Picarelli Antonio, Sabbatella Luigi, Di Tola Marco, Di Cello Teresa, Vetrano Stefania, Anania Maria Cristina
Department of Clinical Sciences, University of Rome La Sapienza, Italy.
Am J Gastroenterol. 2002 Jan;97(1):95-8. doi: 10.1111/j.1572-0241.2002.05426.x.
Serum antiendomysial antibodies (EMAs), highly sensitive and specific serological markers of celiac disease (CD), are detectable in culture media of biopsy samples from CD patients. This finding can be considered an in vitro evidence that intestinal mucosa is a site of EMA production. To confirm this finding, we investigated the presence of EMAs and of anti-tissue transglutaminase (anti-tTG), recently identified as the autoantigen of the EMA, in fecal supernatants of CD patients.
Twenty-one newly diagnosed CD patients, 10 treated CD patients on a gluten-free diet, and 14 control disease patients on a gluten-containing diet were enrolled. Twenty-four-hour stool collections and fecal supernatants were obtained from all patients in the study. Biopsy cultures were also performed. IgA EMAs were detected in sera, culture media, and fecal supernatants. IgA, IgG, IgM, and IgE anti-gliadin antibodies (AGAs) and IgA anti-tTG antibodies were measured in fecal supernatants. The weights, water content, and pHs of the 24-h stool collections were also measured.
In all untreated CD patients EMAs were detectable in sera, culture media, and fecal supernatants. In treated CD patients, EMAs were detected only in culture media after in vitro gliadin challenge. No EMAs were detected in controls. Anti-tTG levels were higher in untreated CD patients than in treated CD patients and controls. IgA AGA levels were higher in untreated CD patients than in treated CD and control patients, whereas IgM AGAs were higher in both untreated and treated CD patients than in controls. No statistically significant differences were observed for IgG and IgE AGAs among the above-mentioned populations. Fecal weights, water content, and pHs were higher in untreated CD than in control patients.
The presence of EMAs in fecal supernatants represents the in vivo proof that intestinal mucosa is a site of EMA production. Furthermore, EMA detection in the stools could be a simple and useful additional tool to clarify diagnosis in the patchy conditions of CD.
血清抗肌内膜抗体（EMA）是乳糜泻（CD）高度敏感且特异的血清学标志物，在CD患者活检样本的培养基中可检测到。这一发现可被视为肠道黏膜是EMA产生部位的体外证据。为证实这一发现，我们研究了CD患者粪便上清液中EMA以及近期被确定为EMA自身抗原的抗组织转谷氨酰胺酶（抗tTG）的存在情况。
纳入21例新诊断的CD患者、10例接受无麸质饮食治疗的CD患者以及14例接受含麸质饮食的对照疾病患者。收集所有研究患者的24小时粪便样本并获取粪便上清液。同时进行活检培养。检测血清、培养基和粪便上清液中的IgA EMA。检测粪便上清液中的IgA、IgG、IgM和IgE抗麦醇溶蛋白抗体（AGA）以及IgA抗tTG抗体。还测量了24小时粪便样本的重量、含水量和pH值。
在所有未治疗的CD患者中，血清、培养基和粪便上清液中均可检测到EMA。在接受治疗的CD患者中，仅在体外麦醇溶蛋白激发后培养基中检测到EMA。对照患者中未检测到EMA。未治疗的CD患者抗tTG水平高于接受治疗的CD患者和对照患者。未治疗的CD患者IgA AGA水平高于接受治疗的CD患者和对照患者，而未治疗和接受治疗的CD患者IgM AGA水平均高于对照患者。上述人群中IgG和IgE AGA未观察到统计学显著差异。未治疗的CD患者粪便重量、含水量和pH值高于对照患者。
粪便上清液中EMA的存在代表了肠道黏膜是EMA产生部位的体内证据。此外，粪便中EMA检测可能是在CD局部病变情况下辅助明确诊断的一种简单且有用的工具。
