Gastric mucosal cracked and cobblestone‐like changes resulting from proton pump inhibitor use

Miyamoto, Shuichi; Kato, Mototsugu; Tsuda, Momoko; Matsumoto, Kana; Muranaka, Toshiya; Abiko, Satoshi; Ono, Masayoshi; Mizushima, Takeshi; Omori, Saori; Yamamoto, Keiko; Mabe, Katsuhiro; Ono, Shoko; Kudo, Takahiko; Shimizu, Yuichi; Sakamoto, Naoya

doi:10.1111/den.12765

Cited by 19 publications

(36 citation statements)

References 20 publications

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“…We defined CLM as numerous uneven, flat, elevated mucosa like “cobblestones” in gastric corpus (Fig. 3a, b) [12, 14, 15]. We searched for the presence of these 3 findings for all objectives.…”

Section: Methodsmentioning

confidence: 99%

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Factors Associated with Gastric Black Spot, White Flat Elevated Mucosa, and Cobblestone-Like Mucosa: A Cross-Sectional Study

Hatano¹,

Haruma

Kamada

et al. 2018

Digestion

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Background/Aims: Previous studies have reported a possible relevance between proton pump inhibitor (PPI) use and 3 new gastric mucosal changes: black spots (BSs), white flat elevated mucosa (WFEM), and cobblestone-like mucosa (CLM). The aim of this study was to investigate the association between these mucosal changes and multiple factors including PPI use. Methods: All subjects who underwent a routine esophagogastroduodenoscopy (EGD) were successively enrolled. Endoscopists carried out the EGD after being blinded about information on patient PPI usage and determined the presence of these mucosal changes. The ratio of each factor was compared in cases with and without each gastric finding. Results: Out of 1,214 patients, BSs were recognized in 75 (6.2%) cases, WFEM in 59 (4.9%), and CLM in 41 (3.4%). In logistic regression analysis, PPI use was significantly correlated with all of these findings (BSs: OR 2.94; 95% CI 1.66–5.21), (WFEM: OR 3.58; 95% CI 1.94–6.61), and (CLM: OR 4.57; 95% CI 2.34–9.96), and Helicobacter pylori eradication was related to BSs (OR 3.01; 95% CI 1.73–5.24) and WFEM (OR 2.11; 95% CI 1.08–4.11). Decision-tree analyses showed that H. pylori eradication was associated with all findings. Conclusions: All of the considered findings were correlated with PPI and H. pylori eradication.

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Section: Methodsmentioning

confidence: 99%

“…Histological examination of the gastric mucosa of patients with CLM found parietal cell protrusion, cystic dilation of fundic gland, and cytoplasmic vacuolation [14, 15]. In cases with BSs, brownish pigmentations in fundic gland cysts were found in addition to these pathological findings [11].…”

Section: Introductionmentioning

confidence: 99%

Factors Associated with Gastric Black Spot, White Flat Elevated Mucosa, and Cobblestone-Like Mucosa: A Cross-Sectional Study

Hatano¹,

Haruma

Kamada

et al. 2018

Digestion

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“…Similarly, fundic gland polyps developed from long-term PPI use in a patient without H. pylori infection [5]. Recently, we reported that gastric mucosal changes such as GCM and GCSM result from the use of PPIs in a patient without current H. pylori infection [11].…”

Section: Glands Kumar Et Al Demonstrated That Oxyntic Gland Dilatatmentioning

confidence: 99%

“…The normal fundic glands exhibit no PCPs and are not dilated. The major axis of the lumen of the normal fundic gland is usually <50 µm [11]. Large-size oxyntic gland dilatations were detected by EUS as sporadic small a-echoic lesions.…”

Section: Glands Kumar Et Al Demonstrated That Oxyntic Gland Dilatatmentioning

confidence: 99%

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Endoscopic ultrasonography features of gastric mucosal cobblestone-like changes from a proton-pump inhibitor

Miyamoto

Kudo

Kato

et al. 2017

Clin J Gastroenterol

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A 68-year-old man with no symptoms presented to Hokkaido University Hospital for esophagogastroduodenoscopy screening. He had a history of Helicobacter pylori eradication. Initial esophagogastroduodenoscopy showed no gastric cobblestone-like mucosa or gastric cracked mucosa. After 1 year, he received esomeprazole (20 mg) once daily for heartburn at another hospital.Esophagogastroduodenoscopy was performed after 2 years of esomeprazole administration. Endoscopic findings showed that after H. pylori eradication, according to the Kyoto classification, gastric cobblestone-like mucosa presented in the gastric body area. Dilation of the oval crypt opening and intervening part in the gastric cobblestone-like mucosa was detected by endoscopy with narrow band imaging. Endoscopic ultrasonography revealed a thick gastric second layer and sporadic small a-echoic lesions in the low-echoic thickened second layer in the gastric cobblestone-like mucosa. The gastric cobblestone-like mucosa biopsy specimen showed parietal cell protrusions and oxyntic gland dilatations.Recently, we reported that gastric mucosal changes such as gastric cracked mucosa and gastric cobblestone-like mucosa were caused by proton-pump inhibitors; however, the gastric cobblestone-like mucosa was not examined by endoscopic ultrasonography. In this case, endoscopic ultrasonography findings suggested that oxyntic gland dilatations caused the elevated gastric mucosa, such as gastric cobblestone-like mucosa, from the use of proton-pump inhibitors.3

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Endoscopic findings and outcomes of gastric mucosal changes relating to potassium‐competitive acid blocker and proton pump inhibitor therapy

Shinozaki,

Osawa,

Miura

et al. 2024

DEN Open

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Gastric mucosal changes associated with long‐term potassium‐competitive acid blocker and proton pump inhibitor (PPI) therapy may raise concern. In contrast to that for PPIs, the evidence concerning the safety of long‐term potassium‐competitive acid blocker use is scant. Vonoprazan (VPZ) is a representative potassium‐competitive acid blocker released in Japan in 2015. In order to shed some comparative light regarding the outcomes of gastric mucosal lesions associated with a long‐term acid blockade, we have reviewed six representative gastric mucosal lesions: fundic gland polyps, gastric hyperplastic polyps, multiple white and flat elevated lesions, cobblestone‐like gastric mucosal changes, gastric black spots, and stardust gastric mucosal changes. For these mucosal lesions, we have evaluated the association with the type of acid blockade, patient gender, Helicobacter pylori infection status, the degree of gastric atrophy, and serum gastrin levels. There is no concrete evidence to support a significant relationship between VPZ/PPI use and the development of neuroendocrine tumors. Current data also shows that the risk of gastric mucosal changes is similar for long‐term VPZ and PPI use. Serum hypergastrinemia is not correlated with the development of some gastric mucosal lesions. Therefore, serum gastrin level is unhelpful for risk estimation and for decision‐making relating to the cessation of these drugs in routine clinical practice. Given the confounding potential neoplastic risk relating to H. pylori infection, this should be eradicated before VPZ/PPI therapy is commenced. The evidence to date does not support the cessation of clinically appropriate VPZ/PPI therapy solely because of the presence of these associated gastric mucosal lesions.

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Gastric mucosal cracked and cobblestone‐like changes resulting from proton pump inhibitor use

Abstract: Novel GCM and GCSM endoscopic findings in the corpus area seem to be strongly associated with PPI use.

Cited by 19 publications

References 20 publications

Factors Associated with Gastric Black Spot, White Flat Elevated Mucosa, and Cobblestone-Like Mucosa: A Cross-Sectional Study

Factors Associated with Gastric Black Spot, White Flat Elevated Mucosa, and Cobblestone-Like Mucosa: A Cross-Sectional Study

Endoscopic ultrasonography features of gastric mucosal cobblestone-like changes from a proton-pump inhibitor

Endoscopic findings and outcomes of gastric mucosal changes relating to potassium‐competitive acid blocker and proton pump inhibitor therapy

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