目的:最近的研究表明幽门螺杆菌与代谢功能障碍相关的脂肪变性肝病(MASLD)之间存在关联。我们的目的是评估幽门螺杆菌毒力基因与肝损伤和纤维化的非侵入性标志物在MASLD受试者的关联。
方法:共选择362例经胃镜检查的消化不良患者。生物化学,临床参数,超声,FIB-4得分,通过振动控制瞬态弹性成像(VCTE)测量肝脏硬度(LSM),胃活检,和幽门螺杆菌毒力基因(cagA,vacA)进行了评估。
结果:一个队列由61%的女性和39%的男性组成,中位年龄为52(40-60)岁。MASLD在42%中观察到,45%的幽门螺杆菌阳性。在共病代谢条件下没有观察到关于幽门螺杆菌状态的差异。在MASLD队列中,幽门螺杆菌阳性与较高的AST相关,ALT,FIB-4和LSM。的确,cagA/vacA-s1/m1阳性等位基因组合的携带者与较高的AST相关,ALT,FIB-4和LSM,但不是cagA/vacA-s1/m1阴性。对于幽门螺杆菌阳性的VCTE(≥8kPa)的显着/晚期纤维化高风险的OR为2.56(95%CI,1.2-5.75),对于cagA/vacA-s1/-m1阳性等位基因携带者为4.01(95%CI,1.38-11.56),但cagA/vacA-s1/-m1阴性无显著关联。在调整了年龄之后,性别,糖尿病,BMI和高血压对于幽门螺杆菌阳性的VCTE≥8kPa的OR为2.43(95%CI,1.88-12.44),cagA/vacA-s1/m1阳性等位基因携带者为4.06(95%CI,1.22-14.49)。
结论:在我们的患有MASLD的FD患者队列中,幽门螺杆菌与肝损伤和纤维化的非侵入性标志物相关。cagA/vacA-s1/m1阳性等位基因组合的携带者通过VCTE显示出显著/晚期纤维化的独立风险。
OBJECTIVE: Recent studies have suggested an association between H. pylori and metabolic dysfunction associated steatotic liver disease (MASLD). We aim to evaluate the association of H. pylori virulence genes with non-invasive markers of liver injury and fibrosis in MASLD subjects.
METHODS: A total of 362 dyspeptic patients who underwent gastroscopy were selected. Biochemical, clinical parameters, ultrasound, FIB-4 score, liver stiffness measurement (LSM) by vibration-controlled transient elastography (VCTE), gastric biopsies, and H. pylori virulence genes (cagA, vacA) were evaluated.
RESULTS: A cohort comprised of 61 % women and 39 % men with a median age of 52 (40-60) years. MASLD was observed in 42 %, and H. pylori-positive in 45 %. No differences were observed regarding H. pylori status at co-morbid metabolic conditions. In MASLD cohort, H. pylori-positive was associated with higher AST, ALT, FIB-4 and LSM. Indeed, carriers of cagA/vacA-s1/m1-positive allelic combination were associated with higher AST, ALT, FIB-4 and LSM but not cagA/vacA-s1/m1-negative. The OR for high-risk of significant/advanced- fibrosis by VCTE (≥8 kPa) with H. pylori-positive was 2.56 (95 % CI, 1.2-5.75) and for cagA/vacA-s1/-m1-positive allelic carriers was 4.01 (95 % CI, 1.38-11.56), but non-significant association in cagA/vacA-s1/-m1-negative. After adjusting for age, gender, diabetes, BMI and hypertension the OR for VCTE ≥8 kPa with H. pylori-positive was 2.43 (95 % CI, 1.88-12.44), and cagA/vacA-s1/m1-positive allelic carriers was 4.06 (95 % CI, 1.22-14.49).
CONCLUSIONS: In our cohort of FD patients with MASLD, H. pylori was associated with non-invasive markers of liver injury and fibrosis. Carriers of cagA/vacA-s1/m1-positive allelic combination showed an independent risk of significant/advanced fibrosis by VCTE.