十二指肠胃泌素瘤与萎缩性胃炎的新关联：病例报告及文献综述

Lendel Irina, Manni Andrea, Ruggiero Francesca M

Divisionof Endocrinology, Diabetes, and Metabolism, The Penn State Milton S.Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA.

Endocr Pract. 2007 Nov-Dec;13(7):770-5. doi: 10.4158/EP.13.7.770.

OBJECTIVE

To describe a patient with a duodenal gastrinoma in a setting of atrophic gastritis and hypergastrinemia.

METHODS

We present historical features and results of laboratory and genetic evaluation in a woman with duodenal gastrinoma and hypergastrinemia due to atrophic gastritis.

RESULTS

In a 46-year-old woman with a history of stable pituitary microprolactinoma, multiple gastrointestinal symptoms developed and prompted the performance of an esophagogastroduodenoscopy in conjunction with small bowel biopsies. A 2-mm duodenal gastrin-producing neuroendocrine tumor was discovered. The tumor stained negative for serotonin and somatostatin and involved the mucosa and submucosa. Immunohistochemical staining of the gastrinoma tissue with a monoclonal antibody to the cholecystokinin-B (gastrin) receptor was negative. The patient's random serum gastrin level was elevated at 990 pg/mL. She had been taking pantoprazole for 4 weeks before that test. After pantoprazole therapy was discontinued, the serum gastrin level remained elevated at 403 pg/mL. There was no family history of multiple endocrine neoplasia type 1, and genetic testing for the MEN1 mutation was negative. An upper endoscopy with measurement of gastric pH and performance of gastric biopsies confirmed the presence of chronic atrophic gastritis. This finding was consistent with the patient's persistently elevated serum gastrin levels.

CONCLUSION

Patients with atrophic gastritis and associated hypergastrinemia are known to have a high frequency of hypergastrinemia-induced gastric carcinoid tumors, some of which are actual gastrinomas or are thought to arise from the G cells of the stomach. Gastrin is a well-recognized growth factor for many tissues. We postulate that hypergastrinemia in this patient might have had a trophic effect on the duodenal G cells and led to gastrinoma development. No gastrin receptors were detected on the gastrinoma cells; however, that result might have been attributable to technical (fixation or antibody) or tumor (dedifferentiation) problems.

目的

描述一名患有十二指肠胃泌素瘤且伴有萎缩性胃炎和高胃泌素血症的患者。

方法

我们呈现了一名因萎缩性胃炎导致十二指肠胃泌素瘤和高胃泌素血症的女性患者的病史特征以及实验室和基因评估结果。

结果

一名46岁女性，有稳定的垂体微泌乳素瘤病史，出现多种胃肠道症状，促使其进行了食管胃十二指肠镜检查并取小肠活检。发现了一个2毫米的十二指肠产胃泌素神经内分泌肿瘤。该肿瘤血清素和生长抑素染色为阴性，累及黏膜和黏膜下层。用抗胆囊收缩素 - B（胃泌素）受体单克隆抗体对胃泌素瘤组织进行免疫组化染色为阴性。患者随机血清胃泌素水平升高至990 pg/mL。在该检测前她已服用泮托拉唑4周。泮托拉唑治疗停药后，血清胃泌素水平仍升高至403 pg/mL。无1型多发性内分泌腺瘤家族史，MEN1突变基因检测为阴性。上消化道内镜检查测量胃pH值并取胃活检证实存在慢性萎缩性胃炎。这一发现与患者持续升高的血清胃泌素水平相符。

结论

已知萎缩性胃炎及相关高胃泌素血症患者发生高胃泌素血症诱导的胃类癌肿瘤的频率较高，其中一些实际上是胃泌素瘤或被认为起源于胃的G细胞。胃泌素是许多组织公认的生长因子。我们推测该患者的高胃泌素血症可能对十二指肠G细胞有营养作用并导致胃泌素瘤的发生。在胃泌素瘤细胞上未检测到胃泌素受体；然而，该结果可能归因于技术（固定或抗体）或肿瘤（去分化）问题。