Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis

Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, a...
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Autor*in:	Fadista, João [verfasserIn] Skotte, Line [verfasserIn] Courraud, Julie [verfasserIn] Geller, Frank [verfasserIn] Gørtz, Sanne [verfasserIn] Wohlfahrt, Jan [verfasserIn] Melbye, Mads [verfasserIn] Cohen, Arieh S. [verfasserIn] Feenstra, Bjarke [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Übergeordnetes Werk:	Enthalten in: Metabolomics - Berlin : Springer, 2005, 17(2021), 1 vom: Jan.
Übergeordnetes Werk:	volume:17 ; year:2021 ; number:1 ; month:01

Links:	Volltext

DOI / URN:	10.1007/s11306-020-01763-2

Katalog-ID:	SPR042633567

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245	1	0	\|a Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
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520			\|a Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life.
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700	1		\|a Gørtz, Sanne \|e verfasserin \|4 aut
700	1		\|a Wohlfahrt, Jan \|e verfasserin \|4 aut
700	1		\|a Melbye, Mads \|e verfasserin \|4 aut
700	1		\|a Cohen, Arieh S. \|e verfasserin \|4 aut
700	1		\|a Feenstra, Bjarke \|e verfasserin \|4 aut
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author_variant	j f jf l s ls j c jc f g fg s g sg j w jw m m mm a s c as asc b f bf
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allfields	10.1007/s11306-020-01763-2 doi (DE-627)SPR042633567 (DE-599)SPRs11306-020-01763-2-e (SPR)s11306-020-01763-2-e DE-627 ger DE-627 rakwb eng 540 ASE 42.15 bkl Fadista, João verfasserin aut Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life. Skotte, Line verfasserin aut Courraud, Julie verfasserin aut Geller, Frank verfasserin aut Gørtz, Sanne verfasserin aut Wohlfahrt, Jan verfasserin aut Melbye, Mads verfasserin aut Cohen, Arieh S. verfasserin aut Feenstra, Bjarke verfasserin aut Enthalten in Metabolomics Berlin : Springer, 2005 17(2021), 1 vom: Jan. (DE-627)482838671 (DE-600)2182289-X 1573-3890 nnns volume:17 year:2021 number:1 month:01 https://dx.doi.org/10.1007/s11306-020-01763-2 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_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_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_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_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_2118 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_2472 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_4126 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 17 2021 1 01
spelling	10.1007/s11306-020-01763-2 doi (DE-627)SPR042633567 (DE-599)SPRs11306-020-01763-2-e (SPR)s11306-020-01763-2-e DE-627 ger DE-627 rakwb eng 540 ASE 42.15 bkl Fadista, João verfasserin aut Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life. Skotte, Line verfasserin aut Courraud, Julie verfasserin aut Geller, Frank verfasserin aut Gørtz, Sanne verfasserin aut Wohlfahrt, Jan verfasserin aut Melbye, Mads verfasserin aut Cohen, Arieh S. verfasserin aut Feenstra, Bjarke verfasserin aut Enthalten in Metabolomics Berlin : Springer, 2005 17(2021), 1 vom: Jan. (DE-627)482838671 (DE-600)2182289-X 1573-3890 nnns volume:17 year:2021 number:1 month:01 https://dx.doi.org/10.1007/s11306-020-01763-2 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_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_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_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_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_2118 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_2472 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_4126 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 17 2021 1 01
allfields_unstemmed	10.1007/s11306-020-01763-2 doi (DE-627)SPR042633567 (DE-599)SPRs11306-020-01763-2-e (SPR)s11306-020-01763-2-e DE-627 ger DE-627 rakwb eng 540 ASE 42.15 bkl Fadista, João verfasserin aut Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life. Skotte, Line verfasserin aut Courraud, Julie verfasserin aut Geller, Frank verfasserin aut Gørtz, Sanne verfasserin aut Wohlfahrt, Jan verfasserin aut Melbye, Mads verfasserin aut Cohen, Arieh S. verfasserin aut Feenstra, Bjarke verfasserin aut Enthalten in Metabolomics Berlin : Springer, 2005 17(2021), 1 vom: Jan. (DE-627)482838671 (DE-600)2182289-X 1573-3890 nnns volume:17 year:2021 number:1 month:01 https://dx.doi.org/10.1007/s11306-020-01763-2 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_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_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_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_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_2118 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_2472 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_4126 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 17 2021 1 01
allfieldsGer	10.1007/s11306-020-01763-2 doi (DE-627)SPR042633567 (DE-599)SPRs11306-020-01763-2-e (SPR)s11306-020-01763-2-e DE-627 ger DE-627 rakwb eng 540 ASE 42.15 bkl Fadista, João verfasserin aut Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life. Skotte, Line verfasserin aut Courraud, Julie verfasserin aut Geller, Frank verfasserin aut Gørtz, Sanne verfasserin aut Wohlfahrt, Jan verfasserin aut Melbye, Mads verfasserin aut Cohen, Arieh S. verfasserin aut Feenstra, Bjarke verfasserin aut Enthalten in Metabolomics Berlin : Springer, 2005 17(2021), 1 vom: Jan. (DE-627)482838671 (DE-600)2182289-X 1573-3890 nnns volume:17 year:2021 number:1 month:01 https://dx.doi.org/10.1007/s11306-020-01763-2 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_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_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_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_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_2118 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_2472 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_4126 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 17 2021 1 01
allfieldsSound	10.1007/s11306-020-01763-2 doi (DE-627)SPR042633567 (DE-599)SPRs11306-020-01763-2-e (SPR)s11306-020-01763-2-e DE-627 ger DE-627 rakwb eng 540 ASE 42.15 bkl Fadista, João verfasserin aut Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life. Skotte, Line verfasserin aut Courraud, Julie verfasserin aut Geller, Frank verfasserin aut Gørtz, Sanne verfasserin aut Wohlfahrt, Jan verfasserin aut Melbye, Mads verfasserin aut Cohen, Arieh S. verfasserin aut Feenstra, Bjarke verfasserin aut Enthalten in Metabolomics Berlin : Springer, 2005 17(2021), 1 vom: Jan. (DE-627)482838671 (DE-600)2182289-X 1573-3890 nnns volume:17 year:2021 number:1 month:01 https://dx.doi.org/10.1007/s11306-020-01763-2 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_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_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_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_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_2118 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_2472 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_4126 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.15 ASE AR 17 2021 1 01
language	English
source	Enthalten in Metabolomics 17(2021), 1 vom: Jan. volume:17 year:2021 number:1 month:01
sourceStr	Enthalten in Metabolomics 17(2021), 1 vom: Jan. volume:17 year:2021 number:1 month:01
format_phy_str_mv	Article
institution	findex.gbv.de
dewey-raw	540
isfreeaccess_bool	true
container_title	Metabolomics
authorswithroles_txt_mv	Fadista, João @@aut@@ Skotte, Line @@aut@@ Courraud, Julie @@aut@@ Geller, Frank @@aut@@ Gørtz, Sanne @@aut@@ Wohlfahrt, Jan @@aut@@ Melbye, Mads @@aut@@ Cohen, Arieh S. @@aut@@ Feenstra, Bjarke @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	482838671
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id	SPR042633567
language_de	englisch
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Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. 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author	Fadista, João
spellingShingle	Fadista, João ddc 540 bkl 42.15 Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
authorStr	Fadista, João
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topic_title	540 ASE 42.15 bkl Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
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title	Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
ctrlnum	(DE-627)SPR042633567 (DE-599)SPRs11306-020-01763-2-e (SPR)s11306-020-01763-2-e
title_full	Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
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author_browse	Fadista, João Skotte, Line Courraud, Julie Geller, Frank Gørtz, Sanne Wohlfahrt, Jan Melbye, Mads Cohen, Arieh S. Feenstra, Bjarke
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title_sort	integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
title_auth	Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
abstract	Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life.
abstractGer	Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life.
abstract_unstemmed	Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. Conclusions We detected lower levels of certain metabolites in IHPS, possibly reflecting different feeding patterns in the first days of life.
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title_short	Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis
url	https://dx.doi.org/10.1007/s11306-020-01763-2
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author2	Skotte, Line Courraud, Julie Geller, Frank Gørtz, Sanne Wohlfahrt, Jan Melbye, Mads Cohen, Arieh S. Feenstra, Bjarke
author2Str	Skotte, Line Courraud, Julie Geller, Frank Gørtz, Sanne Wohlfahrt, Jan Melbye, Mads Cohen, Arieh S. Feenstra, Bjarke
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doi_str	10.1007/s11306-020-01763-2
up_date	2024-07-03T13:58:08.106Z
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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">SPR042633567</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519193051.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">210109s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s11306-020-01763-2</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR042633567</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)SPRs11306-020-01763-2-e</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s11306-020-01763-2-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">540</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">42.15</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Fadista, João</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</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">Introduction Infantile hypertrophic pyloric stenosis (IHPS) is caused by hypertrophy of the pyloric sphincter muscle. Objectives Since previous reports have implicated lipid metabolism, we aimed to (1) investigate associations between IHPS and a wide array of lipid-related metabolites in newborns, and (2) address whether detected differences in metabolite levels were likely to be driven by genetic differences between IHPS cases and controls or by differences in early life feeding patterns. Methods We used population-based random selection of IHPS cases and controls born in Denmark between 1997 and 2014. We randomly took dried blood spots of newborns from 267 pairs of IHPS cases and controls matched by sex and day of birth. We used a mixed-effects linear regression model to evaluate associations between 148 metabolites and IHPS in a matched case–control design. Results The phosphatidylcholine PC(38:4) showed significantly lower levels in IHPS cases (P = 4.68 × $ 10^{−8} $) as did six other correlated metabolites (four phosphatidylcholines, acylcarnitine AC(2:0), and histidine). Associations were driven by 98 case–control pairs born before 2009, when median age at sampling was 6 days. No association was seen in 169 pairs born in 2009 or later, when median age at sampling was 2 days. More IHPS cases than controls had a diagnosis for neonatal difficulty in feeding at breast (P = 6.15 × $ 10^{−3} $). Genetic variants known to be associated with PC(38:4) levels did not associate with IHPS. 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Integrating genetics with newborn metabolomics in infantile hypertrophic pyloric stenosis

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