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要旨●[症例1]はH. pylori未感染胃粘膜の患者で,既往に逆流性食道炎がありPPIを継続内服中であった.味覚異常を契機に酢酸亜鉛50mgの服用が開始された.5か月後には胃体上部後壁大彎を中心に,白苔を伴う発赤びらんを散在性に認めた.最終的に酢酸亜鉛起因性胃粘膜傷害が強く疑われた.[症例2]もH. pylori未感染胃粘膜の患者で,逆流性食道炎のためボノプラザン内服中であった.味覚障害に対して酢酸亜鉛100mgが投与された.9か月後のEGDにて胃体部や胃穹窿部に白苔を伴うびらんと周囲の発赤粘膜,瘢痕所見を多発性に認めた.17か月後には潰瘍性病変となり,明らかに増悪した.酢酸亜鉛起因性胃粘膜傷害を疑い25mgに減量したところ,潰瘍は閉鎖し発赤瘢痕に改善した.
The first case involved a 90-year-old male patient who had undergone esophagogastroduodenoscopy(EGD)for an annual examination of gastroesophageal reflux disease(GERD). The second case involved a 70-year-old male patient who had undergone EGD for GERD. Both patients complained of an abnormal taste and were diagnosed with hypozincemia with a serum zinc level of 69 and 72μg/dL(normal range:80−130μg/dL). Both patients were orally administered with zinc acetate 5 and 9 months before the examination. Endoscopy revealed erosions with white-coated mucosa surface adhesions and erythema on the greater curvature to the posterior side of the gastric body. EGD performed after 9−17 months revealed ulcers and scars on the posterior wall and greater curvature of the upper gastric body. Furthermore, redness was observed on the anterior wall. Biopsied specimens showed gastric erosions and ductal distortion with exudate on the surface, and overall epithelial cells demonstrated infarct-like necrosis(ghost-like appearance). Therefore, we diagnosed the gastric mucosal injury as a zinc acetate-associated gastric lesion based on the endoscopic results and oral zinc acetate administration history. We discontinued zinc acetate to solve these gastric lesions. Our cases demonstrate the importance of recognizing the typical endoscopic findings of a zinc acetate-associated gastric lesion to enable its prompt diagnosis during EGD.
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