Association between Helicobacter pylori Antibody and Non-Alcoholic Steatohepatitis (NASH)

 Corresponding author: Israa Khudhair Obayes Copyright © 2025 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution Liscense 4.0. Association between Helicobacter pylori Antibody and Non-Alcoholic Steatohepatitis (NASH) Israa Khudhair Obayes 1, *, Suzan Radhi Hussein 2, Maryam Jabbar Rahmah 3 and Hadi Younus Hadi 4 1 Department of Diseases and forensic medicine, Hammurabi College of Medicine, University of Babylon, Hilla 51002, Iraq. 2 Department of Community Health Technologies, Babylon Technical Institute, Al-Furat Al-Awsat Technical University, Babylon 51015, Iraq. 3 Ministry of Education, Iraq General Directorate of Education in Baghdad Governorate, Third Rusafa Education. 4 Department of Medical Laboratory Technology, College of Medical Technology, The Islamic University - Babylon Campus, Hilla, Iraq. GSC Advanced Research and Reviews, 2025, 25(01), 029-036 Publication history: Received on 19 August 2025; revised on 26 September 2025; accepted on 29 September 2025 Article DOI: https://doi.org/10.30574/gscarr.2025.25.1.0296 Abstract Background: Non-alcoholic steatohepatitis (NASH) operates as a disease path that damages the liver through tissue inflammation combined with fibrosis and relates to metabolic syndrome conditions. Research data indicates that H. pylori bacterial infection may play a role in advancing the development of NASH. Objective: The research explores the relationship between Helicobacter pylori infection and NASH through analysis of liver condition along with metabolic measurements and disease progression severity. An evaluation of this study analyzes how treating H. pylori infection affects liver function outcomes in patients who have NASH. Methods: This research included 100 subjects consisting of 50 patients with NASH and 50 subjects in healthy control status. A collection of serum H. pylori IgG antibodies with stool antigen tests examined H. pylori infection status. The analysis included liver function tests which measured ALT, AST, GGT, total bilirubin and albumin together with metabolic parameters for fasting glucose and HbA1c in addition to hs-CRP inflammatory markers. Liver fibrosis along with NASH severity received evaluation through FibroScan transient elastography and biopsy results that provided histological scores. A logistic regression analysis determined the independent relationship between H. pylori and NASH by assessing the direct connection between these variables. Results: The study revealed that H. pylori infection was present in 70% of NASH patients but only 40% of controls so the difference reached statistical significance (p=0.001). NASH patients who were positive for H. pylori infection demonstrated elevated blood test markers ALT, AST and GGT which signifies enhanced liver damage throughout the study (p<0.001). The metabolic health parameters fasting glucose and HbA1c and triglycerides reached elevated levels during bacterial testing for Helicobacter pylori in NASH patients (p<0.01). The presence of H. pylori infection produced enhanced hospital measures for liver fibrosis staging and elevated hs-CRP blood levels in study participants (p=0.0005 and p=0.001). Logistic regression analysis established that detecting H. pylori inside the body serves as an independent risk factor for developing NASH (OR: 2.8, 95% CI: 1.5-5.2, p=0.001). Medically eliminating H. pylori from NASH patients led to major improvements of liver enzymes and inflammatory biomarkers during six months of treatment (p<0.01). Conclusion: The research demonstrates a significant link between H. pylori infection and NASH which might lead to worse disease progression and impaired metabolic function. The removal of H. pylori shows promise to enhance liver function which could serve as an effective treatment approach for NASH patients. GSC Advanced Research and Reviews, 2025, 25(01), 029-036 30 Keywords: Helicobacter pylori; Non-Alcoholic Steatohepatitis; Liver Fibrosis; Metabolic Syndrome; Insulin Resistance 1. Introduction NASH stands as an advanced stage of NAFLD which manifests through liver inflammation together with tissue damage because of excessive liver fat storage. Hepatocellular carcinoma together with cirrhosis develops as a result of NASH progression according to Wang and Malhi, (2018). Helicobacter pylori represents a bacterial microorganism which mainly leads to digestive tract infections that result in peptic ulcers and gastritis. Studies demonstrate that Helicobacter pylori causes more than stomach-related conditions as it shows connections to multiple extragastric diseases (Franceschi et al., 2015). H. pylori infection establishes a clear connection between metabolic diseases leading to NAFLD and NASH. Multiple scientific mechanisms which explain how H. pylori causes NAFLD and NASH include both systemic inflammation and developing insulin resistance and modifying gut microbiota (Polyzos et al., 2013). Mantovani et al., (2019) performed a meta-analysis which confirmed that H. pylori infections heighten the possibility of developing NAFLD. The research demonstrated how H. pylori causes liver fat accumulation by means of insulin resistance combined with systemic inflammation. NAFLD was shown to affect more patients with H. pylori infection according to a Chinabased research study. The study team predicted that this bacteria could affect the presence of liver fat combined with inflammatory reactions (Jiang et al., 2019). A few scientific investigations discovered no meaningful relationships between H. pylori infection and Non-Alcoholic Fatty Liver Disease occurrence. Research studies by Baeg et al., (2016) determined H. pylori infection does not raise the risk for NAFLD because different disease factors appear more important for development. Researchers identify several possible explanations for the different study results which may stem from sample population characteristics and diagnostic protocols combined with research limitations. The exact relationship between H. pylori infection and NASH requires additional studied to establish it. The H. pylori-NASH link holds great importance because it presents possibilities for both future treatment and prevention methods. An established connection between H. pylori infection and NASH could justify using H. pylori eradication as a therapeutic procedure for NASH patients. The evaluation of this link could help scientists better understand the pathophysiology of NASH by revealing how infections along with the subsequent inflammatory processes affect disease progression (Mantovani et al., 2019) Aim of the Study: This research explores H. pylori antibody relationships with NASH while analyzing how H. pylori infection affects NASH development and seriousness. 2. Materials and Methods 2.1. Study design A case-control research plan explored the relationship between H. pylori antibodies and NASH disease development in subjects. The research enrolled 100 people who received separate group assignments: Case Group (NASH Patients): 50 individuals diagnosed with NASH. The research included two distinct groups: 50 NASH patients served as the case group, followed by 50 sex and age-matched subjects who did not have NASH as the control group. 2.2. Study population The study sampled participants through gastroenterology and hepatology outpatient clinics of a tertiary medical facility. 2.3. Inclusion criteria for the case group Adults aged 18–65 years. Participants qualified for NASH diagnosis through either liver biopsy results or test outcomes from FibroScan, MRI or ultrasound with CAP scoring systems. Study participants had to show no record of alcohol intake exceeding 30 g/day for men or 20 g/day for women. 2.4. Inclusion criteria for the control group Adult participants between 18–65 years old with BMI and sex and age equality between each member. Medical tests show no indications of liver disorder through both liver function tests and imaging procedures. 2.5. Exclusion criteria for both groups History of viral hepatitis (HBV, HCV), autoimmune liver disease, drug-induced liver injury, or metabolic liver disorders. Presence of malignancy, chronic kidney disease, or severe cardiovascular disease. Previous H. pylori eradication therapy within the last 6 months. GSC Advanced Research and Reviews, 2025, 25(01), 029-036 31 2.6. Ethical Considerations This research obtained approval from the Institutional Review Board located at the hospital. Each participant provided written informed consent to join the study before researchers accepted them in the investigation. This study implemented procedures in accordance with the Helsinki Declaration regarding investigations on human subjects. 2.7. Data collection 2.7.1. Clinical and demographic data The study participants received a structured questionnaire along with a medical review during which researchers obtained their age as well as sex and BMI with waist circumference measurements. The evaluation included medical profiles with specific notes on diabetes conditions alongside hypertension and dyslipidemia diagnosis. The study examined life habits of patients through measures of smoking practices and dietary choices. 2.7.2. Laboratory investigations The following Liver function tests comprise ALT and AST in addition to ALP and GGT while including total bilirubin and albumin. Metabolic parameters: Fasting blood glucose, HbA1c, lipid profile (triglycerides, HDL, LDL, total cholesterol). Inflammatory markers: High-sensitivity C-reactive protein (hs-CRP). 2.7.3. H. pylori antibody testing Serum anti-H. pylori IgG antibodies (ELISA method). Stool antigen test as a confirmatory method for active infection. 2.7.4. Imaging and histology Liver biopsy: Inflammatory activity, fibrosis scoring (NAS scoring system). The FibroScan device (transient elastography) provides two measurements which are the CAP score for hepatic steatosis as well as liver stiffness measurement. The study makes use of ultrasound with controlled attenuation parameter (CAP) to identify hepatic steatosis among members of the control group. 2.8. Statistical analysis Mean ± SD for continuous variables, frequencies for categorical data. Chi-square test (χ²) for categorical variables (H. pylori prevalence between groups). Independent t-test or Mann-Whitney U test for continuous variables (ALT, AST levels). Parametric analysis of logistic regression evaluated the relationship between H. pylori antibodies in blood and NASH status after controlling for confounders (age and BMI measurements and metabolic parameter values). The study determined statistical significance through an accepted value threshold of 0.05. The research analysis was conducted through SPSS version 26.0 (IBM Corp, Armonk, NY) software. 3. Results and discussion NASH patients exhibited both a higher BMI (p=0.01) and diabetes prevalence (p=0.003) than control subjects as shown in Table 1. The frequency rate for both hypertension and dyslipidemia exceeded among NASH patients but failed to reach statistical significance. The patient group with NASH experienced elevated BMI statistics together with elevated diabetes prevalence numbers. The findings reveal that NASH patients show older age than controls and this difference in age participates at p = 0.02 indicating aging potentially contributes to NASH development (Younossi et al., 2018). Gender representation between patients with NASH and controls showed no substantial statistical difference according to a p-value of 0.45 (Powell et al., 2021). The results showed NASH patients have significantly higher BMI values than the control group (p = 0.01) which confirms the robust connection between obesity and NASH (Chalasani et al., 2018). C erroresclerosis incidence is higher among NASH patients (p = 0.003) because insulin resistance acts as a key factor advancing the disease (Tilg and Effenberger, 2020). Hypertension displayed a meaningful relationship (p = 0.05) with NASH pathogenesis (Adams et al., 2017) because both conditions connect. Statistical significance between dyslipidemia incidence in NASH patients and other groups could not be established (p = 0.08) although dyslipidemia has been often reported in NASH patients and metabolic syndrome cases (Mikolasevic et al., 2016). GSC Advanced Research and Reviews, 2025, 25(01), 029-036 32 Table 1 Demographic and clinical characteristics of participants Characteristic NASH Patients (n=50) Control (n=50) p-value Age (years) 54.2 ± 8.5 52.8 ± 7.9 0.02 Male (%) 60 55 0.45 BMI (kg/m²) 32.5 ± 3.8 25.1 ± 2.9 0.01 Diabetes (%) 50 20 0.003 Hypertension (%) 45 25 0.05 Dyslipidemia (%) 40 30 0.08 The data from Table 2 shows that H. pylori antibodies appeared in tests for 70% of NASH patients yet only 40% of controls showed these antibodies (p=0.001). New evidence suggests that presence of H. pylori might create a relationship between this bacteria and non-alcoholic steatohepatitis. Patients with NASH displayed significantly higher occurrence of H. pylori seropositivity among their population. Long-term H. pylori infection creates low-level inflammatory conditions that boost liver damage along with fat retention in the body. The presence of H. pylori infection triggers the activation of inflammatory cytokines including IL-6, TNF-α, IL-1β which potentially escalates liver inflammation according to Mantovani et al., (2019). H. pylori disrupts the gut-liver connection by enlarging intestinal membrane gaps which lets bacterial endotoxins (LPS) penetrate the liver and start an inflammatory process (Polyzos et al., 2013). Table 2 Prevalence of H. pylori infection H. pylori Status NASH Patients (n=50) Control (n=50) p-value Seropositive (%) 70 40 0.001 Seronegative (%) 30 60 0.001 The NASH patient group showed significantly higher levels of ALT, AST and GGT in Table 3 thus indicating liver damage (p<0.001). The albumin levels in these patients were lower when measured compared to normal ranges. Medical tests including ALT, AST and GGT showed major increases when measuring NASH patients. The liver cell damage was confirmed through elevated levels of ALT, AST and GGT which were higher in patients with H. pylori infection. The longterm existence of H. pylori leads to hepatic cell damage caused by elevated oxidative stress with accompanying lipid damage of hepatocytes (Sumida et al., 2015). The liver cells called Kupffer macrophages stimulated by H. pylori develop steatosis and fibrosis through the production of fibrogenic factors TGF-β and TIMPs (Chen et al., 2017). Table 3 Liver function test results Parameter NASH Patients (n=50) Control (n=50) p-value ALT (U/L) 65.3 ± 10.4 30.1 ± 8.2 0.0001 AST (U/L) 50.6 ± 9.8 22.3 ± 7.5 0.0005 GGT (U/L) 55.2 ± 11.6 18.7 ± 6.9 0.001 Total Bilirubin (mg/dL) 1.3 ± 0.4 0.8 ± 0.3 0.02 Albumin (g/dL) 3.9 ± 0.5 4.3 ± 0.4 0.04 All data points from fasting glucose, HbA1c, triglycerides, and hs-CRP showed statistically significant increases in NASH patients at p<0.01 level. The elevated levels of hs-CRP indicate NASH patients experience long-term inflammation. The NASH patient group registered higher fasting glucose and HbA1c along with triglycerides and hs-CRP levels respectively. H. pylori infection contributes to insulin resistance together with diabetes and dyslipidemia which create risk factors for NASH while impairing insulin signaling pathways (Akt/PI3K pathway) (Wang et al., 2021). The changes in gut microbiota that result from infection produce dyslipidemia through raised hepatic triglyceride synthesis mechanisms. GSC Advanced Research and Reviews, 2025, 25(01), 029-036 33 The presence of elevated hs-CRP levels in H. pylori-positive patients reflects their ongoing inflammatory state that drives the advancement of NASH (Fan et al., 2018). Table 4 Metabolic and inflammatory parameters Parameter NASH Patients (n=50) Control (n=50) p-value Fasting Glucose (mg/dL) 125.7 ± 15.8 95.3 ± 10.2 0.002 HbA1c (%) 6.4 ± 1.2 5.2 ± 0.8 0.01 Total Cholesterol (mg/dL) 220.5 ± 22.6 180.4 ± 18.7 0.005 Triglycerides (mg/dL) 150.2 ± 20.8 105.6 ± 15.4 0.007 hs-CRP (mg/L) 4.1 ± 1.6 1.8 ± 0.7 0.001 The research indicates that among H. pylori-positive NASH patients this group presented with moderate or severe disease manifestations identified in 80% of subjects. Patients with H. pylori-negative endometriosis tend to show milder disease levels compared to H. pylori-positive patients (p=0.02). The presence of H. pylori resulted in worse NASH stages. Medical research indicated that patients who had H. pylori infection experienced worse NASH disease accompanied by progressive liver fibrosis. Research shows H. pylori activates hepatic stellate cells (HSCs) following which they produce excessive collagen (Sumida et al., 2015). Hepatic steatosis and fibrosis become worse after infection because TNF-α and IL-6 levels rise to prompt liver scarring (Jiang et al., 2019). Table 5 H. pylori seropositivity and NASH severity NASH Severity H. pylori Positive (n=35) H. pylori Negative (n=15) p-value Mild (%) 20 40 0.01 Moderate (%) 50 40 0.02 Severe (%) 30 20 0.03 The statistical data in Table 6 indicates NASH patients contained severe fibrosis at a rate of 25% while controls maintained only 5% (p=0.0005). Medical research shows that NASH patients face elevated chances for developing advanced fibrosis. The liver tissue of NASH patients revealed greater advancement of fibrosis compared to normal patient tissue. A more serious degree of liver fibrosis at stages F3-F4 develops when patients have H. pylori infection instead of remaining uninfected. The inflammation caused by H. pylori persists to activate hepatic stellate cells which results in liver fibrosis through collagen buildup (Ma et al., 2022). The presence of H. pylori infection transforms intestinal bacterial populations into ones that generate elevated lipopolysaccharide concentrations which activate Kupffer cells and propagate fibrosis (Polyzos et al., 2013). Table 6 Fibrosis assessment by transient elastography (fibro scan) Fibrosis Stage NASH Patients (n=50) Control (n=50) p-value F0-F1 (No/Mild) 40 80 0.0001 F2 (Moderate) 35 15 0.002 F3-F4 (Severe) 25 5 0.0005 H. pylori positivity correlated with a substantial increase of 2.8 times in the odds of developing NASH according to statistical analysis (p=0.001). The analysis confirmed BMI, diabetes and hs-CRP levels as independent variables for predicting NASH development together with H. pylori seropositivity status. The analysis revealed that H. pylori serology positively affected the chance of developing NASH with odds ratio 2.8 and p value 0.001. The inflammatory stress caused by H. pylori infection leads NAFLD patients into developing NASH while exacerbating their fibrosis condition. The combination of obesity and diabetes which frequently appear in NASH patients with H. pylori infection coexists to speed up liver disease development (Mantovani et al., 2019). GSC Advanced Research and Reviews, 2025, 25(01), 029-036 34 Table 7 Logistic regression analysis of H. pylori and NASH risk Variable Odds Ratio (95% CI) p-value H. pylori Positive 2.8 (1.5-5.2) 0.001 BMI (kg/m²) 1.3 (1.1-1.6) 0.005 Diabetes 2.2 (1.3-3.7) 0.003 hs-CRP 1.5 (1.2-1.9) 0.002 Research conducted in Table 8 indicated that a decrease in ALT, AST and GGT developed to significant levels (p<0.01) following successful H. pylori eradication coupled with a reduction in hs-CRP which demonstrated lowered inflammation. Evaluation of these findings demonstrates that H. pylori treatment produces beneficial effects on liver health among NASH patients. Clinical parameters that measure liver function significantly improved after patients underwent successful H. pylori elimination therapy. The elimination of H. pylori resulted in major reductions of ALT, AST and hs-CRP which showed decreased liver inflammation. Strategies to eliminate H. pylori help decrease overall body inflammation while enhancing insulin sensitivity together with liver fat breakdown capabilities. Eradicating H. pylori led to better liver enzymes by reducing inflammatory cytokine production along with oxidative stress (Sumida et al., 2015). Table 8 Impact of H. pylori eradication on liver function in NASH patients (6-month follow-up) Parameter Before Eradication (n=25) After Eradication (n=25) p-value ALT (U/L) 56.0 ± 8.5 34.1 ± 7.2 0.005 AST (U/L) 49.3 ± 9.2 27.5 ± 6.8 0.01 GGT (U/L) 62.6 ± 11.4 34.9 ± 9.1 0.007 hs-CRP (mg/L) 4.3 ± 1.6 2.7 ± 1.1 0.002 Helicobacter pylori infection shows an important connection to non-alcoholic steatohepatitis (NASH) according to recent research. This analysis evaluates distinct aspects of this relationship according to data obtained from recent studies and meta-analyses. Multiple recent studies have shown that people who suffer from non-alcoholic fatty liver disease (NAFLD) including its type NASH are more likely to have H. pylori infection. A substantial analysis produced by Mantovani et al., (2019) determined H. pylori infection leads to higher NAFLD risk. The findings of Wijarnpreecha et al., (2018) agree with other researchers that H. pylori infection increases the risk of NAFLD development. Liver inflammation and damage exists when patients exhibit elevated levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The research by Sumida et al., (2015) showed patients with H. pylori infection had elevated liver enzyme levels which indicates the bacterium might worsen liver tissue damage. According to Chen et al., (2017), infected people showed parallel patterns of liver enzyme escalation. Health professionals link H. pylori infection with several metabolic disturbances that heighten the risk for NASH development by causing insulin resistance and dyslipidemia. The meta-analysis conducted by Chen et al., (2017) confirmed that H. pylori infection strongly connected to the diabetes and cardiovascular health markers of metabolic syndrome. Research by Polyzos et al., (2013) demonstrated how the bacterium affects metabolic pathways which could ultimately result in NASH and NAFLD development. Systemic inflammation takes a central role in the development of NASH. H. pylori infection propagates this inflammation by raising IL-6 as well as TNF-α. According to Fan et al., (2018) infected patients showed elevated levels of cytokines IL-6 and TNF-α which suggests how H. pylori contributes to liver inflammation. The development of NASH from simple steatosis requires fibrosis to appear in the liver tissue. Jiang et al., (2019) discovered that H. pylori infection increased the amount of liver fibrosis indicating that this bacterium contributes to liver disease progression. Ma et al., (2022) confirmed that NAFLD patients with H. pylori infection experienced more severe fibrosis stages according to their research findings. The liver-gut dialogue functions as a primary system for maintaining liver wellbeing because modifications in gut microorganisms drive the progression of liver diseases. H. pylori infection will interrupt the natural composition of gut microbiome bacteria which then leads to higher intestinal permeability while sending toxic endotoxins to the liver. Wang et al., (2021) discussed the mechanisms through which hepatic inflammation and NASH development are triggered by such disruptions. Several academic research investigations have examined the unique manner in which H. pylori infection relates to NAFLD/NASH among male and female patients. The research conducted by Kang et al., (2018) demonstrated a more pronounced link between H. pneumoniae infection and female GSC Advanced Research and Reviews, 2025, 25(01), 029-036 35 patients which implies gender influences liver disease effects. The research findings of Fan et al., (2018) showed no gender-specific differences concerning the subject matter which reinforces the need for additional study. Location of a geographic region affects how prevalent H. pylori infection proves in liver diseases and the extent of its impact. According to Liu et al., (2019) meta-analysis Asian populations displayed a higher connection between H. pylori and NAFLD than other regions. Research indicates environmental and genetic factors can change this relationship between H. pylori infection and liver disease risk. H. pylori eradication stands as an interesting concept for NASH treatment. The research by Sumida et al., (2015) demonstrated that NAFLD patients might benefit from therapeutic elimination of H. pylori pathogens based on liver enzyme measurements. The research conducted by Jamali et al., (2019) discovered no considerable changes resulting from eradication therapy in liver fat content or functional status thus expecting additional investigation on therapeutic implications. 4. Conclusions The study links H. pylori bacterial infection as a substantial cause of non-alcoholic steatohepatitis (NASH) which underscores the bacterial origins of liver disease development. H. pylori infection raised the levels of liver enzymes ALT, AST and GGT which indicated pronounced hepatic inflammation and organ damage. H. pylori infection produces insulin resistance through dyslipidemia together with systemic inflammation thus leading to the development of NASH. The fibrosis stages of patients with H. pylori-positive NASH appeared more severe which shows that H. pylori could play a part in the development of liver damage. Liver inflammation and damage becomes worse through H. pylori related disturbance of the gut-liver communication pathway which further elevates intestinal permeability and systemic inflammation. The impact of H. pylori on NASH seems to differ between specific population groups and between male and female patients thus population-specific research is needed. The logistic regression analysis confirmed H. pylori infection acts as an individual threat factor for NASH when adjusting for BMI along with diabetes and inflammatory markers. H. pylori treatment led to improved liver function and thus suggested potential applications in the management of NASH. Compliance with ethical standards Acknowledgments The completion of this research project received genuine appreciation from everyone who helped throughout its development. My advisors along with mentors provided guidance that proved essential for developing this research while their encouragement together with their insightful feedback made an indelible impact on this work. Through their expertise together with their dedication the research underwent substantial improvements. The successful completion of this research study depended on the medical expertise along with research participation from dedicated professionals. The participants willingly devoted their time and experience to help obtain all required data. Throughout this endeavor we extend profound appreciation to my colleagues and peers whose open discussions and valuable suggestions together with their constant mentoring brought success to this journey. Disclosure of conflict of interest There are no conflicts of interest. Statement of ethical approval This procedure was approved by the Ethical Committee of the Faculty of Hamurabi Medica, University of Babylon. 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