Bardella M T, Valenti L, Pagliari C, Peracchi M, Farè M, Fracanzani A L, Fargion S
Department Medical Sciences, IRCCS Ospedale Maggiore Policlinico di Milano, University of Milan, Via F. Sforza, 35, 20122 Milan, Italy.
Dig Liver Dis. 2004 May;36(5):333-6. doi: 10.1016/j.dld.2004.01.012.
A non-negligible percentage of patients with non-alcoholic fatty liver disease, a leading cause of hepatic progressive disorder related to insulin resistance, have no metabolic risk factors, and abnormal intestinal permeability has been suggested to be involved in the pathogenesis of the liver damage. Coeliac disease, a curable disorder characterised by inflammatory mucosal damage, may show hepatic histological features similar to steatohepatitis. Conflicting data have been reported on the prevalence of coeliac disease in non-alcoholic steatohepatitis.
To search for coeliac disease in a series of patients with non-alcoholic fatty liver disease by screening with anti-tissue transglutaminase and anti-endomysium antibodies.
Fifty-nine consecutive patients with hypertransaminasemia and non-alcoholic fatty liver disease, 38 (64%) with steatohepatitis. Anti-endomysium antibodies were assayed by indirect immunofluorescence, IgA anti-tissue transglutaminase by ELISA. Patients who tested positive underwent HLA DQ typing and endoscopy.
Tissue transglutaminase antibodies were positive in six (10%) patients and anti-endomysium in two (3.4%); only two (3.4%), positive for both anti-endomysium positive and anti-transglutaminase, resulted to have coeliac disease based on histological findings. After 6 months of gluten-free diet, liver enzymes normalised.
The prevalence of silent coeliac disease is 3.4% in patients with non-alcoholic fatty liver. The inclusion of anti-endomysium antibodies test in studying patients with non-alcoholic fatty liver and persistent biochemical abnormalities has to be taken into account, since positivity for tissue transglutaminase antibodies, in the absence of confirmatory anti-endomysium antibodies, is not sufficient to perform diagnostic endoscopy.
非酒精性脂肪性肝病是与胰岛素抵抗相关的肝脏进行性疾病的主要原因,相当比例的此类患者没有代谢危险因素,且肠道通透性异常被认为参与了肝损伤的发病机制。乳糜泻是一种以炎症性黏膜损伤为特征的可治愈疾病,可能表现出与脂肪性肝炎相似的肝脏组织学特征。关于非酒精性脂肪性肝炎中乳糜泻的患病率,已有相互矛盾的数据报道。
通过抗组织转谷氨酰胺酶和抗肌内膜抗体筛查,在一系列非酒精性脂肪性肝病患者中寻找乳糜泻。
连续纳入59例高转氨酶血症和非酒精性脂肪性肝病患者,其中38例(64%)为脂肪性肝炎。抗肌内膜抗体通过间接免疫荧光法检测,IgA抗组织转谷氨酰胺酶通过酶联免疫吸附测定法检测。检测呈阳性的患者接受HLA DQ分型和内镜检查。
6例(10%)患者的组织转谷氨酰胺酶抗体呈阳性,2例(3.4%)抗肌内膜抗体呈阳性;仅2例(3.4%)抗肌内膜抗体和抗转谷氨酰胺酶均呈阳性的患者根据组织学结果被诊断为乳糜泻。无麸质饮食6个月后,肝酶恢复正常。
非酒精性脂肪性肝病患者中无症状乳糜泻的患病率为3.4%。在研究非酒精性脂肪性肝病和持续性生化异常的患者时,应考虑纳入抗肌内膜抗体检测,因为在没有抗肌内膜抗体确认的情况下,组织转谷氨酰胺酶抗体阳性不足以进行诊断性内镜检查。