrinogenemia is a qualitative fibrinogen disorder in which functional fibrinogen level is reduced with normal antigenic level. <br><b> Case report:</b> Herein we present the case of a 59-year-old female with recurrent gastrointestinal bleeds, that turned out to be an unusual manifestation of congenital dysf

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28

Kotlín, R., A. Sobotková, J. Suttnar, P. Salaj, T. Riedel, and J. E. Dyr. "P047 Acquired dysfibrinogenemia associated with multiple myeloma." Blood Reviews 21 (August 2007): S101. http://dx.doi.org/10.1016/s0268-960x(07)70122-4.

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29

Kotlín, Roman, Eliška Ceznerova, Stikarová Jana, et al. "Four Cases of Aaplha Dysfibrinogenemia in Childhood." Blood 126, no. 23 (2015): 4697. http://dx.doi.org/10.1182/blood.v126.23.4697.4697.

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Abstract Introduction Hemostasis in childhood differs from that of adults; and the hemostatic system is still developing during childhood. These differences offer a protective advantage to children with hemorrhagic and thrombotic complications. Plasma levels of coagulation factors (except for fibrinogen, factor V and factor VIII), as well as plasma levels of protein C, protein S and antithrombin are reduced. Hereditary dysfibrinogenemia is a rare disorder wherein an inherited abnormality in fibrinogen structure may result in defective fibrin function and/or structure. Clinical symptoms may var

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30

Bin, Qiong, Fang Liang, Dan-yan Ou, Hai-rong Cui, and Jian-ming Luo. "Two symptomatic cases of dysfibrinogenemia in China." Blood Coagulation & Fibrinolysis 26, no. 5 (2015): 564–71. http://dx.doi.org/10.1097/mbc.0000000000000290.

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31

Munoz, Javier, Jessica Schering, Angela Lambing, et al. "The dilemma of inherited dysfibrinogenemia during pregnancy." Blood Coagulation & Fibrinolysis 23, no. 8 (2012): 775–77. http://dx.doi.org/10.1097/mbc.0b013e328358e96d.

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32

Mori, Takehiko, Mitsuru Murata, Masatoshi Wakui, et al. "Acquired dysfibrinogenemia following allogeneic bone marrow transplantation." American Journal of Hematology 56, no. 4 (1997): 294–95. http://dx.doi.org/10.1002/(sici)1096-8652(199712)56:4<294::aid-ajh17>3.0.co;2-9.

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33

Merkulova, Alona A., Steven C. Mitchell, Sergei Merkulov, Alisa S. Wolberg, Neerman-Arbez Marguerite, and Alvin H. Schmaier. "Acquired Dysfibrinogenemia Krakow III after Everolimus Therapy." Blood 134, Supplement_1 (2019): 4934. http://dx.doi.org/10.1182/blood-2019-131319.

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A 45 yo woman with a medical history of common variable immunodifficiency (CVID) was referred for a bleeding disorder. The bleeding was manifested daily with ecchymosis and epistaxis, but prior to the visit, she developed a lower pelvic mass that was a massive hematoma requiring transfusion. In 2011 she had a splenectomy for thrombocytopenia. After splenectomy, her liver enlarged and one year prior to being seen, she was started on everolimus as part of a protocol to reduce her liver size. Bleeding started 3-6 months after starting everolimus treatment, first manifesting with recurrent lower g

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34

Khare, Manika, Vijay Kumar, Sadhna Marwah, A. S. Nigam, and Gurdeep Buxi. "Dysfibrinogenemia with Subgaleal Hematoma: An Unusual Presentation." Indian Journal of Hematology and Blood Transfusion 32, S1 (2015): 239–41. http://dx.doi.org/10.1007/s12288-015-0606-2.

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35

Yamanaka, Yoshihiko, Kyousuke Takeuchi, Makoto Sugimoto, Asomi Sato, Satoshi Nakago, and Takeshi Maruo. "Dysfibrinogenemia during pregnancy treated successfully with fibrinogen." Acta Obstetricia et Gynecologica Scandinavica 82, no. 10 (2003): 972–73. http://dx.doi.org/10.1034/j.1600-0412.2003.00211.x.

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36

La Gioia, A., A. Barsotti, M. Petrini, F. Veneziani, and A. Lofaro. "A new case of dysfibrinogenemia: Fibrinogen pontedera." Thrombosis Research 61 (January 1991): 111. http://dx.doi.org/10.1016/0049-3848(91)90622-4.

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37

Hessel, B., S. Stenbjerg, J. Dyr, B. Kudryk, L. Therkildsen, and B. Blombäck. "Fibrinogen Aarhus — a new case of dysfibrinogenemia." Thrombosis Research 42, no. 1 (1986): 21–37. http://dx.doi.org/10.1016/0049-3848(86)90193-3.

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38

Miesbach, Wolfgang A., D. K. Galanakis, and Inge Scharrer. "Congenital Dysfibrinogenemia - Clinical Manifestations in Relation to the Fibrinogen Gene Mutation." Blood 106, no. 11 (2005): 2138. http://dx.doi.org/10.1182/blood.v106.11.2138.2138.

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Abstract The congenital dysfibrinogenemia is a rare clotting disorder which is based on a structural defect in the fibrinogen molecule. Approximately 350 cases of unrelated families with dysfibrinogenemia have been reported. Of these, the structural defects have been determined in nearly 170 families. Patients and methods: We describe the clinical manifestations in 50 patients from 19 families from Frankfurt. Up to now the underlying structural defect could be found in 43/50 (86 %) of the patients and 14/19 (74 %) of the families (Galanakis, New York, von Depka, Hannover). Results: In 19 famil

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39

Purohit, AbhishekH L., HaraP Pati, Mukul Aggrawal, and Mrinalini Kotru. "Platelet aggregation study: valuable aid to diagnose dysfibrinogenemia." Egyptian Journal of Haematology 40, no. 1 (2015): 11. http://dx.doi.org/10.4103/1110-1067.155783.

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40

Okumura, Nobuo, and Fumiko Terasawa. "Analysis for dysfibrinogenemia and hypofibrinogenemia with electrophoretic methods." SEIBUTSU BUTSURI KAGAKU 44, no. 4 (2000): 283–88. http://dx.doi.org/10.2198/sbk.44.283.

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41

Ducloy-Bouthors, A. S., A. F. Dalmas-Laurent, N. Coutty, et al. "P10 ROTEM® analysis for dysfibrinogenemia in pregnancy." Thrombosis Research 123 (January 2009): S142. http://dx.doi.org/10.1016/s0049-3848(09)70055-6.

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42

Dawson, N. A., C. F. Barr, and B. M. Alving. "Acquired Dysfibrinogenemia. Paraneoplastic Syndrome in Renal Cell Carcinoma." Journal of Urology 134, no. 2 (1985): 428. http://dx.doi.org/10.1016/s0022-5347(17)47198-9.

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43

Imafuku, Yuji, Kyoko Tanaka, Kiyoaki Takahashi та ін. "Identification of a dysfibrinogenemia of γR275C (Fibrinogen Fukushima)". Clinica Chimica Acta 325, № 1-2 (2002): 151–56. http://dx.doi.org/10.1016/s0009-8981(02)00293-0.

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44

Depoorter, M., and S. Eeckhoudt. "A dysfibrinogenemia leading to resistance to bovine thrombin." Acta Clinica Belgica 69, no. 6 (2014): 451–53. http://dx.doi.org/10.1179/2295333714y.0000000058.

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45

Kotlín, Roman, Bohumír Blažek, Jiří Suttnar, Martin Malý, Jan Kvasnička, and Jan E. Dyr. "Dysfibrinogenemia in childhood: two cases of congenital dysfibrinogens." Blood Coagulation & Fibrinolysis 21, no. 7 (2010): 640–48. http://dx.doi.org/10.1097/mbc.0b013e32833e4284.

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46

Yan, Jie, Donghong Deng, Peng Cheng, Lin Liao, Meiling Luo, and Faquan Lin. "Management of dysfibrinogenemia in pregnancy: A case report." Journal of Clinical Laboratory Analysis 32, no. 3 (2017): e22319. http://dx.doi.org/10.1002/jcla.22319.

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47

Al-Fawaz, I. M., and A. M. A. Gader. "Severe Congenital Dysfibrinogenemia (Fibrinogen-Riyadh): A Family Study." Acta Haematologica 88, no. 4 (1992): 194–97. http://dx.doi.org/10.1159/000204685.

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48

Dawson, Nancy A., Charles F. Barr, and Barbara M. Alving. "Acquired dysfibrinogenemia. Paraneoplastic syndrome in renal cell carcinoma." American Journal of Medicine 78, no. 4 (1985): 682–86. http://dx.doi.org/10.1016/0002-9343(85)90414-0.

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49

Ashby, Mark A., and John Lazarchick. "Case Report: Acquired Dysfibrinogenemia Secondary to Mithramycin Toxicity." American Journal of the Medical Sciences 292, no. 1 (1986): 53–55. http://dx.doi.org/10.1097/00000441-198607000-00011.

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50

Batorova, Angelika, Daniela Horvathova, Martin Mistrik, Philippe de Moerloose, and Marguerite Neerman-Arbez. "Genetic and Phenotypic Analysis of Families with Inherited Hypo- and Dys-Fibrinogenemia. Fibrinogen Bratislava." Blood 106, no. 11 (2005): 1794. http://dx.doi.org/10.1182/blood.v106.11.1794.1794.

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Abstract Inherited hypofibrinogenemia (hypo-FBG) and dysfibrinogenemia (dys-FBG) are rare blood coagulation disorders caused by quantitative or qualitative defects of fibrinogen. We reviewed the clinical course in 47 individuals with dys-FBG and 16 patients with hypo-FBG with median fibrinogen coagulant/antigen levels of 0.76/2.8 and 1.1/1.2 g/L, respectively. Genetic analysis was performed in 5 families (16 individuals) with dys-FBG and 4 families (8 individuals) with hypo-FBG. In the dysfibrinogenemia group 21 (45%) individuals were asymptomatic, 24(51%) patients suffered from bleeding and/o

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