Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.

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 tocilizu...

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Autores principales:	Sho Mokuda, Yosuke Murata, Naoya Sawada, Kenichiro Matoba, Akihiro Yamada, Makoto Onishi, Yasuaki Okuda, Kazuo Jouyama, Eiji Sugiyama, Kiyoshi Takasugi
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/95ca42b5c6ca459fb627e05c4c2b9400
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spelling	oai:doaj.org-article:95ca42b5c6ca459fb627e05c4c2b94002021-11-18T09:01:43ZTocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.1932-620310.1371/journal.pone.0069944https://doaj.org/article/95ca42b5c6ca459fb627e05c4c2b94002013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23936360/?tool=EBIhttps://doaj.org/toc/1932-6203Factor 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.Sho MokudaYosuke MurataNaoya SawadaKenichiro MatobaAkihiro YamadaMakoto OnishiYasuaki OkudaKazuo JouyamaEiji SugiyamaKiyoshi TakasugiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e69944 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sho Mokuda Yosuke Murata Naoya Sawada Kenichiro Matoba Akihiro Yamada Makoto Onishi Yasuaki Okuda Kazuo Jouyama Eiji Sugiyama Kiyoshi Takasugi Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.
description	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.
format	article
author	Sho Mokuda Yosuke Murata Naoya Sawada Kenichiro Matoba Akihiro Yamada Makoto Onishi Yasuaki Okuda Kazuo Jouyama Eiji Sugiyama Kiyoshi Takasugi
author_facet	Sho Mokuda Yosuke Murata Naoya Sawada Kenichiro Matoba Akihiro Yamada Makoto Onishi Yasuaki Okuda Kazuo Jouyama Eiji Sugiyama Kiyoshi Takasugi
author_sort	Sho Mokuda
title	Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.
title_short	Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.
title_full	Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.
title_fullStr	Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.
title_full_unstemmed	Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.
title_sort	tocilizumab induced acquired factor xiii deficiency in patients with rheumatoid arthritis.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/95ca42b5c6ca459fb627e05c4c2b9400
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Tocilizumab induced acquired factor XIII deficiency in patients with rheumatoid arthritis.

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