NAFLD is a common metabolic disorder that affects approximately 13%-30% of the general population, although its underlying mechanism still remains to be defined. Several factors, such as genetic, environmental, metabolic, and behavioral factors, contribute to the pathogenesis of NAFLD[18]. In recent years, some scientific investigations have revealed possible connections between H. pylori infection and NAFLD[19].
In current study, we found that H. pylori infection was significantly associated with NAFLD. Of note, H. pylori infection remained an independent risk factor of NAFLD morbidity following ruling out some confounding factors, such as age, carotid plaque, blood pressure, blood lipids, blood glucose, and liver enzymes (OR = 1.35,P = 0.036).
This might imply that H. pylori infected individuals wound have a 35% higher risk of NAFLD than those without H. pylori infection. This is consistent with the results of meta-analysis by Zhou et al. who showed that a positive link between H. pylori infection and the risk of NAFLD[9].
At present, the preliminary idea that NAFLD would be the hepatic manifestation of the metabolic syndrome is changed, and it is considered that it might actually precede metabolic syndrome[20]. When analyzed in conjunction with metabolic syndrome, we found that higher weight, SBP, DBP, higher levels of TC, TG, LDL-C, FPG, and BMI were observed in NAFLD group than those of in non-NAFLD group (all P < 0.05). Moreover, we also found that DBP, FPG, TG, and BMI were significant risk factors for NAFLD. Accordingly, we speculate that a cross-talk may exist between the NAFLD and metabolic syndrome components. As previously reported by other studies, metabolic syndrome itself is one of the key risk factors for NAFLD, and vice versa[21].
A large body of literature has described that H. pylori infection is closely related to NAFLD and metabolic syndrome[22–25]. In current study, the effects of H. pylori infection on some key indicators of metabolic syndrome (SBP, DBP, FPG, BMI, TC, TG, HDL-C, and LDL-C) were analyzed. Interesting, we found that the levels of TC and LDL-C were higher in H. pylori-positive group than in H. pylori-negative group (P < 0.05). Accordingly, H. pylori infection may contribute to the increase of TC and LDL-C. This is in agreement with other reports. A large-scale meta-analysis shows that H. pylori infection significantly affects the serum lipid profile, which might lead to various severe dyslipidemia-related diseases[26]. However, in this study, we failed to identify the impacts of H. pylori infection on other metabolic syndrome indicators, including SBP, DBP, FPG, BMI, TG, and HDL-C. We suggest that there are some reasons why our findings may differ from other studies. Firstly, our study population with a higher level of education was drawn from government affiliated institutions in Dali region. Compared with the rural population, they are likely to be more concerned about their health conditions, and have the awareness about the disease prevention. Secondly, subjects were given advance notification of some dos and don’ts prior to blood collection, especially eating habits. To some extent, some biochemical indicators of subjects in the original living environment, such as blood lipid, blood glucose, liver and kidney function, might be underestimated after the adjustment of dietary structure. Thus, our findings may be biased by the subjects with a good living environment, good habit, better dietary structure and good health awareness.
Several potential limitations of this study merit consideration. First, the current study is a single-center, small sample size, and retrospective research. Second, no follow-up of the subjects was performed. Third, only subjects of health check-up were involved in this study, and the results may not be generalizable to other populations. Larger cohorts including different subjects with different backgrounds are needed to further validate our findings.