Gut microbiota and intestinal immunity-A crosstalk in irritable bowel syndrome.

Irritable bowel syndrome (IBS), one of the most prevalent functional gastrointestinal disorders, is characterized by recurrent abdominal pain and abnormal defecation habits, resulting in a severe healthcare burden worldwide. The pathophysiological mechanisms of IBS are multi-factorially involved, including food antigens, visceral hypersensitivity reactions, and the brain-gut axis. Numerous studies have found that gut microbiota and intestinal mucosal immunity play an important role in the development of IBS in crosstalk with multiple mechanisms. Therefore, based on existing evidence, this paper elaborates that the damage and activation of intestinal mucosal immunity and the disturbance of gut microbiota are closely related to the progression of IBS. Combined with the application prospect, it also provides references for further in-depth exploration and clinical practice.

The role of gut microbiota and metabolites in regulating the immune response in drug-induced enteritis.

Drug-induced enteritis is an inflammatory disease changing in the morphology and function of the intestine as a result of medicine damage. With the increase in drug abuse in recent years, the incidence of drug-associated enteritis accordingly rises and becomes an important disease affecting the health and life quality of patients. Hence, elucidating the pathogenesis of drug-induced enteritis and finding cost-effective diagnostic and therapeutic tools have become current research focuses. The gut microbiota and metabolites regulate the immune response, playing a key role in the maintenance of homeostasis in the intestine. Numerous studies have found that many medicines can induce intestinal flora disorders, which are closely related to the development of drug-induced enteritis. Therefore, this paper analyses the role of gut microbiota and metabolites in regulating the immune response, and provides basic research direction and clinical reference strategies for drug-induced enteritis, taking into account the existing applications and perspectives.

Meta-analysis of Virtual Reality Based on Delaying Mild Cognitive Impairment.

ABSTRACT: To further clarify the effectiveness of virtual reality (VR) in improving cognitive function of patients with mild cognitive impairment (MCI) through meta-analysis, we searched the PubMed, Web of Science, Scopus, MEDLINE, and Cochrane centers for controlled trials of VR in patients with MCI. All analyses were performed using RevMan (Version 5.3; Cochrane Collaboration, Oxford, United Kingdom). The selected data were extracted as 2 × 2 table. All included studies were weighted and aggregated. According to the inclusion criteria and exclusion criteria, five articles were selected for meta-analysis. There was no bias or heterogeneity in the results. We found that the diamond is on the right side of the vertical line and does not intersect with the vertical line. We determined the following values: odds ratio, 1.34; 95% confidence interval, 0.31-2.37; z = 2.55; p = 0.01. VR can effectively improve the cognitive function of MCI patients and delay cognitive impairment, which can be further developed as a treatment to delay the development of MCI.

Teprenone ameliorates diclofenac-induced small intestinal injury via inhibiting protease activated receptors 1 and 2 activity.

OBJECTIVE: This study aimed to investigate specific protein expression of injured intestinal mucosa induced by diclofenac, and explore the protective effects of teprenone on it. METHODS: Intestinal damage of Sprague Dawley male rats was gradually induced by the intragastric administration of diclofenac. After the last drug administration, the intestinal mucosa was taken off with an interval of 24 h, subsequently, its general histological injury and ultrastructure were observed and analysed by a transmission electron microscope. The expression levels of PAR1 and PAR2 protein were detected by immunohistochemistry and real-time polymerase chain reaction (PCR). RESULTS: The Reuter and Chiu scores of small intestinal damage were 5.63 ± 1.30 and 4.25 ± 0.70 respectively in the model group, which could be protected by teprenone (100 mg/kg⋅day) with the degree of 55.7% and 44%. Optical microscopy and transmission electron microscope showed that intestinal mucosa and ultrastructure were severely damaged. Distributed in the cytoplasm or aligned with the nucleus, the expression of PAR1 and PAR2 was significantly upregulated after the administration of diclofenac, while it was relieved after the treatment of teprenone. CONCLUSION: Our study presents a new view that teprenone might protect NSAIDs-induced (diclofenac) intestinal injury via suppressing the expression of PAR1 and PAR2.

Comparing endoscopic mucosal resection with endoscopic submucosal dissection: the different endoscopic techniques for colorectal tumors.

BACKGROUND: Endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD) are used for the removal of colorectal tumors. There are no current guidelines or consensus on the optimal treatment strategy for these lesions. A meta-analysis was conducted to compare the effectiveness and safety of ESD and EMR for colorectal tumors. METHODS: For the years 1966 until October 2014, Medline, PubMed, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials were searched for articles comparing the effectiveness and safety of ESD and EMR. STATA 11.0 and RevMan 5.0 were used for meta-analysis and publication bias. RESULTS: Seventeen articles were included in this meta-analysis. ESD was more effective than EMR in endoscopic complete resection rate (odds ratio [OR] = 2.81; 95% confidence interval [CI], 1.39-5.70; Z = 2.86; P = 0.004) and pathologic complete resection rate (OR = 2.81; 95% CI, 1.39-5.70; Z = 2.86; P = 0.004). ESD resulted in a higher perforation rate (OR = 5.27; 95% CI, 2.75-10.08; Z = 5.01; P < 0.00001) and a lower recurrence rate (OR = 0.14; 95% CI, 0.06-0.30; Z = 5.04; P < 0.00001). The tumor size was larger in the ESD group (OR = 3.09; 95% CI, 1.54-4.63; Z = 3.92; P < 0.0001), and the procedure time was longer in the ESD group (OR = 21.39; 95% CI, 10.33-32.46; Z = 3.79; P = 0.0002). But bleeding rate did not differ significantly (OR = 1.34; 95% CI, 0.81-2.20; Z = 1.14; P = 0.25). There was no publication bias analyzed by Begg test and Egger test. CONCLUSIONS: The study indicates that ESD is the better treatment for colorectal tumors for its higher complete resection rate despite the longer procedure time and higher perforation rate.

A study of the association of vitamin D receptor (VDR) as a predictive biomarker for immune checkpoint inhibitor therapy with immune invasion in colon adenocarcinoma.

Colon adenocarcinoma(COAD) is a primary and aggressive malignancy with the fifth highest mortality rate among cancers, and it is important to discover new strategies. The online database was used to analyze the correlation between Vitamin D receptor (VDR) and COAD, and further explore the immune infiltration and related gene networks.The expression and methylation levels of VDR was analyzed by using Timer database, GEPIA platform and UALCAN database. GeneMANIA database was used to analyze and obtain gene networks that are closely linked to VDR. UALCAN database was used to score the gene effects of VDR in colorectal cancer cell lines. The cBioPortal database was used for the detection of gene mutations. The survival curve analysis was carried out using the GEPIA database. The relationship between VDR expression and immune cell infiltration was analyzed by using the timer database and TISIDB database. TISIDB database was used to obtain VDR-related drug targets.The expression of VDR was significantly lower in COAD(p<0.05). The methylation level of VDR was significantly higher in COAD (p<0.05). The gene mutation rate of VDR in COAD was 2 %. OS and DFS were not associated with changes in the VDR gene in patients with COAD. VDR expression was correlated with CD4+T cell infiltration, macrophage infiltration, neutrophil infiltration, and dendritic cell infiltration. VDR has a clear correlation with ADORA2A, BTLA, CD160, CD244, CD274, CD96, CSF1R, CTLA4, HAVCR2, IL10, IDO1, LAG3, LGALS9, PDCD1, PDCD1LG2, PVRL2, TGFB1, TGFBR1, TIGIT and VTCN1.The expression of VDR is associated with immune infiltration in patients with COAD. VDR may be a new candidate biomarker for determining the level of immune infiltration and predicting immune checkpoint inhibitor therapy.

A screening study of high-risk groups for liver fibrosis in patients with metabolic dysfunction-associated fatty liver disease.

The purpose of this study was to explore the correlation between Hashimoto's thyroiditis and Metabolic dysfunction-associated fatty liver disease (MAFLD), and at the same time to screen high-risk groups for liver fibrosis in MAFLD, find out the high-risk related indicators. The physical examination population was included as the study subjects and was grouped according to the diagnostic criteria for MAFLD. APRI > 1 or NFS > 0.676 or FIB-4 > 2.67were used to assess people at high risk of liver fibrosis, and logistic regression analysis was used to identify risk factors associated with high risk of liver fibrosis in MAFLD. ROC curves are used to look for indicators of diagnostic value. The proportion of people with Hashimoto's thyroiditis was lower in the MAFLD group. The MAFLD high-risk group for liver fibrosis had higher TSH levels, lower FT3 and FT4 levels, higher TGAB levels, and differences in biochemical markers. Age, BMI, FBG, and AST are risk factors for the high risk of liver fibrosis in MAFLD patients. ROC curve analysis showed that the AUC of age was 0.741 (0.721-0.761), and the optimal stage value was 57.5 years, while the AUC of AST was 0.729 (0.707-0.751), and the optimal cut-off value was 39.5 U/L. Age, BMI, FBG, and AST are risk factors for the high risk of liver fibrosis in MAFLD patients.The age is greater than or equal to 57.5 years, or the AST is greater than or equal to 39.5 U/L, indicating that the MAFLD patients are at high risk of liver fibrosis.

Effect of multimorbidity on depressive status in older Chinese adults: evidence from the China Health and Retirement Longitudinal Study (CHARLS).

OBJECTIVE: This study aims to further explore the relevant influencing factors of depression and explore the correlation between multimorbidity coexistence and depression to find the goals and methods of early intervention of depression in the elderly. DESIGN: This study adopts a cross-sectional approach. SETTING: The study population of this project came from the China Health and Retirement Longitudinal Study. Depression was grouped according to the 10-item version of Centre for Epidemiological Research Depression Scale. Chronic diseases, height, weight, grip strength, education, marital status, alcohol consumption, exercise and other indicators were included in the analysis. PARTICIPANTS: 2239 adults over 60 years of age were included. RESULTS: The proportion of women in the depression group was higher (p<0.001). The depression group had a lower grip strength than the control group (p<0.05). The sleep duration was shorter in the depression group (p<0.001). There were differences in education, marital status and alcohol consumption in the depression group (p<0.05). The depression group might have more types of coexisting chronic diseases (p<0.001). The depression group was more likely to have hypertension, dyslipidaemia, chronic lung diseases, heart attack, stroke, stomach disease and memory-related disease. Grip strength was connected with the risk of depression in the elderly (0.971 (95% CI 0.959 to 0.984)). Sleep (0.827 (95% CI 0.785 to 0.872) and education level (0.790 (95% CI 0.662 to 0.942) were related to the risk of depression in the elderly. Concomitant chronic diseases could affect the risk of depression in the elderly (1.455 (95% CI 1.243 to 1.703)). CONCLUSION: The coexistence of multiple chronic diseases and depression is very common in the elderly. The coexistence of multiple chronic diseases is more common in older women and older depressed people. With the increase in the number of chronic diseases, the risk of depression in the elderly is significantly increased.

Changes in M6A methylation: A key factor in the vicious cycle of flora -gut aging.

The aging process significantly impacts the gastrointestinal tract and various bodily systems, exacerbating age-related diseases. Research suggests a correlation between an imbalance in intestinal flora and gut aging, yet the precise mechanism remains incompletely elucidated. Epigenetic modifications, particularly m6A methylation, play a pivotal role in driving aging and are closely associated with gut aging. Maintaining a healthy balance of intestinal microbes is contingent upon m6A methylation, which is believed to be crucial in the vicious cycle of gut aging and intestinal flora. This article highlights the importance of m6A methylation in the nexus between gut aging and flora. It proposes the potential for targeted m6A methylation to break the vicious cycle of gut aging and flora imbalance, offering novel perspectives on attenuating or reversing gut aging.

Endoscopic submucosal dissection for treatment of gastric submucosal tumors originating from the muscularis propria layer.

BACKGROUND AND AIMS: We aimed to study the feasibility of endoscopic submucosal dissection (ESD) for the removal of gastric muscularis propria tumors and to evaluate the efficacy and safety of ESD for this treatment. METHODS: Eighteen patients with gastric SMTs originating from the muscularis propria were treated by ESD between July 2008 and July 2011. Tumor characteristics, complications, en bloc resection rate, and local recurrence rate were evaluated. RESULTS: Among the 18 patients, 11 were women (61.1 %). The median age was 65.3 ± 6.3 years old (range 30-71 years old). Seventeen tumors were resected completely by ESD (success rate 94.4 %). The mean tumor size as determined by endoscopic ultrasound was 2.6 ± 1.2 cm (range 1.0-3.5 cm). The histological diagnosis was gastrointestinal stromal tumor for 13 lesions and leiomyoma for four tumors. The mean operation time was 90 ± 38 min (range 50-120 min), and the average blood loss was 20 ml. Two patients developed perforation, which was closed by endoscopic methods with metallic clips. The tumor was closely adhered to the muscularis propria and was convex to the enterocoelia in one case. No single case had severe complications, such as GI bleeding, peritonitis, or abdominal abscess, and there were no other immediate post-procedure complications. CONCLUSIONS: ESD is a safe, effective, well-tolerated, and minimally invasive therapy for the intraluminal SMTs originating from gastric muscularis propria with relatively few complications. Although there is a risk of perforation which has become manageable endoscopically.

Proton pump inhibitors are not the key for therapying non-steroidal anti-inflammatory drugs-induced small intestinal injury.

The ability of non-steroidal anti-inflammatory drugs (NSAIDs) to injure the small intestine has been well established in humans and animals. Proton pump inhibitors (PPIs) are frequently prescribed to reduce gastric and duodenal injury caused in high-risk patients taking NSAIDs. However, scarce information is available concerning the effects of PPIs on intestinal damage induced by NSAIDs, and the suppression of gastric acid secretion by PPIs is hard to provide any protection against the damage caused by NSAIDs in the small intestine. The present study was designed to examine the effects of intragastric treatment of two PPIs widely used in clinical practice, namely omeprazole and pantoprazole, on the intestinal damage induced by administration of diclofenac in rat. Male SD rats were treated with omeprazole or pantoprazole for 9 days, with concomitant treatment with anti-inflammatory doses of diclofenac on the final 5 days. The anatomical lesion, villous height, the thickness, and the section area of small intestine were quantitatively analyzed. The change of ultrastructural organization was observed. Endotoxin level in blood was measured by photometry. Epidermal growth factor was observed by immunohistochemistry. Omeprazole and pantoprazole didn't decrease the macroscopic and histologic damage induced by diclofenac in the rat's small intestine. In the two PPI groups, villous height was (89.6 ± 11.8 and 92.6 ± 19.3 µm) lower than which of the control group (P < 0.05). The thickness became thinning, and the section area became small. LPS levels in the portal blood of omeprazole and pantoprazole were (4.36 ± 1.26 and 4.25 ± 1.17 EU/ml), significantly higher than in controls (P < 0.05). The EFG of PPI group descended significantly compared with the control group (P < 0.05). Omeprazole and pantoprazole cannot protect the small intestine from the damage induced by diclofenac in the conscious rat. PPIs cannot repair NSAID-induced intestinal damage at least in part because of significant lesion in mechanical barrier function and reduction in epidermal growth factor.

Correlation analysis of PBX family with immune invasion and drug sensitivity in colon adenocarcinoma.

Objedtive: Pre-B cell leukemia (PBX) has been found to be associated with cancer, but poorly studied with colon adenocarcinoma (COAD). In this study, the correlation between PBX family and COAD pathogenesis and immune cytokine infiltration was further explored by analyzing online tumor databases, in order to find new biomarkers for the diagnosis of COAD. Methods: The online database was used to analyze gene differential expression, methylation level, gene mutation rate, immune infiltration difference, drug sensitivity, and so on. Results: PBX1 and PBX3 decreased in COAD. PBX2 and PBX4 increased. The expression of PBX1 and PBX2 in different clinical stages was different. PBX4 was valuable for the prognosis of COAD. PBX family has correlation between COAD and immune infiltration. PBX2 was correlated with different pathological stages. PBX3 had the highest gene mutation rate, followed by PBX1, PBX2 and PBX4. PBX1, PBX2 and PBX4 were correlated with the sensitivity of multiple drugs. Conclusion: The PBX family is differentially expressed in COAD and has a genetic mutation, and its protein network is closely related to the HOX family and is associated with immune infiltration of COAD.

Application of artificial intelligence in colorectal cancer screening by colonoscopy: Future prospects (Review).

Colorectal cancer (CRC) has become a severe global health concern, with the third­high incidence and second­high mortality rate of all cancers. The burden of CRC is expected to surge to 60% by 2030. Fortunately, effective early evidence­based screening could significantly reduce the incidence and mortality of CRC. Colonoscopy is the core screening method for CRC with high popularity and accuracy. Yet, the accuracy of colonoscopy in CRC screening is related to the experience and state of operating physicians. It is challenging to maintain the high CRC diagnostic rate of colonoscopy. Artificial intelligence (AI)­assisted colonoscopy will compensate for the above shortcomings and improve the accuracy, efficiency, and quality of colonoscopy screening. The unique advantages of AI, such as the continuous advancement of high­performance computing capabilities and innovative deep­learning architectures, which hugely impact the control of colorectal cancer morbidity and mortality expectancy, highlight its role in colonoscopy screening.

PARs in the inflammation-cancer transformation of CRC.

Colorectal cancer (CRC) is one of the common malignancies with a global trend of increasing incidence and mortality. There is an urgent need to identify new predictive markers and therapeutic targets for the treatment of CRC. Protease-activated receptors (PARs) are a class of G-protein-coupled receptors, with currently identified subtypes including PAR1, PAR2, PAR3 and PAR4. Increasingly, studies suggest that PARs play an important role in the growth and metastasis of CRC. By targeting multiple signaling pathways may contribute to the pathogenesis of CRC. In this review, we first describe recent studies on the role of PARs in CRC inflammation-cancer transformation, focusing on the important role of PARs in signaling pathways associated with inflammation-cancer transformation, and summarize the progress of research on PARs-targeted drugs.

TLR5 Signaling in the Regulation of Intestinal Mucosal Immunity.

Toll-like receptor 5 (TLR5) is a pattern recognition receptor that specifically recognizes flagellin and consequently plays a crucial role in the control of intestinal homeostasis by activating innate and adaptive immune responses. TLR5 overexpression, on the other hand, might disrupt the intestinal mucosal barrier, which serves as the first line of defense against harmful microbes. The intestine symbiotic bacteria, mucous layer, intestinal epithelial cells (IECs), adherens junctions (such as tight junctions and peripheral membrane proteins), the intestinal mucosal immune system, and cytokines make up the intestinal mucosal barrier. Impaired barrier function has been linked to intestinal illnesses such as inflammatory bowel disease (IBD). IBD is a persistent non-specific inflammatory illness of the digestive system with an unknown cause. It is now thought to be linked to infection, environment, genes, immune system, and the gut microbiota. The significance of immunological dysfunction in IBD has received more attention in recent years. The purpose of this paper is to explore TLR5's position in the intestinal mucosal barrier and its relevance to IBD.

Effects of different doses of lithium on the central nervous system in the rat valproic acid model of autism.

Epidemiological studies have shown that low doses of lithium in the environment can have beneficial effects on mental health. Autism spectrum disorder, a neurodevelopmental disorder in which patients exhibit abnormal behaviors, pharmacological interventions usually relied on a range of psychotropic medications. However, such medications often produce severe side effects or are ineffective in symptoms. Finding alternative ways to improve abnormal behaviors in individuals with autism are warranted, in which case lithium may be a relatively safe and effective medication. Lithium salt therapy is used to treat a variety of neuropsychiatric disorders and has neuroprotective effects. In this study, we investigated the effects of different doses of lithium on neurobehavioural disorders using the rat model of autism established by valproic acid (VPA) injection. Lithium was observed to have an ameliorative effect on the social cognitive, social memory and anxiety levels in the rat model of autism. Immunofluorescence staining showed that subchronic LiCl administration (1.0 mmol/kg) significantly reduced the number of Iba-1 positive cells in the CA1 region of the hippocampus in VPA group and brought it close to the levels of control group. Significantly lower levels of the pro-inflammatory marker IL-6 were observed in the hippocampus and serum after lithium treatment. In addition, the lithium treatment increased the levels of H3K9 acetylation in the hippocampus of VPA-exposed rats. The results showed a defensive effect of environment-related lithium exposure doses on neurobehavioural deficits in the rat valproic acid model of autism, suggesting that it may be a potential drug for the treatment of autism.

Improving intestinal inflammaging to delay aging? A new perspective.

Greying population is becoming an increasingly critical issue for social development. In advanced aging context, organismal multiple tissues and organs experience a progressive deterioration, initially presenting with functional decline, followed by structural disruption and eventually organ failure. The aging of the gut is one of the key links. Decreased gut function leads to reduced nutrient absorption and can perturb systemic metabolic rates. The degeneration of the intestinal structure causes the migration of harmful components such as pathogens and toxins, inducing pathophysiological changes in other organs through the "brain-gut axis" and "liver-gut axis". There is no accepted singular underlying mechanism of aged gut. While the inflamm-aging theory was first proposed in 2000, the mutual promotion of chronic inflammation and aging has attracted much attention. Numerous studies have established that gut microbiome composition, gut immune function, and gut barrier integrity are involved in the formation of inflammaging in the aging gut. Remarkably, inflammaging additionally drives the development of aging-like phenotypes, such as microbiota dysbiosis and impaired intestinal barrier, via a broad array of inflammatory mediators. Here we demonstrate the mechanisms of inflammaging in the gut and explore whether aging-like phenotypes in the gut can be negated by improving gut inflammaging.

Small cell lung cancer presenting as dermatomyositis: mistaken for single connective tissue disease.

Dermatomyositis (DM) is well-known to be associated with several types of malignancy. This case emphasizes the importance of a thorough examination for an underlying cancer, in patients with the symptoms of dermatomyositis. We report the case of a 62-year-old Chinese man who presented with a two-month history of edema of face and neck, together with erythema of the eyelids diagnosed of small cell lung cancer. Initially, it was thought to be single connective tissue disease such as DM. This study highlights the importance of a thorough physical examination when visiting a patient.

[The effects of milk and milk products on non-steroidal anti-inflammatory drug induced intestinal damage in rats].

OBJECTIVE: To investigate the effect of milk and milk products on morphological structure and epidermal growth factor (EGF) of non-steroidal anti-inflammatory drugs (NSAIDs) induced small intestinal damage in animals. METHODS: Eighty male SD rats were randomly divided into 5 groups: control group, diclofenac group, diclofenac with 10% low fat milk group, diclofenac with 10% colostrum group and diclofenac with yoghurt group. The animals with milk or colostrum or yoghurt were fed for 5 days before the administration of diclofenac with 15 mg/kg by gavage, once. Then they were observed the scores of anatomical lesion and the scores of tissue damage of mucous membrane and the height of villous at the 24(th) and 48(th) hour after making the models. Observation of the change of ultrastructural organization of mucous membrane was carried out with transmission and scanning electron microscope and immunohistochemistry of EGF. RESULTS: The scores of anatomical lesion and tissue damage of mucous membrane of the colostrum group were lower than those of the diclofenac group (P < 0.05). The heights of the pile on small intestine of the 24(th) and 48(th)hour of the colostrum group were (145.7 ± 16.5) µm and (139.2 ± 19.0) µm, respectively. They were higher than those of the diclofenac group [(119.2 ± 19.2) µm and (105.4 ± 18.4) µm, P < 0.05]. However there was no difference of the scores and the height among diclofenac group, milk group and yoghurt group. TEM and SEM of tissues showed that the cytoplasmic membrane and other cellular components of villous epithelial cells were well preserved in colostrum group, and the microvilli in the milk group and yoghurt group were ablated more obviously. The positive area of EGF of small intestine [(6170.5 ± 1483.9) µm(2)] were higher 48 h after administration of diclofenac compared with the diclofenac group (P < 0.05). The expression of EGF in milk and yoghurt group were no significant statistical difference with the diclofenac group. CONCLUSION: Bovine colostrum may have a beneficial effect in prevention of NSAIDs induced small intestinal injuries and preserve mechanical barrier of small intestinal mucosa which is probably relative to EGF.

Study on the independent effect of thyroid hormone based on uric acid level on NAFLD.

OBJECTIVE: This study aims to explain the correlation among non-alcoholic fatty liver disease (NAFLD), hyperuricemia, and thyroid function and to find independent risk factors for each other. METHODS: Data were obtained from subjects who underwent health examination in the Health Promotion Centre of Sir Run Run Shaw Hospital of Zhejiang University from January 2017 to February 2019. The diagnosis of NAFLD was according to the clinical diagnosis of the guidelines. Serum uric acid (SUA) > 360 µmol/L (female) and SUA > 420 µmol/L (male) were enrolled in the hyperuricemia group. R software was used for statistical analysis. RESULTS: 55,449 subjects were included in the analysis. 34.27% of patients were classified as NAFLD group (N=19004), and 65.73% of patients were classified as non-NAFLD group (N=36445). The levels of gender ratio, age, BMI, waist circumference, systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), HbA1c, triglyceride (TG), high-density lipoprotein (HDLC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea nitrogen (BUN), creatinine (CR), FT3, FT4, and TSH were significantly different between the non-NAFLD group and NAFLD group. Age, BMI, waist circumference, DBP, fFBG, HbA1c, total cholesterol (TC), low-density lipoprotein (LDLC), AST, and UA were all independent risk factors for NAFLD. In the normal uric acid group, variables other than SBP and TSH were independent factors of NAFLD. In the hyperuricemia group, all variables except SBP, FT4, and TSH were independent factors of NAFLD. CONCLUSION: The level of uric acid is related to the occurrence of NAFLD. Hyperuricemia is one of the independent risk factors of NAFLD. TSH level is not related to the occurrence of NAFLD, while FT3 and FT4 may be related to NAFLD.