Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency

Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembo...
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Autor*in:	Koken Ameku [verfasserIn] Mariko Higa [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Übergeordnetes Werk:	In: Case Reports in Hematology - Hindawi Limited, 2011, (2018)
Übergeordnetes Werk:	year:2018

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1155/2018/5217301

Katalog-ID:	DOAJ030480655

Internformat


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520			\|a Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard.
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publishDate	2018
allfields	10.1155/2018/5217301 doi (DE-627)DOAJ030480655 (DE-599)DOAJ7ebcac8cef7f4d99868c4235a84c287c DE-627 ger DE-627 rakwb eng RC633-647.5 Koken Ameku verfasserin aut Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard. Diseases of the blood and blood-forming organs Mariko Higa verfasserin aut In Case Reports in Hematology Hindawi Limited, 2011 (2018) (DE-627)668311819 (DE-600)2627639-2 20906579 nnns year:2018 https://doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/article/7ebcac8cef7f4d99868c4235a84c287c kostenfrei http://dx.doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/toc/2090-6560 Journal toc kostenfrei https://doaj.org/toc/2090-6579 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2018
spelling	10.1155/2018/5217301 doi (DE-627)DOAJ030480655 (DE-599)DOAJ7ebcac8cef7f4d99868c4235a84c287c DE-627 ger DE-627 rakwb eng RC633-647.5 Koken Ameku verfasserin aut Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard. Diseases of the blood and blood-forming organs Mariko Higa verfasserin aut In Case Reports in Hematology Hindawi Limited, 2011 (2018) (DE-627)668311819 (DE-600)2627639-2 20906579 nnns year:2018 https://doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/article/7ebcac8cef7f4d99868c4235a84c287c kostenfrei http://dx.doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/toc/2090-6560 Journal toc kostenfrei https://doaj.org/toc/2090-6579 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2018
allfields_unstemmed	10.1155/2018/5217301 doi (DE-627)DOAJ030480655 (DE-599)DOAJ7ebcac8cef7f4d99868c4235a84c287c DE-627 ger DE-627 rakwb eng RC633-647.5 Koken Ameku verfasserin aut Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard. Diseases of the blood and blood-forming organs Mariko Higa verfasserin aut In Case Reports in Hematology Hindawi Limited, 2011 (2018) (DE-627)668311819 (DE-600)2627639-2 20906579 nnns year:2018 https://doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/article/7ebcac8cef7f4d99868c4235a84c287c kostenfrei http://dx.doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/toc/2090-6560 Journal toc kostenfrei https://doaj.org/toc/2090-6579 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2018
allfieldsGer	10.1155/2018/5217301 doi (DE-627)DOAJ030480655 (DE-599)DOAJ7ebcac8cef7f4d99868c4235a84c287c DE-627 ger DE-627 rakwb eng RC633-647.5 Koken Ameku verfasserin aut Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard. Diseases of the blood and blood-forming organs Mariko Higa verfasserin aut In Case Reports in Hematology Hindawi Limited, 2011 (2018) (DE-627)668311819 (DE-600)2627639-2 20906579 nnns year:2018 https://doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/article/7ebcac8cef7f4d99868c4235a84c287c kostenfrei http://dx.doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/toc/2090-6560 Journal toc kostenfrei https://doaj.org/toc/2090-6579 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2018
allfieldsSound	10.1155/2018/5217301 doi (DE-627)DOAJ030480655 (DE-599)DOAJ7ebcac8cef7f4d99868c4235a84c287c DE-627 ger DE-627 rakwb eng RC633-647.5 Koken Ameku verfasserin aut Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard. Diseases of the blood and blood-forming organs Mariko Higa verfasserin aut In Case Reports in Hematology Hindawi Limited, 2011 (2018) (DE-627)668311819 (DE-600)2627639-2 20906579 nnns year:2018 https://doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/article/7ebcac8cef7f4d99868c4235a84c287c kostenfrei http://dx.doi.org/10.1155/2018/5217301 kostenfrei https://doaj.org/toc/2090-6560 Journal toc kostenfrei https://doaj.org/toc/2090-6579 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2018
language	English
source	In Case Reports in Hematology (2018) year:2018
sourceStr	In Case Reports in Hematology (2018) year:2018
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Diseases of the blood and blood-forming organs
isfreeaccess_bool	true
container_title	Case Reports in Hematology
authorswithroles_txt_mv	Koken Ameku @@aut@@ Mariko Higa @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
hierarchy_top_id	668311819
id	DOAJ030480655
language_de	englisch
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topic_title	RC633-647.5 Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency
topic	misc RC633-647.5 misc Diseases of the blood and blood-forming organs
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title	Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency
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title_full	Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency
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title_sort	rivaroxaban treatment for warfarin-refractory thrombosis in a patient with hereditary protein s deficiency
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title_auth	Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency
abstract	Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard.
abstractGer	Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard.
abstract_unstemmed	Protein S (PS) deficiency, an autosomal dominant hereditary thrombophilia, is more prevalent in East Asian populations than in Caucasians. PS-deficient patients have historically been administered a heparin product followed by warfarin for the treatment and secondary prevention of venous thromboembolism (VTE). However, warfarin can be ineffective or causes detrimental effects in rare cases. While direct oral anticoagulants (DOACs) are being increasingly used for the treatment and prevention of VTE, their efficacy in PS-deficient patients has not been established. We describe a 91-year-old woman who presented with chronic bilateral lower leg swelling with VTE that was refractory to warfarin anticoagulation therapy for over 1 year. Her recurrent VTE was diagnosed as quantitative hereditary PS deficiency. Rivaroxaban was administered as maintenance therapy instead of warfarin; after 8 weeks, the severities of the patient’s leg swelling and venous ulcerations were significantly reduced with rivaroxaban compared to warfarin, thus demonstrating the efficacy of rivaroxaban for warfarin-refractory chronic VTE associated with hereditary PS deficiency. This case illustrates that rivaroxaban can potentially serve as therapeutic agents to treat warfarin-refractory VTE in PS-deficient patients. Further investigations are required to confirm the efficacy of rivaroxaban on the long term in this regard.
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title_short	Rivaroxaban Treatment for Warfarin-Refractory Thrombosis in a Patient with Hereditary Protein S Deficiency
url	https://doi.org/10.1155/2018/5217301 https://doaj.org/article/7ebcac8cef7f4d99868c4235a84c287c http://dx.doi.org/10.1155/2018/5217301 https://doaj.org/toc/2090-6560 https://doaj.org/toc/2090-6579
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