NAFLD、Hp感染与结直肠息肉的关系

摘要/Abstract

摘要： 目的探讨非酒精性脂肪肝(NAFLD)、Hp感染与结直肠息肉的关系。方法纳入2021年6月至2022年5月合肥市第二人民医院经结肠镜及病理检查明确诊断结直肠息肉患者133例,其中增生性息肉54例,腺瘤性息肉79例。另选70名健康体检者。检测所有患者的总胆固醇(CHOL)、低密度脂蛋白(LDL)、幽门螺杆菌(Hp)及血清胃泌素17(G-17),胃蛋白酶Ⅰ(PGⅠ)与胃蛋白酶Ⅱ(PGⅡ)的比值(PGR)。二元logistic回归分析发生结肠息肉的影响因素;观察NAFLD、胃组织病理、Hp感染等指标在增生性和腺瘤性息肉间差异;分析腺瘤性息肉伴肠上皮瘤变进展与G17等指标的差异。结果年龄>60岁(χ²=7.436,P=0.006,OR=2.657)、Hp感染(χ²=17.702,P<0.001,OR=4.650)、PGR(χ²=10.794,P=0.001,OR=1.129)、胃泌素17升高(χ²=4.471,P=0.034,OR=3.706)与结肠息肉发生相关。腺瘤性息肉组Hp阳性占75.9%(60/79)高于增生组59.3%(32/54)(χ²=4.190,P=0.041)、腺瘤组NAFLD的构成比32.9%(26/79)高于增生组的14.8%(8/54)(χ²=5.520,P=0.019)、腺瘤组年龄>60岁占81.0%较增生组64.8%高(χ²=4.423,P=0.035),合并胃癌前病变(30.4%比44.4%)和G17升高(17.7%比11.1%)、PGR水平(14.18±7.74比13.93±8.75)二组差异无统计学意义(P>0.05)。腺瘤性息肉患者进展期组较非进展组NAFLD占比(20.8%比38.2%)、G17升高比率(41.7%比34.5%)差异无统计学意义(P>0.05);进展组吸烟率37.5%高于非进展组16.4%(χ²=4.243,P=0.039)、伴有癌前状态的严重慢性胃病比率45.8%较非进展组的23.6%高(χ²=3.892,P=0.049)、Hp感染率91.7%高于非进展组的69.1%(χ²=4.662,P=0.031)。结论结直肠息肉患者的腺瘤性息肉发生和进展与胃癌前病变、HP感染和NFALD有一定的关联。

关键词: 幽门螺杆菌, 非酒精性脂肪肝, 结直肠息肉

Abstract: Objective To explore the association between non-alcoholic fatty liver disease (NAFLD), Helicobacter pylori(Hp) infection, and the incidence of colorectal polyps.Methods From June 2021 to May 2022, a total of 133 patients diagnosed with colorectal polyps through colonoscopy and pathological examination were included in the experimental group. This group comprised 54 cases of hyperplastic polyps and 79 cases of adenomatous polyps. Additionally, 70 patients without colorectal polyps were selected as the control group. In all patients, various parameters, including total cholesterol (CHOL), low-density lipoprotein (LDL), HP antibody, serum gastrin 17 (G-17) and pepsinogen Ⅰ(PG-Ⅰ)/ pepsinogen Ⅱ (PG-II) ratio(PGR) were measured. Binary logistic regression analysis was utilized to assess the impact of each index on the occurrence of colonic polyps. The patients were subsequently categorized into two groups: the proliferative polyp group and the adenomatous polyp group. The differences in NAFLD, gastric histopathology, HP infection, adenomatous polyps with intestinal epithelial neoplasia and seurm G-17 levels between the two groups were observed in the study.Results The occurrence of colon polyps was found to be significantly associated with being older than 60 years (χ²=7.436,P=0.006, OR=2.657), Hp infection (χ²=17.702,P<0.001, OR=4.650), PGR (χ²=10.794,P=0.001,OR=1.129) and elevated levels of serum G-17 (χ²=4.471,P=0.034, OR=3.706). In the adenomatous polyp group, the HP-positive ratio was 75.9%, significantly higher than the 59.3% in the hyperplastic group(χ²=4.190, P=0.041). Similarly, the prevalence of NAFLD in the adenoma group was 32.9%, exceeding the 14.8% in the hyperplastic group (χ²=5.520, P=0.019). The percentage of patients older than 60 years in the adenoma group was 81.0%, which was higher compared to 64.8% in the hyperplasia group (χ²=4.423, P=0.035). No significant differences were observed in the proportion of precancerous lesions (30.4%vs44.4%), the increase rate of G-17 (17.7%vs11.1%), and the level of PGR (14.18±7.74 vs 13.93±8.75) between the two groups(P>0.05). Between the advanced and non-advanced groups, there were no significant differences in the proportion of NAFLD (20.8%vs38.2%) and the increase rate of G-17 (41.7% vs 34.5%) (P>0.05). However, the smoking rate in the advanced group was 37.5%, markedly higher than 16.4% in the non-advanced group(χ²=4.243, P=0.039), and the rate of severe chronic stomach disease with precancer was 45.8% in the advanced group compared to 23.6% in the non-progressive group (χ²=3.892,P=0.049). The HP infection rate was significantly higher in the advanced group(91.7%) compared to the non-advanced group(69.1%) (χ²=4.662, P=0.031).Conclusion The development and progression of colorectal polyps, particularly adenomatous polyps, are linked to gastric precancerous lesions, Hp infection and NAFLD. Effectively treating and preventing severe chronic gastric conditions and NAFLD, as well as the comprehensive eradication of HP, hold significantly potential in both the prevention and management of colorectal polyps.

Key words: Helicobacter pylori, Non-alcoholic fatty liver disease, Colorectal polyps

胡召锁, 姚春艳, 金娟, 严波, 陈正徐. NAFLD、Hp感染与结直肠息肉的关系[J]. 肝脏, 2023, 28(12): 1472-1475.

HU Zhao-suo, YAO Chun-yan, JIN Juan, YAN Bo, CHEN Zheng-xu. Correlation between non-alcoholic fatty liver disease, Helicobacter pylori infection, and the incidence of colorectal polyps[J]. Chinese Hepatolgy, 2023, 28(12): 1472-1475.

参考文献

[1] Dubé C, Yakubu M, McCurdy BR, et al. Risk of advanced adenoma, colorectal cancer, and colorectal cancer mortality in people with low-risk adenomas at baseline colonoscopy: a systematic review and meta-analysis[J]. Am J Gastroenterol, 2017,112:1790-801.
[2] Khan AA. Exploring polyps to colon carcinoma voyage: can blocking the crossroad halt the sequence? J Cancer Res Clin Oncol, 2021,147(8):2199-2207.
[3] 芦波. 幽门螺杆菌感染与结直肠肿瘤的风险:一项系统综述和荟萃分析[J]. 中华医学杂志,2022,102(22):1682-1682.
[4] Zumkeller N, Brenner H, Chang-Claude J, et al. Helicobacter pylori infection, interleukin-1 gene polymorphisms and the risk of colorectal cancer: evidence from a case-control study in Germany[J]. Eur J Cancer, 2007,43:1283-1289.
[5] Loke SS, Chuah SK. Factors associated with colorectal polyps in middle-aged and elderly populations[J]. Int J Environ Res Public Health, 2022, 19(12):7543.
[6] Cheng Y, Han J, Li Q, et al. Metabolic obesity phenotypes: a friend or foe of digestive polyps?-An observational study based on National Inpatient Database[J]. Metabolism, 2022,132:155201.
[7] Milano A, Bianco MA, Buri L, et al. Metabolic syndrome is a risk factor for colorectal adenoma and cancer: a study in a white population using the harmonized criteria[J]. Therap Adv Gastroenterol, 2019,12:1756284819867839.
[8] 柏愚,杨帆,马丹,等.中国早期结直肠癌筛查及内镜诊治指南(2014年,北京)[J].胃肠病学,2015,20(06):345-365.
[9] 非酒精性脂肪性肝病防治指南(2018更新版)[J].传染病信息,2018,31(05):393-402+420.
[10] Mohamed AK, Elhassan NM, Awhag ZA, et al. Prevalence of helicobacter pylori among sudanese patients diagnosed with colon polyps and colon cancer using immunohistochemistry technique[J]. BMC Res Notes, 2020,13(1):322.
[11] Mizuno S, Morita Y, Inui T, et al. Helicobacter pylori infection is associated with colon adenomatous polyps detected by high-resolution colonoscopy[J]. Int J Cancer, 2005, 117(6):1058-1059.
[12] Teimoorian F, Ranaei M, Hajian Tilaki K, et al. Association of helicobacter pylori infection with colon cancer and adenomatous polyps[J]. Iran J Pathol, 2018, 13(3):325-332.
[13] Konturek SJ, Konturek PC, Hartwich A, et al. Helicobacter pylori infection and gastrin and cyclooxygenase expression in gastric and colorectal malignancies[J]. Regul Pept, 2000,93:13Y19.
[14] Fireman Z, Trost L, Kopelman Y, et al. Helicobacter pylori: seroprevalence and colorectal cancer[J]. Isr Med Assoc J, 2000,2:6Y9.
[15] 王晓瑾. 功能性消化不良及肠易激综合征的临床诊治[J].中华全科医师杂志,2015,14 (5): 321-323.
[16] 陈磊, 全俊, 张旭东, 等.老年人肠易激综合征并功能性消化不良与胃肠激素相关性研究[J] .中华老年医学杂志,2015,34 (4): 394-396.
[17] Sonnenberg A, Turner KO, Genta RM. Associations between gastric histopathology and the occurrence of colonic polyps[J]. Colorectal Dis, 2020,22(7):814-817.
[18] Xie C, Wen P, Su J, et al. Elevated serum triglyceride and low-density lipoprotein cholesterol promotes the formation of colorectal polyps[J]. BMC Gastroenterol, 2019,19(1):195.
[19] Lesmana CRA, Pakasi LS, Sudoyo AW, et al. The Clinical Significance of Colon Polyp Pathology in Nonalcoholic Fatty Liver Disease (NAFLD) and Its Impact on Screening Colonoscopy in Daily Practice[J]. Can J Gastroenterol Hepatol, 2020, 2020:6676294.
[20] Narasimhan SD, Yen K, Tissenbaum HA. Converging pathways in lifespan regulation[J]. Curr Biol, 2009,19:R65
[21] 秦邈,王海鹏,宋宝,等. 胰岛素抵抗及糖脂代谢相关分子与结直肠息肉的关系[J]. 中华肿瘤杂志,2021,43(05):553-562.
[22] Ocvirk S, O'Keefe SJD. Dietary fat, bile acid metabolism and colorectal cancer[J]. Semin Cancer Biol, 2021,73:347-35.