Dataset Information

Cumulative Betel Quid Chewing and the Risk of Significant Liver Fibrosis in Subjects With and Without Metabolic Syndrome.

ABSTRACT:

Background

Betel quid chewing is associated with metabolic disorders, oral cancer, cardiovascular disease, and chronic liver diseases. Metabolic syndrome (MetS) is also a factor associated with liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). However, studies on the relationship between betel quid and liver fibrosis while also considering MetS are lacking. The aim of this study was thus to investigate the association of betel quid chewing and liver fibrosis with MetS.

Methods

A total of 9,221 subjects were enrolled after excluding subjects <18 years of age, with past history of chronic liver diseases, cancer, significant alcohol consumption, and incomplete data. Betel nut chewing habit was classified into three groups: none, former-chewing, and current-chewing, and cumulative exposure was calculated by multiplying the duration with the quantity. Liver fibrosis was evaluated based on the NAFLD fibrosis score (NFS), which is a composite score of age, hyperglycemia, BMI, platelet count, albumin, and the AST/ALT ratio. Significant liver fibrosis was defined as NFS ≥-1.455.

Results

After adjusting for other variables, MetS was positively associated with significant liver fibrosis. Subjects with both MetS and betel quid chewing had a higher associated risk of significant liver fibrosis than those with neither MetS nor betel quid chewing (adjusted OR: 3.03, 95% CI: 2.04-4.50, p < 0.001). Betel quid chewing was associated with significant liver fibrosis (adjusted OR: 2.00, 95% CI: 1.14-3.49, p = 0.015) in subjects with MetS, but not in subjects without.

Conclusion

Metabolic syndrome increased the associated risk of significant liver fibrosis. Cumulative betel quid exposure increased the associated risk of significant liver fibrosis in subjects with MetS, but not in subjects without.

SUBMITTER: Chou YT

PROVIDER: S-EPMC8873786 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Publications

Cumulative Betel Quid Chewing and the Risk of Significant Liver Fibrosis in Subjects With and Without Metabolic Syndrome.

Chou Yu-Tsung YT Sun Zih-Jie ZJ Shen Wei-Chen WC Yang Yi-Ching YC Lu Feng-Hwa FH Chang Chih-Jen CJ Li Chung-Yi CY Wu Jin-Shang JS

Frontiers in nutrition 20220211

<h4>Background</h4>Betel quid chewing is associated with metabolic disorders, oral cancer, cardiovascular disease, and chronic liver diseases. Metabolic syndrome (MetS) is also a factor associated with liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). However, studies on the relationship between betel quid and liver fibrosis while also considering MetS are lacking. The aim of this study was thus to investigate the association of betel quid chewing and liver fibrosis with MetS.<h4>Me ...[more]

PMID: 35223941

Similar Datasets

Project description:BackgroundBetel quid chewing is a common habit widely practiced in Southern Asian populations. However, variations are seen in the content of a betel quid across the different countries. Factors associated with commencement and cessation of this habit has been numerously studied. Unfortunately, data on Malaysian population is non-existent. This study aims to determine the factors associated with the inception and also cessation of betel quid chewing behaviour among Malaysian adults.MethodThis study is part of a nationwide survey on oral mucosal lesions carried out among 11,697 adults in all fourteen states in Malaysia. The questionnaire included sociodemographic information and details on betel quid chewing habit such as duration, type and frequency. The Kaplan-Meier estimates were calculated and plotted to compare the rates for the commencement and cessation of betel quid chewing behaviour. Cox proportional hazard regression models were used to calculate the hazard rate ratios for factors related to commencement or cessation of this habit.ResultsOf the total subjects, 8.2% were found to be betel quid chewers. This habit was more prevalent among females and, in terms of ethnicity, among the Indians and the Indigenous people of Sabah and Sarawak. Cessation of this habit was more commonly seen among males and the Chinese. Females were found to be significantly more likely to start (p < 0.0001) and less likely to stop the quid chewing habit. Females, those over 40 years old, Indians and a history of smoking was found to significantly increase the likelihood of developing a quid chewing habit (p < 0.0001). However, those who had stopped smoking were found to be significantly more likely to promote stopping the habit (p = 0.0064). Cessation was also more likely to be seen among those who chewed less than 5 quids per day (p < 0.05) and less likely to be seen among those who included areca nut and tobacco in their quid (p < 0.0001).ConclusionFactors that influence the development and cessation of this behaviour are gender, age, ethnicity, and also history of smoking habit while frequency and type of quid chewed are important factors for cessation of this habit.

Project description:Betel Quid (BQ) chewing independently contributes to oral, hepatic and esophageal carcinomas. Strong association of breast cancer risk with BQ chewing in Northeast Indian population has been reported where this habit is prodigal. We investigated genomic alterations in breast cancer patients with and without BQ chewing exposure. Twenty six BQ chewers (BQC) and 17 non BQ chewer (NBQC) breast cancer patients from Northeast India were analyzed for genomic alterations and pathway networks using SNP array and IPA. BQC tumors showed significantly (P<0.01) higher total number of alterations, as compared with NBQC tumors, 48 ± 17% versus 32 ± 25 respectively. Incidence of gain in fragile sites in BQC tumors were significantly (P<0.001) higher as compared with NBQC tumors, 34 versus 23% respectively. Two chromosomal regions (7q33 and 21q22.13) were significantly (p<0.05) associated with BQC tumors while two regions (19p13.3-19p12 and 20q11.22) were significantly associated with NBQC tumors. GO terms oxidoreductase and aldo-keto reductase activity in BQC tumors in contrast to G-protein coupled receptor protein signaling pathway and cell surface receptor linked signal transduction in NBQC tumors were enriched in DAVID. One network "Drug Metabolism, Molecular Transport, Nucleic Acid Metabolism" including genes AKR1B1, AKR1B10, ETS2 etc in BQC and two networks "Molecular Transport, Nucleic Acid Metabolism, Small Molecule Biochemistry" and "Cellular Development, Embryonic Development, Organismal Development" including genes RPN2, EMR3, VAV1, NNAT and MUC16 etc were seen in NBQC. Common alterations (>30%) were seen in 27 regions. Three networks were significant in common regions with key roles of PTK2, RPN2, EMR3, VAV1, NNAT, MUC16, MYC and YWHAZ genes. These data show that breast cancer arising by environmental carcinogens exemplifies genetic alterations differing from those observed in the non exposed ones. A number of genetic changes are shared in both tumor groups considered as crucial in breast cancer progression.

Dataset Information

Cumulative Betel Quid Chewing and the Risk of Significant Liver Fibrosis in Subjects With and Without Metabolic Syndrome.

Background

Methods

Results

Conclusion

Publications

Cumulative Betel Quid Chewing and the Risk of Significant Liver Fibrosis in Subjects With and Without Metabolic Syndrome.

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