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Kiyoshi Takasugi - One of the best experts on this subject based on the ideXlab platform.
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tocilizumab induced acquired Factor XIII Deficiency in patients with rheumatoid arthritis
PLOS ONE, 2013Co-Authors: Sho Mokuda, Yosuke Murata, Naoya Sawada, Kenichiro Matoba, Akihiro Yamada, Makoto Onishi, Yasuaki Okuda, Kazuo Jouyama, Eiji Sugiyama, Kiyoshi TakasugiAbstract:Factor XIII is one of the twelve coagulation Factors and also known as a fibrin-stabilizing Factor. In 2012, we encountered a male RA patient with hemorrhagic Factor XIII Deficiency who had been treated with tocilizumab for two years. There are few reports regarding the relationship between tocilizumab (a humanized monoclonal antibody against the interleukin-6 receptor (IL-6R)) and Factor XIII. We measured the Factor XIII activity levels in the plasma of 40 RA patients (10 patients treated without biologics, 30 patients treated with biologics (15 patients treated with necrosis Factor inhibitors and 15 patients treated with tocilizumab)) and 19 healthy controls. Consequently, the tocilizumab group exhibited lower levels than the other three groups according to the Steel-Dwass test (P<0.01). Furthermore, we compared the plasma Factor XIII activity levels and the plasma Factor XIII concentrations in the RA patients treated with biologics. Pearson's correlation test was used to assess the relationship between the Factor XIII activity levels and the plasma Factor XIII concentrations (r=0.449, P=0.019). According to the multiple regression analysis, the treatment with tocilizumab is an independent risk Factor for plasma Factor XIII reduction in RA patients. In conclusion, RA patients treated with tocilizumab, an IL-6R blocker, are at risk of developing acquired Factor XIII Deficiency. The mechanisms underlying the reduced Factor XIII activity observed in RA patients treated with tocilizumab may result from the quantitative reduction in the plasma. These data imply that IL-6 plays an important role in maintaining the Factor XIII activity level.
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Tocilizumab induced acquired Factor XIII Deficiency in patients with rheumatoid arthritis.
PloS one, 2013Co-Authors: Sho Mokuda, Yosuke Murata, Naoya Sawada, Kenichiro Matoba, Akihiro Yamada, Makoto Onishi, Yasuaki Okuda, Kazuo Jouyama, Eiji Sugiyama, Kiyoshi TakasugiAbstract:Factor XIII is one of the twelve coagulation Factors and also known as a fibrin-stabilizing Factor. In 2012, we encountered a male RA patient with hemorrhagic Factor XIII Deficiency who had been treated with tocilizumab for two years. There are few reports regarding the relationship between tocilizumab (a humanized monoclonal antibody against the interleukin-6 receptor (IL-6R)) and Factor XIII. We measured the Factor XIII activity levels in the plasma of 40 RA patients (10 patients treated without biologics, 30 patients treated with biologics (15 patients treated with necrosis Factor inhibitors and 15 patients treated with tocilizumab)) and 19 healthy controls. Consequently, the tocilizumab group exhibited lower levels than the other three groups according to the Steel-Dwass test (P
Ali Canbay - One of the best experts on this subject based on the ideXlab platform.
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rotational thromboelastometry can detect Factor XIII Deficiency and bleeding diathesis in patients with cirrhosis
Liver International, 2017Co-Authors: S Bedreli, Janpeter Sowa, Saraa Malek, Sandra Blomeyer, Antonios Katsounas, Guido Gerken, Fuat H Saner, Ali CanbayAbstract:Background & Aims Patients with progressive liver disease exhibit complex coagulation disorders. Factor XIII plays a crucial role in the last steps of haemostasis, and its Deficiency is associated with an increased incidence of bleeding diathesis. However, current conventional coagulation tests cannot detect Factor XIII Deficiency. In this study, we examined Factor XIII activity and the ability of rotational thromboelastometry to detect Factor XIII Deficiency and bleeding diathesis in patients with cirrhosis. Methods We retrospectively studied 74 patients with cirrhosis, comparing the results of conventional coagulation tests (international normalized ratio, activated partial thromboplastin time, platelet count, fibrinogen level), rotational thromboelastometry, Factor XIII activity and clinical scores. Results Patients with cirrhosis exhibited reduced Factor XIII activity. Factor XIII activity was positively correlated with conventional coagulation parameters and rotational thromboelastometry values, such as maximum clot formation (MCF)extem (r=.48, P<.0001) and MCFfibtem (r=.60, P<.0001). However, maximum lysis (ML)extem and MLaptem were not correlated with Factor XIII activity. Three-month mortality rates (P=.0469) and bleeding complications (P<.0001) were significantly associated with lower Factor XIII activity. Patients with haemorrhage exhibited significantly altered rotational thromboelastometry values. Conclusions Reduced levels of MCFextem and MCFfibtem but not high levels of MLextem and MLaptem are associated with Factor XIII Deficiency in patients with liver disease. Therefore, substituting Factor XIII should be considered for such patients to strengthen clot formation in patients experiencing haemorrhage or those who have undergone interventions.
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Rotational thromboelastometry can detect Factor XIII Deficiency and bleeding diathesis in patients with cirrhosis
Liver international : official journal of the International Association for the Study of the Liver, 2016Co-Authors: S Bedreli, Janpeter Sowa, Saraa Malek, Sandra Blomeyer, Antonios Katsounas, Guido Gerken, Fuat H Saner, Ali CanbayAbstract:Background & Aims Patients with progressive liver disease exhibit complex coagulation disorders. Factor XIII plays a crucial role in the last steps of haemostasis, and its Deficiency is associated with an increased incidence of bleeding diathesis. However, current conventional coagulation tests cannot detect Factor XIII Deficiency. In this study, we examined Factor XIII activity and the ability of rotational thromboelastometry to detect Factor XIII Deficiency and bleeding diathesis in patients with cirrhosis. Methods We retrospectively studied 74 patients with cirrhosis, comparing the results of conventional coagulation tests (international normalized ratio, activated partial thromboplastin time, platelet count, fibrinogen level), rotational thromboelastometry, Factor XIII activity and clinical scores. Results Patients with cirrhosis exhibited reduced Factor XIII activity. Factor XIII activity was positively correlated with conventional coagulation parameters and rotational thromboelastometry values, such as maximum clot formation (MCF)extem (r=.48, P
Daisuke Takahashi - One of the best experts on this subject based on the ideXlab platform.
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Hemorrhagic-acquired Factor XIII Deficiency associated with tocilizumab for treatment of rheumatoid arthritis
International journal of hematology, 2012Co-Authors: Masatake Matsuoka, Tokifumi Majima, Tomohiro Onodera, Masahiro Ieko, Masayoshi Souri, Akitada Ichinose, Takashi Kurita, Yasuhiko Kasahara, Masahiro Inoue, Daisuke TakahashiAbstract:Factor XIII (FXIII) is the final enzyme in the coagulation cascade. Acquired FXIII Deficiency is caused by inhibitors of FXIII or decreased synthesis and/or increased consumption of FXIII, which leads to severe bleeding. Recently, we experienced a case of hemorrhagic-acquired Factor XIII Deficiency that occurred during treatment with the IL-6 inhibitor tocilizumab for rheumatoid arthritis. A 48-year-old man was referred because of right hip pain due to a hematoma. Laboratory findings showed that routine coagulation tests were normal, while FXIII activity was slightly low (52.4 %). The patient was successfully treated with plasma-derived Factor XIII concentrates. The time course of recovery suggests that tocilizumab might have inhibited FXIII production. To our knowledge, this is the first report of acquired Factor XIII Deficiency associated with administering of tocilizumab. When recurrent bleeding is seen during administering of tocilizumab, acquired Factor XIII Deficiency may have been induced, thus attending physicians should consider this disease in a differential diagnosis.
Rosalind Dietrich - One of the best experts on this subject based on the ideXlab platform.
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Factor XIII Deficiency mistaken for battered child syndrome case of correct test ordering negated by a commonly accepted qualitative test with limited negative predictive value
American Journal of Hematology, 2002Co-Authors: Richard S. Newman, Mehrdad Jalili, Bradley J. Kolls, Rosalind DietrichAbstract:We report herein a case of Factor XIII Deficiency that remained undiagnosed until 2 years of age. Part of the delay in diagnosis was a consequence of testing that was performed on a blood sample obtained after plasma transfusion therapy for a life-threatening bleeding episode. Due to insufficient family follow-up after discharge from the hospital, the diagnosis was delayed 1 year until the child was rehospitalized and a pre-transfusion plasma sample was tested. The commonly accepted approach of using only a qualitative test for the diagnosis of Factor XIII Deficiency is challenged by this case report. Am. J. Hematol. 71:328–330, 2002. © 2002 Wiley-Liss, Inc.
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Factor XIII Deficiency mistaken for battered child syndrome: case of "correct" test ordering negated by a commonly accepted qualitative test with limited negative predictive value.
American journal of hematology, 2002Co-Authors: Richard S. Newman, Mehrdad Jalili, Bradley J. Kolls, Rosalind DietrichAbstract:We report herein a case of Factor XIII Deficiency that remained undiagnosed until 2 years of age. Part of the delay in diagnosis was a consequence of testing that was performed on a blood sample obtained after plasma transfusion therapy for a life-threatening bleeding episode. Due to insufficient family follow-up after discharge from the hospital, the diagnosis was delayed 1 year until the child was rehospitalized and a pre-transfusion plasma sample was tested. The commonly accepted approach of using only a qualitative test for the diagnosis of Factor XIII Deficiency is challenged by this case report.
Carl-erik Dempfle - One of the best experts on this subject based on the ideXlab platform.
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Factor XIII Deficiency associated with valproate treatment.
Epilepsia, 2004Co-Authors: Martin Teich, Carl-erik Dempfle, Elke Longin, Stephan KönigAbstract:Summary: Purpose: We present two children who developed a Deficiency of Factor XIII with valproate (VPA) treatment. This coagulation disorder has not been described in association with VPA treatment in children, and only very recently in one adult patient. Results: Both patients showed recurrent epistaxis as major clinical sign of a combination of decreased coagulation parameters (Factor XIII Deficiency with thrombocytopenia and decreased von Willebrand Factor, respectively). A few days after reduction or withdrawal of VPA treatment, clinical symptoms disappeared, and laboratory findings were within normal range. Conclusions: VPA is known to influence the synthetic function of the liver and the number and function of megakaryocytes. Therefore an alteration of the Factor XIII level by VPA is conceivable. Our case reports suggest that bleeding symptoms during VPA treatment may be caused or aggravated by a decreased Factor XIII activity. A determination of Factor XIII activity should be considered before surgical procedures during VPA treatment to minimize the risk of (severe) postsurgical bleeding complications.
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Valproate induces reversible Factor XIII Deficiency with risk of perioperative bleeding
Acta neurologica Scandinavica, 2003Co-Authors: B. Pohlmann-eden, C. N. A. Peters, R. Wennberg, Carl-erik DempfleAbstract:The antiepileptic drug valproic acid (VPA) induces subclinical changes in both the intrinsic and extrinsic coagulation system. However, fatal bleeding is very rare. This study reports a 39-year-old patient who underwent selective amygdalohippocampectomy because of drug-resistant temporal lobe epilepsy. Preoperatively, the patient was on a combined therapy with VPA and topiramate, and routine coagulation laboratory parameters were entirely normal. Epilepsy surgery was immediately followed by severe intracranial bleeding events which promped repeated craniectomy. Extensive laboratory analyses revealed a Factor XIII activity level of 17%, indicating Factor XIII Deficiency confirmed by a reduced XIIIA-antigen. After termination of treatment with VPA, Factor XIII levels returned to normal. Control examinations after 9 and 24 months showed normal range values for all coagulation parameters, including Factor XIII, platelet function, and von Willebrand Factor. To our knowledge, this case is the first description of a well-documented, clinically relevant transient Factor XIII-Deficiency syndrome related to VPA treatment.
