Relationship Between Liver Function and Brain Shrinkage in Patients with Alcohol Dependence
Background: Oxidative stress has been proposed as one of the mechanisms of alcohol‐induced brain shrinkage and alcohol‐induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence. Methods:...
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| Published in | Alcoholism, clinical and experimental research Vol. 36; no. 4; pp. 625 - 632 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.04.2012
Wiley |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background: Oxidative stress has been proposed as one of the mechanisms of alcohol‐induced brain shrinkage and alcohol‐induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence.
Methods: We recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma‐glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3‐week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage.
Results: Patients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender‐stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage.
Conclusions: Our results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients. |
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| AbstractList | Background:
Oxidative stress has been proposed as one of the mechanisms of alcohol‐induced brain shrinkage and alcohol‐induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence.
Methods:
We recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma‐glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3‐week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage.
Results:
Patients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender‐stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage.
Conclusions:
Our results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients. Oxidative stress has been proposed as one of the mechanisms of alcohol-induced brain shrinkage and alcohol-induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence.BACKGROUNDOxidative stress has been proposed as one of the mechanisms of alcohol-induced brain shrinkage and alcohol-induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence.We recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3-week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage.METHODSWe recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3-week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage.Patients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender-stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage.RESULTSPatients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender-stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage.Our results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients.CONCLUSIONSOur results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients. Background: Oxidative stress has been proposed as one of the mechanisms of alcohol-induced brain shrinkage and alcohol-induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence. Methods: We recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3-week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage. Results: Patients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender-stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage. Conclusions: Our results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients. Oxidative stress has been proposed as one of the mechanisms of alcohol-induced brain shrinkage and alcohol-induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence. We recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3-week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage. Patients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender-stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage. Our results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients. Background: Oxidative stress has been proposed as one of the mechanisms of alcohol‐induced brain shrinkage and alcohol‐induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence. Methods: We recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma‐glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3‐week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage. Results: Patients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender‐stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage. Conclusions: Our results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients. |
| Author | Momenan, Reza Walker, Jonathan Rawlings, Robert Heilig, Markus Chen, Chun-Hsin Hommer, Daniel W. |
| AuthorAffiliation | 1 Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health 3 Department of Psychiatry, School of Medicine, Taipei Medical University, Taipei, Taiwan 2 Department of Psychiatry, Taipei Medical University-WanFang Hospital, Taipei, Taiwan |
| AuthorAffiliation_xml | – name: 3 Department of Psychiatry, School of Medicine, Taipei Medical University, Taipei, Taiwan – name: 1 Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health – name: 2 Department of Psychiatry, Taipei Medical University-WanFang Hospital, Taipei, Taiwan |
| Author_xml | – sequence: 1 givenname: Chun-Hsin surname: Chen fullname: Chen, Chun-Hsin organization: From the Laboratory of Clinical and Translational Studies (C-HC, JW, RM, RR, MH, DWH), National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland; Department of Psychiatry (CHC), Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan; and Department of Psychiatry (CHC), School of Medicine, Taipei Medical University, Taipei, Taiwan – sequence: 2 givenname: Jonathan surname: Walker fullname: Walker, Jonathan organization: From the Laboratory of Clinical and Translational Studies (C-HC, JW, RM, RR, MH, DWH), National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland; Department of Psychiatry (CHC), Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan; and Department of Psychiatry (CHC), School of Medicine, Taipei Medical University, Taipei, Taiwan – sequence: 3 givenname: Reza surname: Momenan fullname: Momenan, Reza organization: From the Laboratory of Clinical and Translational Studies (C-HC, JW, RM, RR, MH, DWH), National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland; Department of Psychiatry (CHC), Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan; and Department of Psychiatry (CHC), School of Medicine, Taipei Medical University, Taipei, Taiwan – sequence: 4 givenname: Robert surname: Rawlings fullname: Rawlings, Robert organization: From the Laboratory of Clinical and Translational Studies (C-HC, JW, RM, RR, MH, DWH), National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland; Department of Psychiatry (CHC), Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan; and Department of Psychiatry (CHC), School of Medicine, Taipei Medical University, Taipei, Taiwan – sequence: 5 givenname: Markus surname: Heilig fullname: Heilig, Markus organization: From the Laboratory of Clinical and Translational Studies (C-HC, JW, RM, RR, MH, DWH), National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland; Department of Psychiatry (CHC), Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan; and Department of Psychiatry (CHC), School of Medicine, Taipei Medical University, Taipei, Taiwan – sequence: 6 givenname: Daniel W. surname: Hommer fullname: Hommer, Daniel W. organization: From the Laboratory of Clinical and Translational Studies (C-HC, JW, RM, RR, MH, DWH), National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland; Department of Psychiatry (CHC), Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan; and Department of Psychiatry (CHC), School of Medicine, Taipei Medical University, Taipei, Taiwan |
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| Publisher | Blackwell Publishing Ltd Wiley |
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| References | MutzellS (1992) Computed tomography of the brain, hepatotoxic drugs and high alcohol consumption in male alcoholic patients and a random sample from the general male population. Ups J Med Sci97:183-194. PfefferbaumA, SullivanEV, MathalonDH, ShearPK, RosenbloomMJ, LimKO (1995) Longitudinal changes in magnetic resonance imaging brain volumes in abstinent and relapsed alcoholics. Alcohol Clin Exp Res19:1177-1191. ConigraveKM, DaviesP, HaberP, WhitfieldJB (2003) Traditional markers of excessive alcohol use. Addiction98(Suppl 2):31-43. KonoH, RusynI, YinM, GabeleE, YamashinaS, DikalovaA, KadiiskaMB, ConnorHD, MasonRP, SegalBH, BradfordBU, HollandSM, ThurmanRG (2000) NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease. J Clin Invest106:867-872. PfefferbaumA, RosenbloomM, CrusanK, JerniganTL (1988) Brain CT changes in alcoholics: effects of age and alcohol consumption. Alcohol Clin Exp Res12:81-87. WhitfieldJB (2001) Gamma glutamyl transferase. Crit Rev Clin Lab Sci38:263-355. BanksWA (2005) Blood-brain barrier transport of cytokines: a mechanism for neuropathology. Curr Pharm Des11:973-984. McCrorySJ, FordI (1991) Multivariate analysis of SPECT images with illustrations in Alzheimer's disease. Stat Med10:1711-1718. HuangMC, ChenCH, PengFC, TangSH, ChenCC (2009) Alterations in oxidative stress status during early alcohol withdrawal in alcoholic patients. J Formos Med Assoc108:560-569. DrozdzR, ParmentierC, HachadH, LeroyP, SiestG, WellmanM (1998) Gamma-glutamyltransferase dependent generation of reactive oxygen species from a glutathione/transferrin system. Free Radic Biol Med25:786-792. ZhouZ, WangL, SongZ, LambertJC, McClainCJ, KangYJ (2003) A critical involvement of oxidative stress in acute alcohol-induced hepatic TNF-alpha production. Am J Pathol163:1137-1146. KugelmanA, ChoyHA, LiuR, ShiMM, GozalE, FormanHJ (1994) Gamma-glutamyl transpeptidase is increased by oxidative stress in rat alveolar L2 epithelial cells. Am J Respir Cell Mol Biol11:586-592. CrewsFT, NixonK (2009) Mechanisms of neurodegeneration and regeneration in alcoholism. Alcohol Alcohol44:115-127. PfefferbaumA, RosenbloomMJ, DeshmukhA, SullivanEV (2001) Sex differences in the effects of alcohol on brain structure. Am J Psychiatry158:188-197. LimJS, YangJH, ChunBY, KamS, JacobsDRJr, LeeDH (2004) Is serum gamma-glutamyltransferase inversely associated with serum antioxidants as a marker of oxidative stress?Free Radic Biol Med37:1018-1023. LoftS, OlesenKL, DossingM (1987) Increased susceptibility to liver disease in relation to alcohol consumption in women. Scand J Gastroenterol22:1251-1256. BeckerU, DeisA, SorensenTI, GronbaekM, Borch-JohnsenK, MullerCF, SchnohrP, JensenG (1996) Prediction of risk of liver disease by alcohol intake, sex, and age: a prospective population study. Hepatology23:1025-1029. CrewsF, NixonK, KimD, JosephJ, Shukitt-HaleB, QinL, ZouJ (2006) BHT blocks NF-kappaB activation and ethanol-induced brain damage. Alcohol Clin Exp Res30:1938-1949. EnoiuM, AberkaneH, SalazarJF, LeroyP, GroffenJ, SiestG, WellmanM (2000) Evidence for the pro-oxidant effect of gamma-glutamyltranspeptidase-related enzyme. Free Radic Biol Med29:825-833. MorimotoM, HagbjorkAL, NanjiAA, Ingelman-SundbergM, LindrosKO, FuPC, AlbanoE, FrenchSW (1993) Role of cytochrome P4502E1 in alcoholic liver disease pathogenesis. Alcohol10:459-464. MonteiroMG, MasurJ (1986) Monitoring alcoholism treatment: the appropriateness of choice between gamma GT or MCV evaluation after a short time of abstinence. Alcohol3:223-226. ZalitI, GlassGA, StarkAA (1996) The role of chelators in the catalysis of glutathione-gamma-glutamyl transpeptidase-dependent lipid peroxidation by transition metals. Biochem Mol Biol Int40:1123-1133. FeinG, Di SclafaniV, CardenasVA, GoldmannH, Tolou-ShamsM, MeyerhoffDJ (2002) Cortical gray matter loss in treatment-naive alcohol dependent individuals. Alcohol Clin Exp Res26:558-564. ParesA, CaballeriaJ, BrugueraM, TorresM, RodesJ (1986) Histological course of alcoholic hepatitis. Influence of abstinence, sex and extent of hepatic damage. J Hepatol2:33-42. ChenCH, PanCH, ChenCC, HuangMC (2011) Increased oxidative DNA damage in patients with alcohol dependence and its correlation with alcohol withdrawal severity. Alcohol Clin Exp Res35:338-344. PfefferbaumA, LimKO, ZipurskyRB, MathalonDH, RosenbloomMJ, LaneB, HaCN, SullivanEV (1992) Brain gray and white matter volume loss accelerates with aging in chronic alcoholics: a quantitative MRI study. Alcohol Clin Exp Res16:1078-1089. Urbano-MarquezA, EstruchR, Fernandez-SolaJ, NicolasJM, PareJC, RubinE (1995) The greater risk of alcoholic cardiomyopathy and myopathy in women compared with men. JAMA274:149-154. HaniganMH, FriersonHFJr (1996) Immunohistochemical detection of gamma-glutamyl transpeptidase in normal human tissue. J Histochem Cytochem44:1101-1108. MayneST (2003) Antioxidant nutrients and chronic disease: use of biomarkers of exposure and oxidative stress status in epidemiologic research. J Nutr133(Suppl 3):933S-940S. PfefferbaumA, RosenbloomMJ, ServentiKL, SullivanEV (2004) Brain volumes, RBC status, and hepatic function in alcoholics after 1 and 4 weeks of sobriety: predictors of outcome. Am J Psychiatry161:1190-1196. ZouJ, CrewsF (2006) CREB and NF-kappaB transcription factors regulate sensitivity to excitotoxic and oxidative stress induced neuronal cell death. Cell Mol Neurobiol26:385-405. CourchesneE, ChisumHJ, TownsendJ, CowlesA, CovingtonJ, EgaasB, HarwoodM, HindsS, PressGA (2000) Normal brain development and aging: quantitative analysis at in vivo MR imaging in healthy volunteers. Radiology216:672-682. QinL, WuX, BlockML, LiuY, BreeseGR, HongJS, KnappDJ, CrewsFT (2007) Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration. Glia55:453-462. HamelinkC, HampsonA, WinkDA, EidenLE, EskayRL (2005) Comparison of cannabidiol, antioxidants, and diuretics in reversing binge ethanol-induced neurotoxicity. J Pharmacol Exp Ther314:780-788. ShawS, JayatillekeE, RossWA, GordonER, LeiberCS (1981) Ethanol-induced lipid peroxidation: potentiation by long-term alcohol feeding and attenuation by methionine. J Lab Clin Med98:417-424. PrattDS, KaplanMM (2000) Evaluation of abnormal liver-enzyme results in asymptomatic patients. N Engl J Med342:1266-1271. JunghannsK, BackhausJ, VeltrupC, DagefordeJ, BruckmannH, WetterlingT (2004) Mildly disturbed hepatic and pancreatic function during early abstention from alcohol is associated with brain atrophy and with disturbed psychometric performance. Alcohol Alcohol39:113-118. FataccioliV, AndraudE, GentilM, FrenchSW, RouachH (1999) Effects of chronic ethanol administration on rat liver proteasome activities: relationship with oxidative stress. Hepatology29:14-20. Rashba-StepJ, TurroNJ, CederbaumAI (1993) Increased NADPH- and NADH-dependent production of superoxide and hydroxyl radical by microsomes after chronic ethanol treatment. Arch Biochem Biophys300:401-408. SrivastavaV, BuzasB, MomenanR, OrosziG, PulayAJ, EnochMA, HommerDW, GoldmanD (2010) Association of SOD2, a mitochondrial antioxidant enzyme, with gray matter volume shrinkage in alcoholics. Neuropsychopharmacology35:1120-1128. MomenanR, HommerD, RawlingsR, RuttimannU, KerichM, RioD (1997) Intensity-adaptive segmentation of single-echo T1-weighted magnetic resonance images. Hum Brain Mapp5:194-205. MannK, AckermannK, CroissantB, MundleG, NakovicsH, DiehlA (2005) Neuroimaging of gender differences in alcohol dependence: are women more vulnerable?Alcohol Clin Exp Res29:896-901. ZuccoliG, GallucciM, CapelladesJ, RegnicoloL, TumiatiB, GiadasTC, BottariW, MandrioliJ, BertoliniM (2007) Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. AJNR Am J Neuroradiol28:1328-1331. LatvalaJ, HietalaJ, KoivistoH, JarviK, AnttilaP, NiemelaO (2005) Immune responses to ethanol metabolites and cytokine profiles differentiate alcoholics with or without liver disease. Am J Gastroenterol100:1303-1310. Fernandez-SolaJ, EstruchR, NicolasJM, PareJC, SacanellaE, AntunezE, Urbano-MarquezA (1997) Comparison of alcoholic cardiomyopathy in women versus men. Am J Cardiol80:481-485. KarpDR, ShimookuK, LipskyPE (2001) Expression of gamma-glutamyl transpeptidase protects ramos B cells from oxidation-induced cell death. J Biol Chem276:3798-3804. De MinicisS, BrennerDA (2008) Oxidative stress in alcoholic liver disease: role of NADPH oxidase complex. J Gastroenterol Hepatol23(Suppl 1):S98-S103. HommerDW, MomenanR, KaiserE, RawlingsRR (2001) Evidence for a gender-related effect of alcoholism on brain volumes. Am J Psychiatry158:198-204. Gonzalez-QuintelaA, CamposJ, LoidiL, QuinteiroC, PerezLF, GudeF (2008) Serum TNF-alpha levels in relation to alcohol consumption and common TNF gene polymorphisms. Alcohol42:513-518. JerniganTL, ButtersN, DiTragliaG, SchaferK, SmithT, IrwinM, GrantI, SchuckitM, CermakLS (1991) Reduced cerebral grey matter observed in alcoholics using magnetic resonance imaging. Alcohol Clin Exp Res15:418-427. PaolicchiA, TongianiR, TonarelliP, ComportiM, PompellaA (1997) Gamma-glutamyl transpeptidase-dependent lipid peroxidation in isolated hepatocytes and HepG2 hepatoma cells. Free Radic Biol Med22:853-860. 1997; 80 2009; 44 2006; 30 1991; 15 1991; 10 2000; 216 2004; 161 1992; 16 1997; 5 1992; 97 2005; 29 2003; 98 2007; 28 1986; 2 2005; 100 2004; 39 1986; 3 2004; 37 2006; 26 2008; 23 1996; 23 2003; 163 2000; 29 2010; 35 1997; 22 1999; 29 2005; 314 1988; 12 2011; 35 1995; 19 1993; 300 1995; 274 2007; 55 2003; 133 1998; 25 2001; 276 1987; 22 2002; 26 2000; 106 1993; 10 1994; 11 1996; 40 2001; 38 2000; 342 2008; 42 2009; 108 2005; 11 1981; 98 2001; 158 1996; 44 e_1_2_6_51_1 e_1_2_6_32_1 Zalit I (e_1_2_6_49_1) 1996; 40 e_1_2_6_30_1 Shaw S (e_1_2_6_45_1) 1981; 98 e_1_2_6_19_1 e_1_2_6_36_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_17_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_43_1 e_1_2_6_20_1 e_1_2_6_41_1 e_1_2_6_9_1 e_1_2_6_5_1 e_1_2_6_7_1 e_1_2_6_24_1 e_1_2_6_3_1 e_1_2_6_22_1 e_1_2_6_28_1 e_1_2_6_26_1 e_1_2_6_47_1 e_1_2_6_52_1 e_1_2_6_10_1 e_1_2_6_31_1 e_1_2_6_50_1 Fein G (e_1_2_6_13_1) 2002; 26 e_1_2_6_14_1 e_1_2_6_35_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_18_1 e_1_2_6_39_1 e_1_2_6_16_1 e_1_2_6_37_1 e_1_2_6_42_1 e_1_2_6_21_1 e_1_2_6_40_1 e_1_2_6_8_1 e_1_2_6_4_1 e_1_2_6_6_1 e_1_2_6_25_1 e_1_2_6_48_1 e_1_2_6_23_1 e_1_2_6_2_1 e_1_2_6_29_1 e_1_2_6_44_1 e_1_2_6_27_1 e_1_2_6_46_1 |
| References_xml | – reference: ShawS, JayatillekeE, RossWA, GordonER, LeiberCS (1981) Ethanol-induced lipid peroxidation: potentiation by long-term alcohol feeding and attenuation by methionine. J Lab Clin Med98:417-424. – reference: PfefferbaumA, RosenbloomM, CrusanK, JerniganTL (1988) Brain CT changes in alcoholics: effects of age and alcohol consumption. Alcohol Clin Exp Res12:81-87. – reference: WhitfieldJB (2001) Gamma glutamyl transferase. Crit Rev Clin Lab Sci38:263-355. – reference: JunghannsK, BackhausJ, VeltrupC, DagefordeJ, BruckmannH, WetterlingT (2004) Mildly disturbed hepatic and pancreatic function during early abstention from alcohol is associated with brain atrophy and with disturbed psychometric performance. Alcohol Alcohol39:113-118. – reference: MomenanR, HommerD, RawlingsR, RuttimannU, KerichM, RioD (1997) Intensity-adaptive segmentation of single-echo T1-weighted magnetic resonance images. Hum Brain Mapp5:194-205. – reference: MorimotoM, HagbjorkAL, NanjiAA, Ingelman-SundbergM, LindrosKO, FuPC, AlbanoE, FrenchSW (1993) Role of cytochrome P4502E1 in alcoholic liver disease pathogenesis. Alcohol10:459-464. – reference: De MinicisS, BrennerDA (2008) Oxidative stress in alcoholic liver disease: role of NADPH oxidase complex. J Gastroenterol Hepatol23(Suppl 1):S98-S103. – reference: JerniganTL, ButtersN, DiTragliaG, SchaferK, SmithT, IrwinM, GrantI, SchuckitM, CermakLS (1991) Reduced cerebral grey matter observed in alcoholics using magnetic resonance imaging. Alcohol Clin Exp Res15:418-427. – reference: MutzellS (1992) Computed tomography of the brain, hepatotoxic drugs and high alcohol consumption in male alcoholic patients and a random sample from the general male population. Ups J Med Sci97:183-194. – reference: PfefferbaumA, RosenbloomMJ, ServentiKL, SullivanEV (2004) Brain volumes, RBC status, and hepatic function in alcoholics after 1 and 4 weeks of sobriety: predictors of outcome. Am J Psychiatry161:1190-1196. – reference: QinL, WuX, BlockML, LiuY, BreeseGR, HongJS, KnappDJ, CrewsFT (2007) Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration. Glia55:453-462. – reference: MonteiroMG, MasurJ (1986) Monitoring alcoholism treatment: the appropriateness of choice between gamma GT or MCV evaluation after a short time of abstinence. Alcohol3:223-226. – reference: BeckerU, DeisA, SorensenTI, GronbaekM, Borch-JohnsenK, MullerCF, SchnohrP, JensenG (1996) Prediction of risk of liver disease by alcohol intake, sex, and age: a prospective population study. Hepatology23:1025-1029. – reference: BanksWA (2005) Blood-brain barrier transport of cytokines: a mechanism for neuropathology. Curr Pharm Des11:973-984. – reference: LatvalaJ, HietalaJ, KoivistoH, JarviK, AnttilaP, NiemelaO (2005) Immune responses to ethanol metabolites and cytokine profiles differentiate alcoholics with or without liver disease. Am J Gastroenterol100:1303-1310. – reference: FataccioliV, AndraudE, GentilM, FrenchSW, RouachH (1999) Effects of chronic ethanol administration on rat liver proteasome activities: relationship with oxidative stress. Hepatology29:14-20. – reference: LoftS, OlesenKL, DossingM (1987) Increased susceptibility to liver disease in relation to alcohol consumption in women. Scand J Gastroenterol22:1251-1256. – reference: PfefferbaumA, RosenbloomMJ, DeshmukhA, SullivanEV (2001) Sex differences in the effects of alcohol on brain structure. Am J Psychiatry158:188-197. – reference: EnoiuM, AberkaneH, SalazarJF, LeroyP, GroffenJ, SiestG, WellmanM (2000) Evidence for the pro-oxidant effect of gamma-glutamyltranspeptidase-related enzyme. Free Radic Biol Med29:825-833. – reference: DrozdzR, ParmentierC, HachadH, LeroyP, SiestG, WellmanM (1998) Gamma-glutamyltransferase dependent generation of reactive oxygen species from a glutathione/transferrin system. Free Radic Biol Med25:786-792. – reference: ChenCH, PanCH, ChenCC, HuangMC (2011) Increased oxidative DNA damage in patients with alcohol dependence and its correlation with alcohol withdrawal severity. Alcohol Clin Exp Res35:338-344. – reference: PrattDS, KaplanMM (2000) Evaluation of abnormal liver-enzyme results in asymptomatic patients. N Engl J Med342:1266-1271. – reference: SrivastavaV, BuzasB, MomenanR, OrosziG, PulayAJ, EnochMA, HommerDW, GoldmanD (2010) Association of SOD2, a mitochondrial antioxidant enzyme, with gray matter volume shrinkage in alcoholics. Neuropsychopharmacology35:1120-1128. – reference: ZuccoliG, GallucciM, CapelladesJ, RegnicoloL, TumiatiB, GiadasTC, BottariW, MandrioliJ, BertoliniM (2007) Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. AJNR Am J Neuroradiol28:1328-1331. – reference: CourchesneE, ChisumHJ, TownsendJ, CowlesA, CovingtonJ, EgaasB, HarwoodM, HindsS, PressGA (2000) Normal brain development and aging: quantitative analysis at in vivo MR imaging in healthy volunteers. Radiology216:672-682. – reference: KonoH, RusynI, YinM, GabeleE, YamashinaS, DikalovaA, KadiiskaMB, ConnorHD, MasonRP, SegalBH, BradfordBU, HollandSM, ThurmanRG (2000) NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease. J Clin Invest106:867-872. – reference: PaolicchiA, TongianiR, TonarelliP, ComportiM, PompellaA (1997) Gamma-glutamyl transpeptidase-dependent lipid peroxidation in isolated hepatocytes and HepG2 hepatoma cells. Free Radic Biol Med22:853-860. – reference: HaniganMH, FriersonHFJr (1996) Immunohistochemical detection of gamma-glutamyl transpeptidase in normal human tissue. J Histochem Cytochem44:1101-1108. – reference: KarpDR, ShimookuK, LipskyPE (2001) Expression of gamma-glutamyl transpeptidase protects ramos B cells from oxidation-induced cell death. J Biol Chem276:3798-3804. – reference: HamelinkC, HampsonA, WinkDA, EidenLE, EskayRL (2005) Comparison of cannabidiol, antioxidants, and diuretics in reversing binge ethanol-induced neurotoxicity. J Pharmacol Exp Ther314:780-788. – reference: CrewsFT, NixonK (2009) Mechanisms of neurodegeneration and regeneration in alcoholism. Alcohol Alcohol44:115-127. – reference: KugelmanA, ChoyHA, LiuR, ShiMM, GozalE, FormanHJ (1994) Gamma-glutamyl transpeptidase is increased by oxidative stress in rat alveolar L2 epithelial cells. Am J Respir Cell Mol Biol11:586-592. – reference: ParesA, CaballeriaJ, BrugueraM, TorresM, RodesJ (1986) Histological course of alcoholic hepatitis. Influence of abstinence, sex and extent of hepatic damage. J Hepatol2:33-42. – reference: ZalitI, GlassGA, StarkAA (1996) The role of chelators in the catalysis of glutathione-gamma-glutamyl transpeptidase-dependent lipid peroxidation by transition metals. Biochem Mol Biol Int40:1123-1133. – reference: Gonzalez-QuintelaA, CamposJ, LoidiL, QuinteiroC, PerezLF, GudeF (2008) Serum TNF-alpha levels in relation to alcohol consumption and common TNF gene polymorphisms. Alcohol42:513-518. – reference: ZouJ, CrewsF (2006) CREB and NF-kappaB transcription factors regulate sensitivity to excitotoxic and oxidative stress induced neuronal cell death. Cell Mol Neurobiol26:385-405. – reference: FeinG, Di SclafaniV, CardenasVA, GoldmannH, Tolou-ShamsM, MeyerhoffDJ (2002) Cortical gray matter loss in treatment-naive alcohol dependent individuals. Alcohol Clin Exp Res26:558-564. – reference: ZhouZ, WangL, SongZ, LambertJC, McClainCJ, KangYJ (2003) A critical involvement of oxidative stress in acute alcohol-induced hepatic TNF-alpha production. Am J Pathol163:1137-1146. – reference: HommerDW, MomenanR, KaiserE, RawlingsRR (2001) Evidence for a gender-related effect of alcoholism on brain volumes. Am J Psychiatry158:198-204. – reference: MayneST (2003) Antioxidant nutrients and chronic disease: use of biomarkers of exposure and oxidative stress status in epidemiologic research. J Nutr133(Suppl 3):933S-940S. – reference: Urbano-MarquezA, EstruchR, Fernandez-SolaJ, NicolasJM, PareJC, RubinE (1995) The greater risk of alcoholic cardiomyopathy and myopathy in women compared with men. JAMA274:149-154. – reference: McCrorySJ, FordI (1991) Multivariate analysis of SPECT images with illustrations in Alzheimer's disease. Stat Med10:1711-1718. – reference: ConigraveKM, DaviesP, HaberP, WhitfieldJB (2003) Traditional markers of excessive alcohol use. Addiction98(Suppl 2):31-43. – reference: CrewsF, NixonK, KimD, JosephJ, Shukitt-HaleB, QinL, ZouJ (2006) BHT blocks NF-kappaB activation and ethanol-induced brain damage. Alcohol Clin Exp Res30:1938-1949. – reference: LimJS, YangJH, ChunBY, KamS, JacobsDRJr, LeeDH (2004) Is serum gamma-glutamyltransferase inversely associated with serum antioxidants as a marker of oxidative stress?Free Radic Biol Med37:1018-1023. – reference: PfefferbaumA, SullivanEV, MathalonDH, ShearPK, RosenbloomMJ, LimKO (1995) Longitudinal changes in magnetic resonance imaging brain volumes in abstinent and relapsed alcoholics. Alcohol Clin Exp Res19:1177-1191. – reference: MannK, AckermannK, CroissantB, MundleG, NakovicsH, DiehlA (2005) Neuroimaging of gender differences in alcohol dependence: are women more vulnerable?Alcohol Clin Exp Res29:896-901. – reference: HuangMC, ChenCH, PengFC, TangSH, ChenCC (2009) Alterations in oxidative stress status during early alcohol withdrawal in alcoholic patients. J Formos Med Assoc108:560-569. – reference: PfefferbaumA, LimKO, ZipurskyRB, MathalonDH, RosenbloomMJ, LaneB, HaCN, SullivanEV (1992) Brain gray and white matter volume loss accelerates with aging in chronic alcoholics: a quantitative MRI study. Alcohol Clin Exp Res16:1078-1089. – reference: Rashba-StepJ, TurroNJ, CederbaumAI (1993) Increased NADPH- and NADH-dependent production of superoxide and hydroxyl radical by microsomes after chronic ethanol treatment. Arch Biochem Biophys300:401-408. – reference: Fernandez-SolaJ, EstruchR, NicolasJM, PareJC, SacanellaE, AntunezE, Urbano-MarquezA (1997) Comparison of alcoholic cardiomyopathy in women versus men. 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| Snippet | Background: Oxidative stress has been proposed as one of the mechanisms of alcohol‐induced brain shrinkage and alcohol‐induced hepatotoxicity. The aim of this... Background: Oxidative stress has been proposed as one of the mechanisms of alcohol‐induced brain shrinkage and alcohol‐induced hepatotoxicity. The aim of this... Oxidative stress has been proposed as one of the mechanisms of alcohol-induced brain shrinkage and alcohol-induced hepatotoxicity. The aim of this study was to... Background: Oxidative stress has been proposed as one of the mechanisms of alcohol-induced brain shrinkage and alcohol-induced hepatotoxicity. The aim of this... |
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| SubjectTerms | Addictive behaviors Adult and adolescent clinical studies Age of Onset Aged Aging Aging - physiology Alanine transaminase Albumin Alcohol Dependence Alcoholism Alcoholism - cerebrospinal fluid Alcoholism - pathology Alcoholism - physiopathology Alcoholism and acute alcohol poisoning Aspartate aminotransferase Atrophy Biological and medical sciences Body Mass Index Brain Brain - pathology Brain Shrinkage Cerebrospinal fluid Diagnostic and Statistical Manual of Mental Disorders Drug abuse Drug dependence Educational Status Ethanol Female Hematocrit Humans Image Processing, Computer-Assisted Linear Models Liver Liver - physiopathology Liver Function Liver Function Tests Magnetic Resonance Imaging Male Medical sciences Middle Aged MRI Oxidative stress Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Regression analysis Sex Sex Characteristics Smoking - epidemiology Socioeconomic Factors Substantia alba Toxicology |
| Title | Relationship Between Liver Function and Brain Shrinkage in Patients with Alcohol Dependence |
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