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001-es BibID:	BIBFORM125745
035-os BibID:	(scopus)85197919739 (wos)001252813300001
Első szerző:	Gonda Lénárd (Általános orvos)
Cím:	Monoclonal whole IgG impairs both fibrin and thrombin formation : hemostasis and surface plasmon resonance studies / Gonda Lénárd, Torner Bernadett, Ghansah Harriet, Beke Debreceni Ildikó, Váróczy László, Pénzes-Daku Krisztina, Kappelmayer János
Dátum:	2024
ISSN:	1434-6621
Megjegyzések:	Objectives: Monoclonal gammopathies frequently associate with hemostatic alterations. Thrombotic events occur with high incidence particularly upon treatment, while in rarer cases hemorrhagic diathesis can be observed. The pathology of these tendencies could be caused by thrombocytopenia or hyperviscosity burden of circulating monoclonal antibodies. Studies also suggest interference of monoclonal antibodies with primary hemostasis. We isolated monoclonal whole IgG paraproteins from two myeloma patients to observe their effect on thrombin formation and fibrin polymerization. Methods: Monoclonal whole IgG was prepared from sera of two newly diagnosed untreated multiple myeloma patients and control normal plasma samples. Fibrin formation was measured using thrombin time and dilute prothrombin time tests and thrombin formation was detected with a fluorimetric thrombin generation assay. In addition, molecular interactions were investigated by surface plasmon resonance (SPR). Results: Thrombin time was prolonged upon addition of monoclonal IgG even at 30 g/L by 12 %, increasing up to 36 % at 60 g/L concentration. Dilute prothrombin time was prolonged by 20 % even at 30 g/L. Thrombin generation assay indicated an impairment in thrombin formation at the presence of monoclonal IgG compared to polyclonal at equivalent concentration. By an SPR assay we determined that both clonality IgG preparations interacted with fibrinogen, however interaction with human thrombin was only detected with monoclonal immunoglobulins (KD=1.03 ? 10-7 M). Conclusions: Here we provide evidence that isolated monoclonal whole IgG from myeloma patients can impair both fibrin and thrombin formation and we demonstrate by SPR assay that it interacts with components of the final phase of the coagulation system.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk fibrinogen monoclonal IgG Myelóma multiplex trombin
Megjelenés:	Clinical Chemistry And Laboratory Medicine. - 62 : 9 (2024), p. 1863-1869. -
További szerzők:	Torner Bernadett (1997-) (molekuláris biológus) Ghansah, Harriet (1987-) (PhD) Bekéné Debreceni Ildikó (1970-) (biológus) Váróczy László (1974-) (belgyógyász, haematológus) Pénzes-Daku Krisztina (1978-) (biológus) Kappelmayer János (1960-) (absztraktok)
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001-es BibID:	BIBFORM068933
Első szerző:	Hudák Renáta
Cím:	Laboratory characterization of leukemic cell procoagulants / Renáta Hudák, Ildikó Beke Debreceni, Ivett Deák, Gabriella Gál Szabó, Zsuzsanna Hevessy, Péter Antal-Szalmás, Bjarne Osterud, János Kappelmayer
Dátum:	2017
ISSN:	1434-6621
Megjegyzések:	Background: In acute myeloid leukemias, there is anincreased chance to develop thrombotic disorders. Wehypothesized that in addition to leukemic promyelocytes,monocytic leukemia cells may also have a higher procoagulantactivity.Methods: Fibrin formation was assessed by a one-stageclotting assay using a magnetic coagulometer. The thrombingeneration test (TGT) of magnetically isolated normalhuman monocytes, intact leukemic cells and their isolatedmicroparticles was performed by a fluorimetric assay.Phosphatidylserine (PS) expression of leukemic cells andmicroparticle number determinations were carried out byflow cytometry.Results: All cell lines displayed a significant procoagulantpotential compared to isolated normal human monocytes.In the TGT test, the mean of lagtime and the time to peakparameters were significantly shorter in leukemic cells(3.9?4.7 and 9.9?10.3 min) compared to monocytes (14.9and 26.5 min). The mean of peak thrombin in variousmonocytic leukemia cell lines was 112.1?132.9 nM vs.75.1 nM in monocytes; however, no significant differencewas observed in the ETP parameter. Factor VII-deficientplasma abolished all procoagulant activity, whereas factorXII-deficient plasma did not affect the speed of fibrinformation and thrombin generation but modulated theamount of thrombin. Factor XI-deficient plasma affectedthe time to peak values in one leukemic cell line and alsoattenuated peak thrombin. Leukemia cell-derived microparticlesfrom all three cell lines exerted a procoagulanteffect by significantly shortening the lagtime in TGT; therewas a nonsignificant difference in case of ETP parameter.Conclusions: All investigated monocytic leukemia celllines exhibited significant thrombin generation. This phenomenonwas achieved by the procoagulants on the surfaceof leukemic cells as well as by their microparticles.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban monocytic leukemia tissue factor
Megjelenés:	Clinical Chemistry and Laboratory Medicine 55 : 8 (2017), p. 1215-1223. -
További szerzők:	Bekéné Debreceni Ildikó (1970-) (biológus) Deák Ivett Gál Szabó Gabriella Hevessy Zsuzsanna (1966-) (laboratóriumi szakorvos) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Osterud, Bjarne Kappelmayer János (1960-) (laboratóriumi szakorvos)
Pályázati támogatás:	TÁMOP-4.2.4.A/2-11-1-2012-0001 TÁMOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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