Study of the formation of fibrin clot in cirrhotic patients. An approach to study of acquired dysfibrinogenemia

Regañón, Edelmiro; Vila, Virtudes; Aznar, Justo; Garrido, Guillermo; Estellés, Amparo; Berenguer, J

doi:10.1016/0049-3848(87)90272-6

Cited by 12 publications

(5 citation statements)

References 22 publications

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“…Accordingly, the amplitude and maximal velocity of the TT coagulation curve allowed us to discriminate between hypofibrinogenemia, DIC and heparin inhibition, and FGG p.Arg301(275)Cys dysfibrinogenemia. In future studies, it will be interesting to evaluate the TT coagulation curve parameters from samples of patients who carry different mutations responsible for congenital dysfibrinogenemia and from additional patients with acquired low fibrinogen Clauss levels, in particular case of liver diseases .…”

Section: Discussionmentioning

confidence: 99%

The amplitude of coagulation curves from thrombin time tests allows dysfibrinogenemia caused by the common mutation FGG‐Arg301 to be distinguished from hypofibrinogenemia

Jacquemin

Vanlinthout

Horenbeeck

et al. 2017

Int J Lab Hematology

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Section: Discussionmentioning

confidence: 99%

The amplitude of coagulation curves from thrombin time tests allows dysfibrinogenemia caused by the common mutation FGG‐Arg301 to be distinguished from hypofibrinogenemia

Jacquemin

Vanlinthout

Horenbeeck

et al. 2017

Int J Lab Hematology

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“…Through high-throughput phage display library bio-panning, Wang et al discovered the new peptide pep-20, which selectively targets CD47 and blocks CD47/SIRPα axis [133]. RS17, a different CD47-targeted peptide, was created by using MOE analysis and is demonstrated to selectively bind to CD47's extracellular domain [134]. Due to their smaller size compared to larger biomolecules, peptides have higher tissue penetration and lower systemic toxicity concerns [118,119].…”

Section: Peptidesmentioning

confidence: 99%

“…Additionally, since peptides are simple to generate and store, they could be artificially changed at a minimal cost. Peptide medicines act as vaccines or therapeutic carriers, inducing tumor cell death and preventing angiogenesis, which have demonstrated distinct benefits and broad application potential [133,134].…”

Section: Peptidesmentioning

confidence: 99%

Anti-Tumor Strategies by Harnessing the Phagocytosis of Macrophages

Guo

Tian

et al. 2023

Cancers

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Macrophages are essential for the human body in both physiological and pathological conditions, engulfing undesirable substances and participating in several processes, such as organism growth, immune regulation, and maintenance of homeostasis. Macrophages play an important role in anti-bacterial and anti-tumoral responses. Aberrance in the phagocytosis of macrophages may lead to the development of several diseases, including tumors. Tumor cells can evade the phagocytosis of macrophages, and “educate” macrophages to become pro-tumoral, resulting in the reduced phagocytosis of macrophages. Hence, harnessing the phagocytosis of macrophages is an important approach to bolster the efficacy of anti-tumor treatment. In this review, we elucidated the underlying phagocytosis mechanisms, such as the equilibrium among phagocytic signals, receptors and their respective signaling pathways, macrophage activation, as well as mitochondrial fission. We also reviewed the recent progress in the area of application strategies on the basis of the phagocytosis mechanism, including strategies targeting the phagocytic signals, antibody-dependent cellular phagocytosis (ADCP), and macrophage activators. We also covered recent studies of Chimeric Antigen Receptor Macrophage (CAR-M)-based anti-tumor therapy. Furthermore, we summarized the shortcomings and future applications of each strategy and look into their prospects with the hope of providing future research directions for developing the application of macrophage phagocytosis-promoting therapy.

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“…The production of autoantibodies directed against fibrinogen as a cause of dysfibrinogenemia has been observed in the past [3,4,5,6]. Acquired dysfibrinogenemia occurs mainly as a disorder secondary to liver disease [7,8,9], liver cirrhosis [10, 11], multiple myeloma [12,13,14,15], hepatoma [16, 17], paraneoplastic syndrome [18] or digital ischemia and gangrene [19]. It was reported that acquired dysfibrinogenemia may be associated with drug usage [20, 21], antifibrinogen antibody presence [4] or allogeneic bone marrow transplantation [22].…”

Section: Introductionmentioning

confidence: 99%

Acquired Dysfibrinogenemia Secondary to Multiple Myeloma

et al. 2008

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Abnormal coagulation properties indicative of a dysfibrinogen were found in the plasma of a 72-year-old male with multiple myeloma (IgGĸ, stage IIIA). The patient had high paraprotein concentration (85.75 g/l) and prolonged thrombin time (76.8 s), activated partial thromboplastin time (39.5 s), prothrombin time (23.5 s) and reptilase time (72.0 s). The fibrinogen level was increased. The fibrin polymerization induced by both thrombin and reptilase was impaired. Scanning electron microscopy revealed abnormal clot morphology. After six months of treatment, the paraprotein level decreased (19.48 g/l) and coagulation normalized as well as fibrin polymerization and fibrin clot morphology. It was found that the paraprotein interacts with the γ-chain of fibrinogen. Acquired dysfibrinogenemia associated with multiple myeloma was diagnosed in the 72-year-old patient.

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Study of the formation of fibrin clot in cirrhotic patients. An approach to study of acquired dysfibrinogenemia

Cited by 12 publications

References 22 publications

The amplitude of coagulation curves from thrombin time tests allows dysfibrinogenemia caused by the common mutation FGG‐Arg301 to be distinguished from hypofibrinogenemia

The amplitude of coagulation curves from thrombin time tests allows dysfibrinogenemia caused by the common mutation FGG‐Arg301 to be distinguished from hypofibrinogenemia

Anti-Tumor Strategies by Harnessing the Phagocytosis of Macrophages

Acquired Dysfibrinogenemia Secondary to Multiple Myeloma

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