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Autoimmune Gastritis: Distinct Histological and Immunohistochemical Findings Before Complete Loss of Oxyntic Glands

机译:自身免疫性胃炎:在完全丧失氧化性腺体之前的不同组织学和免疫组织化学发现

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Autoimmune gastritis (AG) can be easily recognized when the histological features are fully developed, but recognizing AG before the complete loss of the oxyntic mucosa is more challenging. One feature of fully developed AG is enterochromaffin cell-like (ECL) hyperplasia, but its presence or absence in earlier stages of AG has not been fully evaluated. A retrospective study of biopsy specimens from 40 patients was performed; all of the patients were originally diagnosed with possible AG based on the presence of lymphocytic infiltration and damage to oxyntic glands and/or the presence of metaplastic epithelium that disproportionately involved the body mucosa. Nineteen cases had follow-up serological studies for anti–parietal cells and/or anti–intrinsic factor antibodies: 13 were positive and 6 negative. The remaining 21 cases were indeterminate because of incomplete testing. The histological findings were similar in the patients who were serologically positive and those who were indeterminate for AG. In all of these cases, the oxyntic mucosa showed lymphoplasmacytic infiltrates within the lamina propria with focal gland infiltration and damage. Sixty-five percent (22/34) of the cases showed intestinal and/or pyloric metaplasia, and 85% (29/34) showed parietal cell pseudohypertrophy. Chromogranin stains were performed in 11 of 13 cases with positive serological markers for AG, and all showed at least linear ECL cell hyperplasia. In contrast, none of the six cases with negative serological studies had linear ECL cell hyperplasia, P < .001. In conclusion, the following constellation of findings supports a diagnosis of AG before the complete loss of oxyntic mucosa: deep or diffuse lymphoplasmacytic infiltrates within the lamina propria with foci of gland infiltration and damage, epithelial metaplasia, parietal cell pseudohypertrophy, and ECL cell hyperplasia at the linear or greater level.
机译:当组织学特征充分发展时,可以很容易地识别自身免疫性胃炎(AG),但是在氧化性粘膜完全消失之前识别AG更具挑战性。完全成熟的AG的特征之一是肠嗜铬细胞样(ECL)增生,但尚未充分评估其在AG早期阶段的存在与否。对40例患者的活检标本进行了回顾性研究。所有患者最初都是根据淋巴细胞浸润和对氧化性腺的损害和/或不完整地累及身体粘膜的化生上皮而被诊断为可能患有AG。 19例接受了抗壁细胞和/或抗内在因子抗体的血清学研究:13例阳性,6例阴性。其余21例由于测试不完整而不确定。血清学阳性的患者和AG不确定的患者的组织学发现相似。在所有这些情况下,催产性粘膜均表现为固有层内淋巴浆细胞浸润,并伴有局灶性腺体浸润和损害。百分之六十五(22/34)的患儿表现为肠和/或幽门化生,而百分之八十五(29/34)的患儿表现为壁细胞假肥大。 13例中有11例进行了嗜铬粒蛋白染色,AG血清学指标阳性,且均显示至少线性ECL细胞增生。相比之下,血清学研究阴性的六例病例均未出现线性ECL细胞增生,P <.001。综上所述,以下发现有助于在氧化性粘膜完全消失之前诊断AG:固有层中的深层或弥漫性淋巴浆细胞浸润伴有腺体浸润和损伤,上皮化生,壁细胞假性肥大和ECL细胞增生线性或更大的水平。

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