Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimula...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	JosÃ© Salvador GarcÃa-Morillo [verfasserIn] Ricardo Blanco-Alonso [verfasserIn] Enrique Morales-Ruiz [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan.

Übergeordnetes Werk:	In: Spanish Journal of Medicine - Permanyer, 2021, 2(2022), 4
Übergeordnetes Werk:	volume:2 ; year:2022 ; number:4

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.24875/SJMED.22000008

Katalog-ID:	DOAJ003326659

Internformat


LEADER	01000caa a22002652 4500
001	DOAJ003326659
003	DE-627
005	20230503010029.0
007	cr uuu---uuuuu
008	230225s2022 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.24875/SJMED.22000008 \|2 doi
035			\|a (DE-627)DOAJ003326659
035			\|a (DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
050		0	\|a RC581-951
100	0		\|a JosÃ© Salvador GarcÃa-Morillo \|e verfasserin \|4 aut
245	1	0	\|a Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis
264		1	\|c 2022
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
520			\|a Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV.
650		4	\|a Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan.
653		0	\|a Specialties of internal medicine
700	0		\|a Ricardo Blanco-Alonso \|e verfasserin \|4 aut
700	0		\|a Enrique Morales-Ruiz \|e verfasserin \|4 aut
773	0	8	\|i In \|t Spanish Journal of Medicine \|d Permanyer, 2021 \|g 2(2022), 4 \|w (DE-627)1756009384 \|x 26965631 \|7 nnns
773	1	8	\|g volume:2 \|g year:2022 \|g number:4
856	4	0	\|u https://doi.org/10.24875/SJMED.22000008 \|z kostenfrei
856	4	0	\|u https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427 \|z kostenfrei
856	4	0	\|u https://www.spanishjmed.com/frame_esp.php?id=73 \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/2696-5631 \|y Journal toc \|z kostenfrei
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_DOAJ
912			\|a SSG-OLC-PHA
912			\|a GBV_ILN_20
912			\|a GBV_ILN_22
912			\|a GBV_ILN_23
912			\|a GBV_ILN_24
912			\|a GBV_ILN_31
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_60
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_65
912			\|a GBV_ILN_69
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_95
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_206
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 2 \|j 2022 \|e 4

Indexfelder

author_variant	j s g m jsgm r b a rba e m r emr
matchkey_str	article:26965631:2022----::opeetlcaenhmngmnoatnurpictpamcnio
hierarchy_sort_str	2022
callnumber-subject-code	RC
publishDate	2022
allfields	10.24875/SJMED.22000008 doi (DE-627)DOAJ003326659 (DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427 DE-627 ger DE-627 rakwb eng RC581-951 JosÃ© Salvador GarcÃa-Morillo verfasserin aut Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV. Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. Specialties of internal medicine Ricardo Blanco-Alonso verfasserin aut Enrique Morales-Ruiz verfasserin aut In Spanish Journal of Medicine Permanyer, 2021 2(2022), 4 (DE-627)1756009384 26965631 nnns volume:2 year:2022 number:4 https://doi.org/10.24875/SJMED.22000008 kostenfrei https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427 kostenfrei https://www.spanishjmed.com/frame_esp.php?id=73 kostenfrei https://doaj.org/toc/2696-5631 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2022 4
spelling	10.24875/SJMED.22000008 doi (DE-627)DOAJ003326659 (DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427 DE-627 ger DE-627 rakwb eng RC581-951 JosÃ© Salvador GarcÃa-Morillo verfasserin aut Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV. Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. Specialties of internal medicine Ricardo Blanco-Alonso verfasserin aut Enrique Morales-Ruiz verfasserin aut In Spanish Journal of Medicine Permanyer, 2021 2(2022), 4 (DE-627)1756009384 26965631 nnns volume:2 year:2022 number:4 https://doi.org/10.24875/SJMED.22000008 kostenfrei https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427 kostenfrei https://www.spanishjmed.com/frame_esp.php?id=73 kostenfrei https://doaj.org/toc/2696-5631 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2022 4
allfields_unstemmed	10.24875/SJMED.22000008 doi (DE-627)DOAJ003326659 (DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427 DE-627 ger DE-627 rakwb eng RC581-951 JosÃ© Salvador GarcÃa-Morillo verfasserin aut Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV. Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. Specialties of internal medicine Ricardo Blanco-Alonso verfasserin aut Enrique Morales-Ruiz verfasserin aut In Spanish Journal of Medicine Permanyer, 2021 2(2022), 4 (DE-627)1756009384 26965631 nnns volume:2 year:2022 number:4 https://doi.org/10.24875/SJMED.22000008 kostenfrei https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427 kostenfrei https://www.spanishjmed.com/frame_esp.php?id=73 kostenfrei https://doaj.org/toc/2696-5631 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2022 4
allfieldsGer	10.24875/SJMED.22000008 doi (DE-627)DOAJ003326659 (DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427 DE-627 ger DE-627 rakwb eng RC581-951 JosÃ© Salvador GarcÃa-Morillo verfasserin aut Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV. Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. Specialties of internal medicine Ricardo Blanco-Alonso verfasserin aut Enrique Morales-Ruiz verfasserin aut In Spanish Journal of Medicine Permanyer, 2021 2(2022), 4 (DE-627)1756009384 26965631 nnns volume:2 year:2022 number:4 https://doi.org/10.24875/SJMED.22000008 kostenfrei https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427 kostenfrei https://www.spanishjmed.com/frame_esp.php?id=73 kostenfrei https://doaj.org/toc/2696-5631 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2022 4
allfieldsSound	10.24875/SJMED.22000008 doi (DE-627)DOAJ003326659 (DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427 DE-627 ger DE-627 rakwb eng RC581-951 JosÃ© Salvador GarcÃa-Morillo verfasserin aut Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV. Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. Specialties of internal medicine Ricardo Blanco-Alonso verfasserin aut Enrique Morales-Ruiz verfasserin aut In Spanish Journal of Medicine Permanyer, 2021 2(2022), 4 (DE-627)1756009384 26965631 nnns volume:2 year:2022 number:4 https://doi.org/10.24875/SJMED.22000008 kostenfrei https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427 kostenfrei https://www.spanishjmed.com/frame_esp.php?id=73 kostenfrei https://doaj.org/toc/2696-5631 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2022 4
language	English
source	In Spanish Journal of Medicine 2(2022), 4 volume:2 year:2022 number:4
sourceStr	In Spanish Journal of Medicine 2(2022), 4 volume:2 year:2022 number:4
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. Specialties of internal medicine
isfreeaccess_bool	true
container_title	Spanish Journal of Medicine
authorswithroles_txt_mv	JosÃ© Salvador GarcÃa-Morillo @@aut@@ Ricardo Blanco-Alonso @@aut@@ Enrique Morales-Ruiz @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	1756009384
id	DOAJ003326659
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ003326659</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230503010029.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230225s2022 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.24875/SJMED.22000008</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ003326659</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC581-951</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">JosÃ© Salvador GarcÃa-Morillo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan.</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Specialties of internal medicine</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ricardo Blanco-Alonso</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Enrique Morales-Ruiz</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Spanish Journal of Medicine</subfield><subfield code="d">Permanyer, 2021</subfield><subfield code="g">2(2022), 4</subfield><subfield code="w">(DE-627)1756009384</subfield><subfield code="x">26965631</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:2</subfield><subfield code="g">year:2022</subfield><subfield code="g">number:4</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.24875/SJMED.22000008</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.spanishjmed.com/frame_esp.php?id=73</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2696-5631</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">2</subfield><subfield code="j">2022</subfield><subfield code="e">4</subfield></datafield></record></collection>
callnumber-first	R - Medicine
author	JosÃ© Salvador GarcÃa-Morillo
spellingShingle	JosÃ© Salvador GarcÃa-Morillo misc RC581-951 misc Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. misc Specialties of internal medicine Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis
authorStr	JosÃ© Salvador GarcÃa-Morillo
ppnlink_with_tag_str_mv	@@773@@(DE-627)1756009384
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut
collection	DOAJ
remote_str	true
callnumber-label	RC581-951
illustrated	Not Illustrated
issn	26965631
topic_title	RC581-951 Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan
topic	misc RC581-951 misc Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. misc Specialties of internal medicine
topic_unstemmed	misc RC581-951 misc Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. misc Specialties of internal medicine
topic_browse	misc RC581-951 misc Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan. misc Specialties of internal medicine
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	Spanish Journal of Medicine
hierarchy_parent_id	1756009384
hierarchy_top_title	Spanish Journal of Medicine
isfreeaccess_txt	true
familylinks_str_mv	(DE-627)1756009384
title	Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis
ctrlnum	(DE-627)DOAJ003326659 (DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427
title_full	Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis
author_sort	JosÃ© Salvador GarcÃa-Morillo
journal	Spanish Journal of Medicine
journalStr	Spanish Journal of Medicine
callnumber-first-code	R
lang_code	eng
isOA_bool	true
recordtype	marc
publishDateSort	2022
contenttype_str_mv	txt
author_browse	JosÃ© Salvador GarcÃa-Morillo Ricardo Blanco-Alonso Enrique Morales-Ruiz
container_volume	2
class	RC581-951
format_se	Elektronische Aufsätze
author-letter	JosÃ© Salvador GarcÃa-Morillo
doi_str_mv	10.24875/SJMED.22000008
author2-role	verfasserin
title_sort	complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis
callnumber	RC581-951
title_auth	Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis
abstract	Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV.
abstractGer	Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV.
abstract_unstemmed	Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	4
title_short	Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis
url	https://doi.org/10.24875/SJMED.22000008 https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427 https://www.spanishjmed.com/frame_esp.php?id=73 https://doaj.org/toc/2696-5631
remote_bool	true
author2	Ricardo Blanco-Alonso Enrique Morales-Ruiz
author2Str	Ricardo Blanco-Alonso Enrique Morales-Ruiz
ppnlink	1756009384
callnumber-subject	RC - Internal Medicine
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
doi_str	10.24875/SJMED.22000008
callnumber-a	RC581-951
up_date	2024-07-03T17:20:12.426Z
_version_	1803579254295756801
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ003326659</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230503010029.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230225s2022 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.24875/SJMED.22000008</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ003326659</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ76f73acc8808493fb4534ee4fdff1427</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC581-951</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">JosÃ© Salvador GarcÃa-Morillo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are characterized by the presence of ANCA, particularly those directed against proteinase 3 (PR3) or myeloperoxidase (MPO). At present, the most accepted pathogenic pathway is based on the pathogenic nature of ANCA, which stimulate neutrophils with the consequent activation of the alternative complement pathway, leading to the production of C5a, an anaphylatoxin which plays a key role in amplifying the inflammatory process in AAV. Remission induction in patients with AAV continues to depend on the use of glucocorticoids (GC) in combination with rituximab or cyclophosphamide. Indeed, there are very limited treatment options and a clear need for strategies that reduce the use of GC without compromising efficacy. Avacopan is the first drug specifically developed for patients with AAV as its mechanism of action inhibits C5aR1, thus acting on one of the pathophysiological mechanisms of AAV.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Complement. Antineutrophil cytoplasmic antibodies-associated vasculitis. Avacopan.</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Specialties of internal medicine</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ricardo Blanco-Alonso</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Enrique Morales-Ruiz</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Spanish Journal of Medicine</subfield><subfield code="d">Permanyer, 2021</subfield><subfield code="g">2(2022), 4</subfield><subfield code="w">(DE-627)1756009384</subfield><subfield code="x">26965631</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:2</subfield><subfield code="g">year:2022</subfield><subfield code="g">number:4</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.24875/SJMED.22000008</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/76f73acc8808493fb4534ee4fdff1427</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.spanishjmed.com/frame_esp.php?id=73</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2696-5631</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">2</subfield><subfield code="j">2022</subfield><subfield code="e">4</subfield></datafield></record></collection>
score	7.399768

Nicht das Richtige dabei?

Schreiben Sie uns!

Complement blockade in the management of antineutrophil cytoplasmic antibodyassociated vasculitis

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?