New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage

Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophag...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Chandrasoma, Parakrama [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Gastroesophageal reflux disease Histopathologic diagnosis Cardiac mucosa Dilated distal esophagus Barrett esophagus

Übergeordnetes Werk:	Enthalten in: European surgery - Wien : Springer, 2002, 51(2019), 6 vom: 06. Nov., Seite 282-290
Übergeordnetes Werk:	volume:51 ; year:2019 ; number:6 ; day:06 ; month:11 ; pages:282-290

Links:	Volltext

DOI / URN:	10.1007/s10353-019-00616-0

Katalog-ID:	SPR009828575

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520			\|a Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma.
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650		4	\|a Dilated distal esophagus \|7 (dpeaa)DE-He213
650		4	\|a Barrett esophagus \|7 (dpeaa)DE-He213
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matchkey_str	article:16824016:2019----::eeiecdfnnteahlgadahgnssfoeeo
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publishDate	2019
allfields	10.1007/s10353-019-00616-0 doi (DE-627)SPR009828575 (SPR)s10353-019-00616-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Chandrasoma, Parakrama verfasserin aut New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma. Gastroesophageal reflux disease (dpeaa)DE-He213 Histopathologic diagnosis (dpeaa)DE-He213 Cardiac mucosa (dpeaa)DE-He213 Dilated distal esophagus (dpeaa)DE-He213 Barrett esophagus (dpeaa)DE-He213 Enthalten in European surgery Wien : Springer, 2002 51(2019), 6 vom: 06. Nov., Seite 282-290 (DE-627)324655363 (DE-600)2029279-X 1682-4016 nnns volume:51 year:2019 number:6 day:06 month:11 pages:282-290 https://dx.doi.org/10.1007/s10353-019-00616-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 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_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 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_4393 GBV_ILN_4700 44.65 ASE AR 51 2019 6 06 11 282-290
spelling	10.1007/s10353-019-00616-0 doi (DE-627)SPR009828575 (SPR)s10353-019-00616-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Chandrasoma, Parakrama verfasserin aut New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma. Gastroesophageal reflux disease (dpeaa)DE-He213 Histopathologic diagnosis (dpeaa)DE-He213 Cardiac mucosa (dpeaa)DE-He213 Dilated distal esophagus (dpeaa)DE-He213 Barrett esophagus (dpeaa)DE-He213 Enthalten in European surgery Wien : Springer, 2002 51(2019), 6 vom: 06. Nov., Seite 282-290 (DE-627)324655363 (DE-600)2029279-X 1682-4016 nnns volume:51 year:2019 number:6 day:06 month:11 pages:282-290 https://dx.doi.org/10.1007/s10353-019-00616-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 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_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 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_4393 GBV_ILN_4700 44.65 ASE AR 51 2019 6 06 11 282-290
allfields_unstemmed	10.1007/s10353-019-00616-0 doi (DE-627)SPR009828575 (SPR)s10353-019-00616-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Chandrasoma, Parakrama verfasserin aut New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma. Gastroesophageal reflux disease (dpeaa)DE-He213 Histopathologic diagnosis (dpeaa)DE-He213 Cardiac mucosa (dpeaa)DE-He213 Dilated distal esophagus (dpeaa)DE-He213 Barrett esophagus (dpeaa)DE-He213 Enthalten in European surgery Wien : Springer, 2002 51(2019), 6 vom: 06. Nov., Seite 282-290 (DE-627)324655363 (DE-600)2029279-X 1682-4016 nnns volume:51 year:2019 number:6 day:06 month:11 pages:282-290 https://dx.doi.org/10.1007/s10353-019-00616-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 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_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 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_4393 GBV_ILN_4700 44.65 ASE AR 51 2019 6 06 11 282-290
allfieldsGer	10.1007/s10353-019-00616-0 doi (DE-627)SPR009828575 (SPR)s10353-019-00616-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Chandrasoma, Parakrama verfasserin aut New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma. Gastroesophageal reflux disease (dpeaa)DE-He213 Histopathologic diagnosis (dpeaa)DE-He213 Cardiac mucosa (dpeaa)DE-He213 Dilated distal esophagus (dpeaa)DE-He213 Barrett esophagus (dpeaa)DE-He213 Enthalten in European surgery Wien : Springer, 2002 51(2019), 6 vom: 06. Nov., Seite 282-290 (DE-627)324655363 (DE-600)2029279-X 1682-4016 nnns volume:51 year:2019 number:6 day:06 month:11 pages:282-290 https://dx.doi.org/10.1007/s10353-019-00616-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 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_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 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_4393 GBV_ILN_4700 44.65 ASE AR 51 2019 6 06 11 282-290
allfieldsSound	10.1007/s10353-019-00616-0 doi (DE-627)SPR009828575 (SPR)s10353-019-00616-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Chandrasoma, Parakrama verfasserin aut New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma. Gastroesophageal reflux disease (dpeaa)DE-He213 Histopathologic diagnosis (dpeaa)DE-He213 Cardiac mucosa (dpeaa)DE-He213 Dilated distal esophagus (dpeaa)DE-He213 Barrett esophagus (dpeaa)DE-He213 Enthalten in European surgery Wien : Springer, 2002 51(2019), 6 vom: 06. Nov., Seite 282-290 (DE-627)324655363 (DE-600)2029279-X 1682-4016 nnns volume:51 year:2019 number:6 day:06 month:11 pages:282-290 https://dx.doi.org/10.1007/s10353-019-00616-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 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_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 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_4393 GBV_ILN_4700 44.65 ASE AR 51 2019 6 06 11 282-290
language	English
source	Enthalten in European surgery 51(2019), 6 vom: 06. Nov., Seite 282-290 volume:51 year:2019 number:6 day:06 month:11 pages:282-290
sourceStr	Enthalten in European surgery 51(2019), 6 vom: 06. Nov., Seite 282-290 volume:51 year:2019 number:6 day:06 month:11 pages:282-290
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Gastroesophageal reflux disease Histopathologic diagnosis Cardiac mucosa Dilated distal esophagus Barrett esophagus
dewey-raw	610
isfreeaccess_bool	true
container_title	European surgery
authorswithroles_txt_mv	Chandrasoma, Parakrama @@aut@@
publishDateDaySort_date	2019-11-06T00:00:00Z
hierarchy_top_id	324655363
dewey-sort	3610
id	SPR009828575
language_de	englisch
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author	Chandrasoma, Parakrama
spellingShingle	Chandrasoma, Parakrama ddc 610 bkl 44.65 misc Gastroesophageal reflux disease misc Histopathologic diagnosis misc Cardiac mucosa misc Dilated distal esophagus misc Barrett esophagus New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage
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topic_title	610 ASE 44.65 bkl New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage Gastroesophageal reflux disease (dpeaa)DE-He213 Histopathologic diagnosis (dpeaa)DE-He213 Cardiac mucosa (dpeaa)DE-He213 Dilated distal esophagus (dpeaa)DE-He213 Barrett esophagus (dpeaa)DE-He213
topic	ddc 610 bkl 44.65 misc Gastroesophageal reflux disease misc Histopathologic diagnosis misc Cardiac mucosa misc Dilated distal esophagus misc Barrett esophagus
topic_unstemmed	ddc 610 bkl 44.65 misc Gastroesophageal reflux disease misc Histopathologic diagnosis misc Cardiac mucosa misc Dilated distal esophagus misc Barrett esophagus
topic_browse	ddc 610 bkl 44.65 misc Gastroesophageal reflux disease misc Histopathologic diagnosis misc Cardiac mucosa misc Dilated distal esophagus misc Barrett esophagus
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title	New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage
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title_full	New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage
author_sort	Chandrasoma, Parakrama
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title_sort	new evidence defining the pathology and pathogenesis of lower esophageal sphincter damage
title_auth	New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage
abstract	Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma.
abstractGer	Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma.
abstract_unstemmed	Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma.
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title_short	New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage
url	https://dx.doi.org/10.1007/s10353-019-00616-0
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up_date	2024-07-04T03:12:03.730Z
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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">SPR009828575</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519161004.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201005s2019 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s10353-019-00616-0</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR009828575</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s10353-019-00616-0-e</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="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.65</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Chandrasoma, Parakrama</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</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">Background Present diagnosis and management of gastroesophageal reflux disease (GERD)has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. Thisis due to failure to identify pathologic changes of early GERD; at present, pathology islimited to management of Barrett esophagus (BE). Methods Convincing evidence have confirmed that cardiac mucosa distal to thesquamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium. Results When cardiac mucosa is recognized as a metaplastic esophageal epithelium, itbecomes self-evident that the present endoscopic definition of the gastro-esophagealjunction is incorrect, and there exists a dilated distal esophagus (DDE) in what isincorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It alsobecomes clear that the length of the DDE correlates with the presence and severity ofGERD and represents the pathology of the entire spectrum of GERD. Further, it allowsrecognition that the DDE, measured as the gap between esophageal squamous epitheliumand gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologicanatomy of damage to the abdominal segment of the lower esophageal sphincter (LES). Conclusion The new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause ofGERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset.Ultimately, such early diagnosis has the potential to reverse the increasing trend ofesophageal adenocarcinoma.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gastroesophageal reflux disease</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Histopathologic diagnosis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cardiac mucosa</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Dilated distal esophagus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Barrett esophagus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">European surgery</subfield><subfield code="d">Wien : Springer, 2002</subfield><subfield code="g">51(2019), 6 vom: 06. 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New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage

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