Abstract
With widespread use of proton pump inhibitors (PPIs) has come characteristic gastric mucosal changes such as parietal cell protrusions (PCPs) and so-called fundic gland polyps (FGPs). Nevertheless, whether these lesions are actually PPI-related gastric mucosal lesions has not been fully clarified. The present study focused on this issue. We firstly examined the purported relation between the emergence of PCPs and PPI use. We also investigated the relation between PPI use and the emergence of cystically dilated glands (CDGs) that can give rise to elevated mucosal lesions such as FGPs. In addition, we performed histopathologic and immunohistochemical analyses to clarify the characteristics of PCPs and PCP-affected gastric oxyntic mucosa. A significant relation between the emergence of PCPs and PPI use was confirmed. In contrast, no significant relation was found between the emergence of CDGs and PPI use. Histologic and immunohistochemical analyses showed PCPs to be hyperplastic lesions. In the PCP-affected oxyntic mucosa, the isthmus-and-neck region of the fundic glands was elongated and the base region was shortened in relation to the total mucosal thickness. These changes were accompanied by an increase in the number of parietal cells and a decrease in the number of chief cells. Immunohistochemical analysis suggested impairment of both parietal cell differentiation and mucous neck-to-chief cell differentiation．Furthermore, our study reinforced the notion that elevated hydrostatic pressure and cytoplasmic edema due to movement of water from interstitial space toward the lumen of oxyntic glands via parietal cells give rise to the formation of PCPs, oxyntic dilatation, and CDGs. The detailed mechanism of PCP formation and its clinical implications are expected to be clarified in future studies.
