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Research Article | Volume 7 Issue 1 (January-June, 2026) | Pages 1 - 4
Impact of Gut-Liver Axis: Hepatic Biochemical and Metabolic Changes Associated with Chronic Gastritis in Iraqi Patients with Helicobacter Pylori
1
Department of physiology and medical physics, College of Medicine, Jabir Ibn Hayyan University for Medical and Pharmaceutical Science, Kufa, Iraq
Under a Creative Commons license
Open Access
Received
Jan. 6, 2026
Revised
Jan. 28, 2026
Accepted
Feb. 19, 2026
Published
Feb. 20, 2026
Abstract

Background: The previous studies refer to Helicobacter pylori infection, which has a wide distribution, affecting about 50 and 90% of people worldwide, to cause inflamed, ulcers, and cancers of the gastric mucosa, and may be related to their transfer via the blood circulation from the gut into the liver.Objective: Therefore, the current study sought to discover the relationship between Helicobacter pylori infection and some biochemical parameters, such as liver enzyme activity and lipid profile, as indicators of liver stress and metabolic disturbance. Methods: This study was conducted on 24 participants, aged 30 to 60 years, of both sexes. The participants were divided into two equal groups (n=12). Group 1 (G) consisted of healthy individuals not infected with Helicobacter pylori, while Group 2 (GG) consisted of patients infected with Helicobacter pylori who exhibited symptoms such as loss of appetite, vomiting, abdominal pain, and heartburn. We work on laboratory analysis of liver function tests and blood lipid profile tests to compare the infected and healthy groups, all these after ensuring that participants are of a similar weight and avoiding obese individuals who may affect the results.Results: Statistical analysis showed a highly significant increase (p<0.001) in the activity of liver enzymes in the H. pylori group (GG) compared to the healthy control group. Furthermore, an increase in the significance of lipid profile, e.g., triglyceride, total cholesterol, and LDL parameters of the infected group compared to the control group. All these indicate to found relation between bacterial infection and liver dysfunction and dyslipidemia associated with this condition. Conclusion: Referenced our study results for the Helicobacter pylori group, which exhibited raised levels of liver enzymes (ALT, AST, ALP) and blood lipid profiles, although bacteria colonize in the gastric mucosa, confirming that the pathological effects of H. pylori extend beyond local gastric lesions to include the stimulation of systemic inflammation.

Keywords
INTRODUCTION

Helicobacter pylori (H. Pylori) is found in more than half the world's population. It is a spiral-shaped, gram-negative bacterium that primarily targets the gastric lining. In addition to its traditional role in the development of ulcers and stomach cancer, emerging scientific evidence suggests the involvement of this bacterium in multiple systemic disorders that extend beyond the digestive tract [1,2].

 

Chronic infection triggers a widespread systemic inflammatory response, leading to general metabolic dysfunction and directly affecting lipid regulation and vital liver functions. Scientific evidence suggests that inflammatory mediators such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) play a pivotal role in modulating lipid levels and liver enzyme concentrations, increasing the likelihood of developing non-alcoholic fatty liver disease or metabolic syndrome [3,4].

 

Given the liver's pivotal role in regulating lipid metabolism, chronic infections or physiological stress negatively impact its functional efficiency, resulting in raised levels of liver enzymes, including ALT, AST, and ALP, in the bloodstream.At the same time, dyslipidemia, which is categorized by raised levels of LDL cholesterol, triglycerides, and total cholesterol, is a common feature among individuals with persistent infections [5,6]. Therefore, the current study sought to discover the relationship between Helicobacter pylori infection and some biochemical parameters, such as liver enzyme activity and lipid profile, as indicators of liver stress and metabolic disturbance.

PATIENTS AND METHODS

Experimental Design

This study was conducted on 24 participants, aged 30 to 60 years, of both sexes. The participants were divided into two equal groups (n=12). Group 1 (G) consisted of healthy individuals not infected with Helicobacter pylori, while Group 2 (GG) consisted of patients infected with Helicobacter pylori who exhibited symptoms such as loss of appetite, vomiting, abdominal pain, and heartburn. We ensure that participants are of a similar weight and avoid obese individuals who may affect the results. This study was conducted at the Gastroenterology Hospital in Najaf, Iraq, in February 2025. Before collecting any samples, the study got the green light from the College of Medicine Research Ethics Committee. Everyone involved gave their informed consent, and the team took every safety precaution to prevent contamination and ensure people's well-being. 

 

Blood Sample Collection

Blood samples were drawn from both healthy and diseased subjects and transferred into standard tubes. They were left at 24 °C to undergo natural clotting. Blood samples were to be centrifuged at 3000 revolutions per minute for 15 minutes at room temperature (this falls within the normal ranges for most lab conditions) to obtain serum. Isolated serum samples were frozen at −20 °C to preserve them for future biochemical analyses.

 

Biochemical Analysis

Liver Function Tests: Using a spectrophotometric apparatus, the serum levels of the aminotransferases (AST and ALT) and alkaline phosphatase (ALP) were recorded. The tests were conducted using standardized diagnostic kits, and beyond the measurements, strict adherence was given to the manufacturer's diagnostic/instructional guidelines. This was done to ensure accuracy. We also consider the medical history of all participants, including diabetes, inflammatory bowel disease, and medication use and other factors that may impact transaminase measurements and the study results.

 

Lipid Profile

In this study, the blood lipid levels of total cholesterol, triglycerides, and HDL cholesterol were assessed by enzyme chromatography through lab serum samples. To estimate greater variance of the lipid levels, calculation models were implemented, employing the Friedwald equation, [7] which was used to determine the concentrations of LDL and VLDL cholesterol.The medical history of all participants was also considered to rule out any factors that might influence the blood lipid measurements.

 

Statistical Analysis

Data were analyzed using SAS software (version 9.1), and results are presented as mean ±standard error. P values ​<0.05 and p<0.01 were considered statistically significant. To accurately describe biochemical parameters, such as liver enzymes and lipid levels, descriptive statistics and the independent samples t-test were used to assess statistically significant differences between study groups.

RESULTS

The study results, as shown in Table 1, demonstrate a statistically extremely significant (p<0.001) increase in the activity of liver enzymes in H.pylori group (GG) to include; ALP (149.67±3.1), and ALT (87.07±2.42), and highly significant (p<0.01) increase in AST (40.9±0.67), and on the other hand showed a statistically significant (p<0.05) increase in blood lipid levels (T.G, T.cholestrol, HDL, LDL, VLDL) in the group infected with H. pylori (GG) compared to the healthy control group (G). This reflects a clear physiological difference in health status and metabolism between the infected and healthy groups of the study.

DISCUSSION

The current study sought to discover the relationship between Helicobacter pylori infection and some biochemical parameters, such as liver enzyme activity and lipid profile, as indicators of liver stress and metabolic disturbance. 

 

The study results demonstrate a significant increase in the activity of liver enzymes, ALP, ALT, and AST respectively. Blood lipid levels – like triglycerides, total cholesterol, HDL, LDL, and VLDL – were statistically higher (p<0.05) in people infected with H. pylori compared to healthy individuals. This really backs up the idea that bacterial infections can mess with your whole system, not just your gut. It shows these effects go way beyond the digestive tract and actually hurt your overall health.

 

Liver Enzyme Alterations

Some statuses, like hepatitis or physiological stress due to H. pylori, lead to marked elevation of liver enzyme levels (ALP, ALT, and AST) in the infected group (GG). It is important to consider the patient's medical history and ensure there are no other diseases or factors affecting liver enzyme activity. This mechanism is explained by the Gut-Liver Axis, whereby the bacteria stimulate the announcement of systemic inflammatory mediators resulting from inflamed gastric mucosa, like IL-6 and tumor necrosis factor-alpha, to the portal circulation, leading to impaired liver function, represented by increased liver enzyme activities.

 

These cytokines then travel to the liver and cause damage to its cell membranes, which in turn leads to the leakage of enzymes into the bloodstream. These conclusions are consistent with those of researcher Luo et al. (2022), who confirmed that chronic gastritis may extend its effect to take a systemic form that directly affects liver tissue [8,5]

 

Table 1: Biochemical Parameters Changes (Liver Function Tests and Lipid Profile) under the Effect of H.Pylori Bacteria. N = 12. Mean±Se

Parameters

G group (n=12)

GG group (n=12)

p-value

ALP (U/L)

45.41±3.05

149.67±3.1

<0.001***

AST (U/L)

25.48±1.14

40.9±0.67

<0.01**

ALT (U/L)

36.39±2.25

87.07±2.42

<0.001***

T.G (mg/dl)

115.75±3.4

193.25±12.1

<0.05*

T. cholesterol (mg/dl)

204.57±2.33

277.23±3.33

<0.05*

HDL (mg/dl)

60.16±2.69

80.58±1.57

<0.05*

LDL (mg/dl)

121.25±1.95

158±3.38

<0.05*

VLDL (mg/dl)

23.15±0.68

38.65±2.42

<0.05*

* Significant at p<0.05, ** Highly Significant at p<0.01, *** Extremely significant at p<0.001

 

Lipid Profile and Metabolic Impact

The analytical data of the lipid profile showed a significant upsurge in the concentrations of total cholesterol, triglycerides, VLDL, and LDL in the blood serum of the infected group. This imbalance in lipid levels is attributed to the effect of chronic infection, which affects lipid metabolism as a result of systemic inflammation caused by Helicobacter pylori bacteria. This, in turn, may lead to inhibition of the activity of the lipoprotein lipase (LPL) enzyme, which is mainly responsible for the process of removing triglycerides from the bloodstream, thus explaining their accumulation and imbalance in those infected [9].

 

In addition, the increased levels of LDL and VLDL in individuals infected with Helicobacter pylori double the risk of cardiovascular complications and metabolic syndrome [10], which reinforces the conclusions of Franceschi et al. study that the metabolic disturbances associated with this bacterium go beyond the local scope of the stomach to form a complex systemic reaction that casts a shadow on the overall biochemical homeostasis [4]. The biochemical changes observed in the Helicobacter pylori infection group are linked to the far-reaching effects of gut microbiota imbalance on the digestive system and overall health. This has been confirmed by studies in recent years, highlighting the pivotal role of gut microbiota and anti-inflammatory interventions in restoring physiological balance. A 2020 study by Bakheet et al. demonstrated that prebiotics and synbiotics, such as fenugreek seeds and Lactobacillus acidophilus, effectively enhance intestinal immune responses and reduce inflammation in experimental models [11,12]. Further studies by Al-Qayem and Bakheet in 2016 corroborate this approach, demonstrating the ability of beneficial bacteria to improve physiological and immunological aspects during inflammatory conditions. Based on the above, this research aims to analyze these findings to explore the possibility of mitigating pathogenic infections, such as Helicobacter pylori, and their associated systemic inflammation and metabolic disorders (as seen in the GG group), by improving the gut microbiome. Therefore, understanding the mechanisms of the gut-hepatobiliary axis is essential for developing integrated therapeutic strategies [13-15]

 

In conclusion, this study improved the understanding that the effects of Helicobacter pylori are not limited to localized lesions in the mucosa of the stomach but extend to cause systemic inflammation and metabolic disturbances that directly affect liver function and lipid balance by our study's laboratory tests that used due to the close connection between them, known as the gut-liver axis. Moreover, our study results show a significant increase in the activity of liver enzymes (ALT, AST, ALP) and cholesterol and triglyceride levels in infected individuals. Figuring out if this bug is the culprit behind gut problems really matters for treatment. Plus, catching it early and getting rid of it right away is key. That’s a big step in prevention, too. It can cut down the chances of developing liver disease and metabolic syndrome down the road.

CONCLUSION AND RECOMMENDATIONS

Our study's results for the Helicobacter pylori group are pretty striking. We found higher levels of liver enzymes like ALT, AST, and ALP, along with altered blood lipid profiles. Even though the bacteria stick to the stomach lining, this really shows that H. pylori's damage goes further than just local stomach issues. It seems to kick off inflammation throughout the whole body. So, we're suggesting doctors add liver function tests and lipid profiles to regular check-ups for these patients. This could help catch metabolic problems early. The study suggested more research into how probiotics might help prevent and treat H. pylori infections. It's a vital step for cutting down long-term health risks tied to that bacteria.

REFERENCE
  1. Bakheet, N. “Impact of infection by H. pylori on gastric parietal cell physiology: review.” Journal of Medical Genetics and Clinical Biology, vol. 2, 2025, pp. 434–439.

  2. Hooi, J.K.Y. et al. “Global prevalence of Helicobacter pylori infection: systematic review and meta-analysis.” Gastroenterology, vol. 153, no. 2, 2017, pp. 420–429.

  3. Maleki, N. et al. “Helicobacter pylori infection and association with chronic diseases: a focus on cardiovascular disease, MASLD, and type 2 diabetes.” Metabol Open, vol. 27, 2025, pp. 100385.

  4. Franceschi, F. et al. “Helicobacter pylori and extragastric diseases.” Helicobacter, vol. 19, 2014, pp. 52–58.

  5. Luo, N. et al. “A functional liver imaging score for preoperative prediction of liver failure after hepatocellular carcinoma resection.” European Radiology, vol. 32, no. 8, 2022, pp. 5623–5632.

  6. Shimamoto, T. et al. “The association of Helicobacter pylori infection with serum lipid profiles: an evaluation based on a combination of meta-analysis and a propensity score-based observational approach.” PLOS ONE, vol. 15, no. 6, 2020, pp. e0234433.

  7. Friedewald, W.T. et al. “Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge.” Clinical Chemistry, vol. 18, 1972, pp. 499–502.

  8. Mohammed, M.K.B. et al. “Pro-inflammatory cytokines of gastric tissues and its role in patients with H. pylori.” Microbial Biosystems, vol. 10, no. 3, 2025, pp. 104–110.

  9. Xie, J. et al. “Association between Helicobacter pylori infection and triglyceride levels: a nested cross-sectional study.” Frontiers in Endocrinology, vol. 14, 2023, pp. 1220347.

  10. Shang, H. et al. “Helicobacter pylori infection increases the risk of dyslipidemia in Chinese non-obese and non-diabetic population from the perspective of age category: a retrospective cross-sectional study.” BMC Infectious Diseases, vol. 25, no. 1, 2025, pp. 814.

  11. Bakheet, N. and Alqayim, M.A. “Improvement of intestinal functional and structural features enhanced with butyric acid produced by fenugreek synbiotic with Lactobacillus acidophilus.” Biochemical and Cellular Archives, vol. 20, 2020, pp. 6047–6057.

  12. Bakheet, N.Z. et al. “Intestinal anti-inflammatory improvement with fenugreek seeds as a prebiotic and synbiotic with Lactobacillus acidophilus in rats experimentally infected with Escherichia coli.” The Iraqi Journal of Veterinary Medicine, vol. 44, no. 2, 2020, pp. 1–14.

  13. Yang, Z. et al. “Gut microbiota metabolism axis in digestive tumors: emerging targets for novel therapies (review).” Experimental and Therapeutic Medicine, vol. 31, no. 4, 2026, pp. 113.

  14. Wang, Y. et al. “Crucial functions of gut microbiota on gut–liver repair.” hLife, vol. 3, no. 8, 2025, pp. 364–385.

  15. Alqayim, M.A.J. and Bakhit, N.Z.M. “Effect of Lactobacillus acidophilus on some physiological and immunological aspects in experimentally induced colitis in rats.” Advances in Animal and Veterinary Sciences, vol. 4, no. 9, 2016, pp. 476–488.

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Impact of Gut-Liver Axis: Hepatic Biochemical and Metabolic Changes Associated with Chronic Gastritis in Iraqi Patients with Helicobacter Pylori © 2026 by Noor Zuhair Bakheet N. Z. licensed under CC BY-NC-ND 4.0
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