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肥厚性淋巴细胞性胃炎患者根除幽门螺杆菌后胃肠道蛋白丢失的缓解情况。

Resolution of gastrointestinal protein loss after Helicobacter pylori eradication in a patient with hypertrophic lymphocytic gastritis.

作者信息

Madisch Ahmed, Aust Daniela, Morgner Andrea, Grossmann Dana, Schmelz Renate, Kropp Joachim, Ehninger Gerhard, Baretton Gustavo, Miehlke Stephan

机构信息

Medical Department I, Technical University Hospital, Dresden, Germany.

出版信息

Helicobacter. 2004 Dec;9(6):629-31. doi: 10.1111/j.1083-4389.2004.00275.x.

Abstract

BACKGROUND

Lymphocytic gastritis is a rare condition found in approximately 1% of dyspeptic patients. An association with Helicobacter pylori infection has been described. Hypertrophic lymphocytic gastritis is a rare cause of gastrointestinal protein loss. Here, we describe a patient with hypertrophic lymphocytic gastritis, in whom gastrointestinal protein loss resolved completely following H. pylori eradication.

CASE REPORT

A 38-year old obese man without gastrointestinal symptoms showed a markedly decreased serum protein (53 g/l, normal 66-85 g/l), a decreased serum albumin (33 g/l, normal 35-52 g/l) and decreased serum immunoglobulin G and immunoglobulin M levels. A renal cause for protein loss was excluded, liver function was normal. Endoscopy of the upper gastrointestinal tract revealed enlarged rigid gastric folds, and an H. pylori-associated lymphocytic gastritis. 99mTc-labelled albumin scintigraphy showed an increased activity in the upper left abdomen compatible with protein secretion in the stomach, and tracer pooling in the upper small bowel. Push enteroscopy with histology demonstrated a normal upper small bowel. Two months after eradication therapy, cure of H. pylori infection was documented and serum protein (71 g/l) and albumin (41 g/l) had returned to normal, while lymphocytic gastritis was still present. One year after eradication therapy endoscopy of the upper gastrointestinal tract and histology and laboratory values were normal.

CONCLUSION

Protein-losing gastropathy caused by H. pylori-associated hypertrophic lymphocytic gastritis can be cured solely by H. pylori eradication therapy.

摘要

背景

淋巴细胞性胃炎是一种罕见疾病,约1%的消化不良患者会出现。已有研究表明其与幽门螺杆菌感染有关。肥厚性淋巴细胞性胃炎是胃肠道蛋白丢失的罕见原因。在此,我们描述了一名肥厚性淋巴细胞性胃炎患者,其胃肠道蛋白丢失在根除幽门螺杆菌后完全缓解。

病例报告

一名38岁无胃肠道症状的肥胖男性,血清蛋白显著降低(53 g/l,正常66 - 85 g/l),血清白蛋白降低(33 g/l,正常35 - 52 g/l),血清免疫球蛋白G和免疫球蛋白M水平降低。排除了肾脏导致蛋白丢失的原因,肝功能正常。上消化道内镜检查发现胃皱襞粗大僵硬,诊断为幽门螺杆菌相关性淋巴细胞性胃炎。99mTc标记白蛋白闪烁扫描显示左上腹活性增加,符合胃内蛋白分泌情况,且示踪剂在小肠上段聚集。推进式小肠镜检查及组织学检查显示上段小肠正常。根除治疗两个月后,记录到幽门螺杆菌感染已治愈,血清蛋白(71 g/l)和白蛋白(41 g/l)恢复正常,但淋巴细胞性胃炎仍存在。根除治疗一年后,上消化道内镜检查、组织学检查及实验室检查结果均正常。

结论

幽门螺杆菌相关性肥厚性淋巴细胞性胃炎所致的失蛋白性胃病仅通过根除幽门螺杆菌治疗即可治愈。

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