Association of serum lactate dehydrogenase levels with non-alcoholic fatty liver disease and advanced hepatic fibrosis in the United States: a cross-sectional study using NHANES data from 2007 to 2018

The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF. In this cross-sectional study, after...

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Published inBMC gastroenterology Vol. 25; no. 1; pp. 467 - 15
Main Authors Zhang, Xiaotong, Liu, Min, Huang, Junjun, Zheng, Ya, Wang, Yuping, Zhou, Yongning
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 01.07.2025
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Abstract The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF. In this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM). Following data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378-6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI (β  = 0.965, 95% CI: 0.014-1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose-response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups. This study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes.
AbstractList The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF. In this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM). Following data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378-6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI ([beta].sub.Q2 vs. Q1 = 0.965, 95% CI: 0.014-1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose-response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups. This study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes.
Background The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF. Methods In this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM). Results Following data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378-6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI ([beta].sub.Q2 vs. Q1 = 0.965, 95% CI: 0.014-1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose-response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups. Conclusions This study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes. Keywords: NAFLD, Lactate dehydrogenase, NHANES, Biomarker, Cross-sectional analysis
BackgroundThe associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF.MethodsIn this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM).ResultsFollowing data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378–6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI (βQ2 vs. Q1 = 0.965, 95% CI: 0.014–1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose–response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups.ConclusionsThis study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes.
The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF. In this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM). Following data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378-6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI (β  = 0.965, 95% CI: 0.014-1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose-response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups. This study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes.
Abstract Background The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF. Methods In this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM). Results Following data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378–6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI (βQ2 vs. Q1 = 0.965, 95% CI: 0.014–1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose–response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups. Conclusions This study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes.
The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF.BACKGROUNDThe associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims to investigate the association between log-transformed LDH levels and the prevalence of NAFLD and AHF.In this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM).METHODSIn this cross-sectional study, after applying specific criteria for inclusion and exclusion, a total of 7,316 individuals were chosen from the 59,842 participants for the final analysis. LDH levels were measured using an enzymatic rate method. A fatty liver index (FLI) greater than or equal to 60 and an NAFLD fibrosis score (NFS) higher than 0.676 were found to be indicative of hepatic steatosis and advanced hepatic fibrosis. Both weighted multivariable linear and logistic regression analyses were used to finish the study. Moreover, additional analyses were performed utilizing weighted stratified analysis and weighted smoothed curve fitting using the generalized additive model (GAM).Following data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378-6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI (βQ2 vs. Q1 = 0.965, 95% CI: 0.014-1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose-response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups.RESULTSFollowing data analysis, the multivariable regression model 3 showed a significant association between the elevated log-transformed LDH levels and AHF (OR: 3.087, 95% CI: 1.378-6.915, P = 0.007). Furthermore, a modest association was observed between log-transformed LDH tertiles and FLI (βQ2 vs. Q1 = 0.965, 95% CI: 0.014-1.916, P = 0.047). However, there was no evidence to prove that there was an association between log-transformed LDH levels and NAFLD in model 3. The weighted smoothed curve fitting using the GAM suggested a linear dose-response effect between log-transformed LDH levels and an increased risk of NAFLD, as well as a non-linear relationship between log-transformed LDH levels with AHF risk. Moreover, the weighted stratified analysis further suggested that the associations of log-transformed LDH with NAFLD and AHF could differ in different population groups.This study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes.CONCLUSIONSThis study indicates that elevated log-transformed LDH levels are associated with an increased prevalence of AHF in our study population. However, the cross-sectional study analysis cannot prove causality, which requires further cohort studies or mechanistic studies to elucidate the precise mechanisms and root causes.
ArticleNumber 467
Audience Academic
Author Wang, Yuping
Zhang, Xiaotong
Liu, Min
Zhou, Yongning
Huang, Junjun
Zheng, Ya
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/40597710$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Lactate dehydrogenase
Biomarker
NAFLD
NHANES
Cross-sectional analysis
Language English
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Snippet The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This study aims...
Background The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This...
BackgroundThe associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been explored. This...
Abstract Background The associations between LDH and non-alcoholic fatty liver disease (NAFLD), as well as advanced hepatic fibrosis (AHF), have not been...
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SubjectTerms Adult
Alcohol
Analysis
Biomarker
Biomarkers
Biopsy
Body mass index
Care and treatment
Complications and side effects
Cross-sectional analysis
Cross-Sectional Studies
Dehydrogenases
Diabetes
Diagnosis
Diseases
Enzymes
Fatty liver
Female
Fibrosis
Health aspects
Hepatitis
Humans
Hypertension
Information management
L-Lactate dehydrogenase
L-Lactate Dehydrogenase - blood
Lactate dehydrogenase
Liver cancer
Liver cirrhosis
Liver Cirrhosis - blood
Liver Cirrhosis - epidemiology
Liver diseases
Male
Marital status
Measurement
Metabolism
Middle Aged
NAFLD
NHANES
Non-alcoholic Fatty Liver Disease - blood
Non-alcoholic Fatty Liver Disease - epidemiology
Nutrition
Nutrition Surveys
Population studies
Prevalence
Reagents
Risk factors
Secondary schools
Steatosis
Time trends (Statistics)
United States
United States - epidemiology
Weight control
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Title Association of serum lactate dehydrogenase levels with non-alcoholic fatty liver disease and advanced hepatic fibrosis in the United States: a cross-sectional study using NHANES data from 2007 to 2018
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linkProvider Directory of Open Access Journals
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