MARC1 p.A165T variant is associated with decreased markers of liver injury and enhanced antioxidant capacity in autoimmune hepatitis

The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-tr...

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Published inScientific reports Vol. 11; no. 1; p. 24407
Main Authors Janik, Maciej K., Smyk, Wiktor, Kruk, Beata, Szczepankiewicz, Benedykt, Górnicka, Barbara, Lebiedzińska-Arciszewska, Magdalena, Potes, Yaiza, Simões, Inês C. M., Weber, Susanne N., Lammert, Frank, Więckowski, Mariusz R., Milkiewicz, Piotr, Krawczyk, Marcin
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 23.12.2021
Nature Publishing Group
Nature Portfolio
Subjects
631/208
692/4020/4021
Adolescent
Adult
Aged
Antioxidants
Antioxidants - metabolism
Catalase
Child
Fatty liver
Female
Gene polymorphism
Genetic diversity
Genetic Predisposition to Disease - genetics
Genetic variance
Genome-Wide Association Study
Genotype
Genotyping
Hepatitis
Hepatitis, Autoimmune - complications
Hepatitis, Autoimmune - genetics
Hepatitis, Autoimmune - metabolism
Hepatitis, Autoimmune - prevention & control
Humanities and Social Sciences
Humans
Liver cancer
Liver Cirrhosis - etiology
Liver Cirrhosis - genetics
Liver Cirrhosis - metabolism
Liver Cirrhosis - prevention & control
Male
Middle Aged
Mitochondria
Mitochondrial Proteins - genetics
multidisciplinary
Oxidoreductases - genetics
Patients
Phenotype
Phenotypes
Polymorphism, Genetic - genetics
Polymorphism, Genetic - physiology
Science
Science (multidisciplinary)
Transplantation
Young Adult
Online AccessGet full text

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Abstract The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-transplanted adults with AIH. In all patients, the MARC1 (rs2642438), HSD17B13 (rs72613567), PNPLA3 (rs738409), TM6SF2 (rs58542926), and MBOAT7 (rs641738) variants were genotyped using TaqMan assays. Mitochondrial damage markers in serum were analyzed in relation to the MARC1 variant. Carriers of the protective MARC1 allele had lower ALT and AST (both P < 0.05). In patients treated for AIH for ≥ 6 months, MARC1 correlated with reduced AST, ALP, GGT (all P ≤ 0.01), and lower APRI (P = 0.02). Patients carrying the protective MARC1 genotype had higher total antioxidant activity (P < 0.01) and catalase levels (P = 0.02) in serum. The PNPLA3 risk variant was associated with higher MELD (P = 0.02) in treated patients, whereas MBOAT7 increased the odds for liver cancer (OR = 3.71). None of the variants modulated the risk of death or transplantation. In conclusion, the MARC1 polymorphism has protective effects in AIH. Genotyping of MARC1 , PNPLA3, and MBOAT7 polymorphisms might help to stratify patients with AIH.
AbstractList Abstract The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-transplanted adults with AIH. In all patients, the MARC1 (rs2642438), HSD17B13 (rs72613567), PNPLA3 (rs738409), TM6SF2 (rs58542926), and MBOAT7 (rs641738) variants were genotyped using TaqMan assays. Mitochondrial damage markers in serum were analyzed in relation to the MARC1 variant. Carriers of the protective MARC1 allele had lower ALT and AST (both P < 0.05). In patients treated for AIH for ≥ 6 months, MARC1 correlated with reduced AST, ALP, GGT (all P ≤ 0.01), and lower APRI (P = 0.02). Patients carrying the protective MARC1 genotype had higher total antioxidant activity (P < 0.01) and catalase levels (P = 0.02) in serum. The PNPLA3 risk variant was associated with higher MELD (P = 0.02) in treated patients, whereas MBOAT7 increased the odds for liver cancer (OR = 3.71). None of the variants modulated the risk of death or transplantation. In conclusion, the MARC1 polymorphism has protective effects in AIH. Genotyping of MARC1, PNPLA3, and MBOAT7 polymorphisms might help to stratify patients with AIH.
The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-transplanted adults with AIH. In all patients, the MARC1 (rs2642438), HSD17B13 (rs72613567), PNPLA3 (rs738409), TM6SF2 (rs58542926), and MBOAT7 (rs641738) variants were genotyped using TaqMan assays. Mitochondrial damage markers in serum were analyzed in relation to the MARC1 variant. Carriers of the protective MARC1 allele had lower ALT and AST (both P < 0.05). In patients treated for AIH for ≥ 6 months, MARC1 correlated with reduced AST, ALP, GGT (all P ≤ 0.01), and lower APRI (P = 0.02). Patients carrying the protective MARC1 genotype had higher total antioxidant activity (P < 0.01) and catalase levels (P = 0.02) in serum. The PNPLA3 risk variant was associated with higher MELD (P = 0.02) in treated patients, whereas MBOAT7 increased the odds for liver cancer (OR = 3.71). None of the variants modulated the risk of death or transplantation. In conclusion, the MARC1 polymorphism has protective effects in AIH. Genotyping of MARC1 , PNPLA3, and MBOAT7 polymorphisms might help to stratify patients with AIH.
The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-transplanted adults with AIH. In all patients, the MARC1 (rs2642438), HSD17B13 (rs72613567), PNPLA3 (rs738409), TM6SF2 (rs58542926), and MBOAT7 (rs641738) variants were genotyped using TaqMan assays. Mitochondrial damage markers in serum were analyzed in relation to the MARC1 variant. Carriers of the protective MARC1 allele had lower ALT and AST (both P < 0.05). In patients treated for AIH for ≥ 6 months, MARC1 correlated with reduced AST, ALP, GGT (all P ≤ 0.01), and lower APRI (P = 0.02). Patients carrying the protective MARC1 genotype had higher total antioxidant activity (P < 0.01) and catalase levels (P = 0.02) in serum. The PNPLA3 risk variant was associated with higher MELD (P = 0.02) in treated patients, whereas MBOAT7 increased the odds for liver cancer (OR = 3.71). None of the variants modulated the risk of death or transplantation. In conclusion, the MARC1 polymorphism has protective effects in AIH. Genotyping of MARC1, PNPLA3, and MBOAT7 polymorphisms might help to stratify patients with AIH.
Abstract The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-transplanted adults with AIH. In all patients, the MARC1 (rs2642438), HSD17B13 (rs72613567), PNPLA3 (rs738409), TM6SF2 (rs58542926), and MBOAT7 (rs641738) variants were genotyped using TaqMan assays. Mitochondrial damage markers in serum were analyzed in relation to the MARC1 variant. Carriers of the protective MARC1 allele had lower ALT and AST (both P < 0.05). In patients treated for AIH for ≥ 6 months, MARC1 correlated with reduced AST, ALP, GGT (all P ≤ 0.01), and lower APRI (P = 0.02). Patients carrying the protective MARC1 genotype had higher total antioxidant activity (P < 0.01) and catalase levels (P = 0.02) in serum. The PNPLA3 risk variant was associated with higher MELD (P = 0.02) in treated patients, whereas MBOAT7 increased the odds for liver cancer (OR = 3.71). None of the variants modulated the risk of death or transplantation. In conclusion, the MARC1 polymorphism has protective effects in AIH. Genotyping of MARC1 , PNPLA3, and MBOAT7 polymorphisms might help to stratify patients with AIH.
The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to evaluate genetic variants previously associated with fatty liver as potential modulators of the AIH phenotype. The study cohort comprised 313 non-transplanted adults with AIH. In all patients, the MARC1 (rs2642438), HSD17B13 (rs72613567), PNPLA3 (rs738409), TM6SF2 (rs58542926), and MBOAT7 (rs641738) variants were genotyped using TaqMan assays. Mitochondrial damage markers in serum were analyzed in relation to the MARC1 variant. Carriers of the protective MARC1 allele had lower ALT and AST (both P < 0.05). In patients treated for AIH for ≥ 6 months, MARC1 correlated with reduced AST, ALP, GGT (all P ≤ 0.01), and lower APRI (P = 0.02). Patients carrying the protective MARC1 genotype had higher total antioxidant activity (P < 0.01) and catalase levels (P = 0.02) in serum. The PNPLA3 risk variant was associated with higher MELD (P = 0.02) in treated patients, whereas MBOAT7 increased the odds for liver cancer (OR = 3.71). None of the variants modulated the risk of death or transplantation. In conclusion, the MARC1 polymorphism has protective effects in AIH. Genotyping of MARC1, PNPLA3, and MBOAT7 polymorphisms might help to stratify patients with AIH.
ArticleNumber 24407
Author Simões, Inês C. M.
Szczepankiewicz, Benedykt
Lebiedzińska-Arciszewska, Magdalena
Janik, Maciej K.
Weber, Susanne N.
Smyk, Wiktor
Więckowski, Mariusz R.
Kruk, Beata
Potes, Yaiza
Krawczyk, Marcin
Lammert, Frank
Górnicka, Barbara
Milkiewicz, Piotr
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  organization: Liver and Internal Medicine Unit, Department of General, Transplant and Liver Surgery, Medical University of Warsaw, European Reference Network on Hepatological Diseases (ERN RARE-LIVER)
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  organization: Liver and Internal Medicine Unit, Department of General, Transplant and Liver Surgery, Medical University of Warsaw, European Reference Network on Hepatological Diseases (ERN RARE-LIVER)
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  surname: Simões
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  organization: Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology Polish Academy of Sciences
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  fullname: Milkiewicz, Piotr
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  publication-title: Hepatology
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Snippet The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was to...
Abstract The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was...
Abstract The clinical picture of autoimmune hepatitis (AIH) varies markedly between patients, potentially due to genetic modifiers. The aim of this study was...
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SubjectTerms 631/208
692/4020/4021
Adolescent
Adult
Aged
Antioxidants
Antioxidants - metabolism
Catalase
Child
Fatty liver
Female
Gene polymorphism
Genetic diversity
Genetic Predisposition to Disease - genetics
Genetic variance
Genome-Wide Association Study
Genotype
Genotyping
Hepatitis
Hepatitis, Autoimmune - complications
Hepatitis, Autoimmune - genetics
Hepatitis, Autoimmune - metabolism
Hepatitis, Autoimmune - prevention & control
Humanities and Social Sciences
Humans
Liver cancer
Liver Cirrhosis - etiology
Liver Cirrhosis - genetics
Liver Cirrhosis - metabolism
Liver Cirrhosis - prevention & control
Male
Middle Aged
Mitochondria
Mitochondrial Proteins - genetics
multidisciplinary
Oxidoreductases - genetics
Patients
Phenotype
Phenotypes
Polymorphism, Genetic - genetics
Polymorphism, Genetic - physiology
Science
Science (multidisciplinary)
Transplantation
Young Adult
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Title MARC1 p.A165T variant is associated with decreased markers of liver injury and enhanced antioxidant capacity in autoimmune hepatitis
URI https://link.springer.com/article/10.1038/s41598-021-03521-3
https://www.ncbi.nlm.nih.gov/pubmed/34949757
https://www.proquest.com/docview/2613008346
https://search.proquest.com/docview/2614240290
https://pubmed.ncbi.nlm.nih.gov/PMC8702547
https://doaj.org/article/69097146d6b5474a9d809acdb7f449e9
Volume 11
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