Diagnosis and therapy of polycythemia vera

Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Lengfelder, Eva - 1951- [verfasserIn] Merx, Kirsten - 1970- [verfasserIn] Hehlmann, Rüdiger - 1941- [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	02. Mai 2006

Anmerkung:	Gesehen am 10.05.2022
Umfang:	9

Übergeordnetes Werk:	Enthalten in: Seminars in thrombosis and hemostasis - New York, NY : Thieme, 1974, 32(2006), 3, Seite 267-275
Übergeordnetes Werk:	volume:32 ; year:2006 ; number:3 ; pages:267-275 ; extent:9

Links:	Volltext Volltext

DOI / URN:	10.1055/s-2006-939438

Katalog-ID:	1801287880

Internformat


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100	1		\|a Lengfelder, Eva \|d 1951- \|e verfasserin \|0 (DE-588)1031229779 \|0 (DE-627)736022775 \|0 (DE-576)378669230 \|4 aut
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520			\|a Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders.
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Indexfelder

author_variant	e l el k m km r h rh
matchkey_str	article:10989064:2006----::igoiadhrpoplc
oclc_num	1341459823
hierarchy_sort_str	02. Mai 2006
publishDate	2006
allfields	10.1055/s-2006-939438 doi (DE-627)1801287880 (DE-599)KXP1801287880 (OCoLC)1341459823 DE-627 ger DE-627 rda eng Lengfelder, Eva 1951- verfasserin (DE-588)1031229779 (DE-627)736022775 (DE-576)378669230 aut Diagnosis and therapy of polycythemia vera Eva Lengfelder, Kirsten Merx, Rüdiger Hehlmann 02. Mai 2006 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 10.05.2022 Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Merx, Kirsten 1970- verfasserin (DE-588)122413091 (DE-627)70589892X (DE-576)293258910 aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Enthalten in Seminars in thrombosis and hemostasis New York, NY : Thieme, 1974 32(2006), 3, Seite 267-275 Online-Ressource (DE-627)342892754 (DE-600)2072469-X (DE-576)279447868 1098-9064 nnns volume:32 year:2006 number:3 pages:267-275 extent:9 https://doi.org/10.1055/s-2006-939438 Verlag Resolving-System lizenzpflichtig Volltext http://www.thieme-connect.de/DOI/DOI?10.1055/s-2006-939438 Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2865 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_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4753 AR 32 2006 3 267-275 9 2013 01 DE-16-250 4131335824 00 --%%-- --%%-- --%%-- --%%-- l01 10-05-22 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1448669367 Lengfelder, Eva 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1460938518 Merx, Kirsten 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_3
spelling	10.1055/s-2006-939438 doi (DE-627)1801287880 (DE-599)KXP1801287880 (OCoLC)1341459823 DE-627 ger DE-627 rda eng Lengfelder, Eva 1951- verfasserin (DE-588)1031229779 (DE-627)736022775 (DE-576)378669230 aut Diagnosis and therapy of polycythemia vera Eva Lengfelder, Kirsten Merx, Rüdiger Hehlmann 02. Mai 2006 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 10.05.2022 Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Merx, Kirsten 1970- verfasserin (DE-588)122413091 (DE-627)70589892X (DE-576)293258910 aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Enthalten in Seminars in thrombosis and hemostasis New York, NY : Thieme, 1974 32(2006), 3, Seite 267-275 Online-Ressource (DE-627)342892754 (DE-600)2072469-X (DE-576)279447868 1098-9064 nnns volume:32 year:2006 number:3 pages:267-275 extent:9 https://doi.org/10.1055/s-2006-939438 Verlag Resolving-System lizenzpflichtig Volltext http://www.thieme-connect.de/DOI/DOI?10.1055/s-2006-939438 Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2865 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_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4753 AR 32 2006 3 267-275 9 2013 01 DE-16-250 4131335824 00 --%%-- --%%-- --%%-- --%%-- l01 10-05-22 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1448669367 Lengfelder, Eva 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1460938518 Merx, Kirsten 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_3
allfields_unstemmed	10.1055/s-2006-939438 doi (DE-627)1801287880 (DE-599)KXP1801287880 (OCoLC)1341459823 DE-627 ger DE-627 rda eng Lengfelder, Eva 1951- verfasserin (DE-588)1031229779 (DE-627)736022775 (DE-576)378669230 aut Diagnosis and therapy of polycythemia vera Eva Lengfelder, Kirsten Merx, Rüdiger Hehlmann 02. Mai 2006 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 10.05.2022 Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Merx, Kirsten 1970- verfasserin (DE-588)122413091 (DE-627)70589892X (DE-576)293258910 aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Enthalten in Seminars in thrombosis and hemostasis New York, NY : Thieme, 1974 32(2006), 3, Seite 267-275 Online-Ressource (DE-627)342892754 (DE-600)2072469-X (DE-576)279447868 1098-9064 nnns volume:32 year:2006 number:3 pages:267-275 extent:9 https://doi.org/10.1055/s-2006-939438 Verlag Resolving-System lizenzpflichtig Volltext http://www.thieme-connect.de/DOI/DOI?10.1055/s-2006-939438 Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2865 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_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4753 AR 32 2006 3 267-275 9 2013 01 DE-16-250 4131335824 00 --%%-- --%%-- --%%-- --%%-- l01 10-05-22 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1448669367 Lengfelder, Eva 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1460938518 Merx, Kirsten 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_3
allfieldsGer	10.1055/s-2006-939438 doi (DE-627)1801287880 (DE-599)KXP1801287880 (OCoLC)1341459823 DE-627 ger DE-627 rda eng Lengfelder, Eva 1951- verfasserin (DE-588)1031229779 (DE-627)736022775 (DE-576)378669230 aut Diagnosis and therapy of polycythemia vera Eva Lengfelder, Kirsten Merx, Rüdiger Hehlmann 02. Mai 2006 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 10.05.2022 Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Merx, Kirsten 1970- verfasserin (DE-588)122413091 (DE-627)70589892X (DE-576)293258910 aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Enthalten in Seminars in thrombosis and hemostasis New York, NY : Thieme, 1974 32(2006), 3, Seite 267-275 Online-Ressource (DE-627)342892754 (DE-600)2072469-X (DE-576)279447868 1098-9064 nnns volume:32 year:2006 number:3 pages:267-275 extent:9 https://doi.org/10.1055/s-2006-939438 Verlag Resolving-System lizenzpflichtig Volltext http://www.thieme-connect.de/DOI/DOI?10.1055/s-2006-939438 Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2865 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_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4753 AR 32 2006 3 267-275 9 2013 01 DE-16-250 4131335824 00 --%%-- --%%-- --%%-- --%%-- l01 10-05-22 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1448669367 Lengfelder, Eva 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1460938518 Merx, Kirsten 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_3
allfieldsSound	10.1055/s-2006-939438 doi (DE-627)1801287880 (DE-599)KXP1801287880 (OCoLC)1341459823 DE-627 ger DE-627 rda eng Lengfelder, Eva 1951- verfasserin (DE-588)1031229779 (DE-627)736022775 (DE-576)378669230 aut Diagnosis and therapy of polycythemia vera Eva Lengfelder, Kirsten Merx, Rüdiger Hehlmann 02. Mai 2006 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 10.05.2022 Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Merx, Kirsten 1970- verfasserin (DE-588)122413091 (DE-627)70589892X (DE-576)293258910 aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Enthalten in Seminars in thrombosis and hemostasis New York, NY : Thieme, 1974 32(2006), 3, Seite 267-275 Online-Ressource (DE-627)342892754 (DE-600)2072469-X (DE-576)279447868 1098-9064 nnns volume:32 year:2006 number:3 pages:267-275 extent:9 https://doi.org/10.1055/s-2006-939438 Verlag Resolving-System lizenzpflichtig Volltext http://www.thieme-connect.de/DOI/DOI?10.1055/s-2006-939438 Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2865 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_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 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_4328 GBV_ILN_4333 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4753 AR 32 2006 3 267-275 9 2013 01 DE-16-250 4131335824 00 --%%-- --%%-- --%%-- --%%-- l01 10-05-22 2013 01 DE-16-250 00 s hd2006 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1448669367 Lengfelder, Eva 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1460938518 Merx, Kirsten 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_3
language	English
source	Enthalten in Seminars in thrombosis and hemostasis 32(2006), 3, Seite 267-275 volume:32 year:2006 number:3 pages:267-275 extent:9
sourceStr	Enthalten in Seminars in thrombosis and hemostasis 32(2006), 3, Seite 267-275 volume:32 year:2006 number:3 pages:267-275 extent:9
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container_title	Seminars in thrombosis and hemostasis
authorswithroles_txt_mv	Lengfelder, Eva @@aut@@ Merx, Kirsten @@aut@@ Hehlmann, Rüdiger @@aut@@
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The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. 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topic	2013 hd2006 2013 wissenschaftlicher Artikel (Zeitschrift) 2013 per_3 2013 s_9 2013 Lengfelder, Eva 2013 III. Medizinische Klinik 2013 Verfasser 2013 pos_1 2013 Merx, Kirsten 2013 pos_2 2013 Hehlmann, Rüdiger 2013 pos_3
topic_unstemmed	2013 hd2006 2013 wissenschaftlicher Artikel (Zeitschrift) 2013 per_3 2013 s_9 2013 Lengfelder, Eva 2013 III. Medizinische Klinik 2013 Verfasser 2013 pos_1 2013 Merx, Kirsten 2013 pos_2 2013 Hehlmann, Rüdiger 2013 pos_3
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title	Diagnosis and therapy of polycythemia vera
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title_full	Diagnosis and therapy of polycythemia vera Eva Lengfelder, Kirsten Merx, Rüdiger Hehlmann
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title_sort	diagnosis and therapy of polycythemia vera
title_auth	Diagnosis and therapy of polycythemia vera
abstract	Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Gesehen am 10.05.2022
abstractGer	Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Gesehen am 10.05.2022
abstract_unstemmed	Polycythemia vera (PV) is a hematopoietic stem cell disorder characterized by a predominant proliferation of the erythroid cell line. The diagnosis is commonly based on the WHO criteria. The acquired V617F mutation in the tyrosine kinase gene JAK2 represents a new molecular marker proving clonality in PV and other chronic myeloproliferative disorders. Phlebotomy is still the treatment of choice to reduce the red cell mass. Low-dose acetylsalicylic acid is successful in the primary prophylaxis of vascular complications. However, the majority of patients require myelosuppressive therapy during the course of their disease due to progressive myeloproliferation. Hydroxyurea still plays a role in patients of all age groups. Interferon α represents an alternative, particularly for younger patients. Apart from sporadic cases of bone marrow transplantation, there is no known curative treatment in PV. To date, the diagnosis of PV was based mainly on clinical criteria. The identification of the JAK2 mutation enables new approaches to the diagnosis, classification, and treatment of PV and of the other myeloproliferative disorders. Gesehen am 10.05.2022
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title_short	Diagnosis and therapy of polycythemia vera
url	https://doi.org/10.1055/s-2006-939438 http://www.thieme-connect.de/DOI/DOI?10.1055/s-2006-939438
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