Development Of Fundic Gland Polyps Research Articles

The association between duration of and indications for proton pump inhibitor use and risk of gastric polyps.

The development of fundic gland polyps (FGPs) is the most common side effect of long-term proton pump inhibitor (PPI) use; however, the effect of drug use characteristics and their impact on the risk of other gastric polyp development remain unclear. We aimed to identify the influence of PPI administration, as well as its duration and dose, in the development of gastric polyps. A prospective cohort study was conducted on consecutive patients who underwent gastroscopy between September 2017 and August 2019. Detailed characteristics of gastric polyps, Helicobacter pylori infection, and PPI use were analyzed. Among the 2723 patients included, gastric polyps (75% FGPs, 22% hyperplastic) were detected in 16.4%, and 60% were prescribed PPI. The risk of FGPs and hyperplastic polyps according to the duration of PPI use were as follows: 2-5 years [odds ratio (95% confidence interval); 2.86 (2.00-4.11) and 2.82 (1.69-4.78)]; 6-9 years [7.42 (5.03-11.01) and 2.32 (1.05-4.78)]; ≥10 years [14.94 (10.36-21.80) and 3.52 (1.67-7.03)]. Multivariate analysis confirmed that the risk of FGPs was 17.16 (11.35-26.23) for ≥10 years of PPI use. Portal hypertension-related conditions were associated with hyperplastic polyps [4.99 (2.71-9.20)]. Duration of and indications for PPI use are the most predictive factors for the development of gastric polyps. Prolonged PPI use increases the risk of polyp development and the number of patients with polyps, which may burden endoscopic practice. Highly selected patients may require particular care despite minimal risk of dysplasia and bleeding generally.

Malignant transformation of fundic gland polyps in familial adenomatous polyposis

Sporadic fundic gland polyps (FGPs) are ubiquitous benign lesions with no potential for malignant transformation. Familial adenomatous polyposis (FAP) is associated with the development of FGPs that are morphologically identical to but genetically distinct from those seen in sporadic cases. The shared aetiology involves disruption of the WNT signalling pathway, however FAP associated cases are predominantly driven by germline APC gene mutations rather than the somatic CTNNB1 gene mutations prevalent in sporadic lesions.

S2158 Fundic Gland Polyp Causes Massive Melena During Induction Chemotherapy With R-EPOCH for DLBCL

INTRODUCTION: Fundic Gland Polyps (FGPs) are hamartomatous cystic lesions in the gastric mucosa, and mostly occur sporadically. Bleeding from an FGP is very rare but has been reported in the setting of long-term PPI use and rare hematologic conditions. Overall, these polyps are considered quite benign. CASE DESCRIPTION/METHODS: A 71-year-old gentleman presented to the hospital in active tumor lysis and was subsequently diagnosed with Diffuse Large B Cell Lymphoma of the non-germinal center type, in a background of 3B follicular lymphoma. He was started on induction chemotherapy with the R-EPOCH regimen (without rituximab given unknown HBV status) and a day later, developed massive melena resulting in hemorrhagic shock. His chemotherapy regimen was stopped and he was resuscitated, requiring multiple transfusions. Once in stable condition, an EGD was performed which found only a benign FGP in a background of chronic atrophic gastritis as a source of the bleed (Figure 1). The pathology revealed pyloric and intestinal metaplasia, consistent with autoimmune gastritis (Figure 2), with no evidence of dysplasia or malignancy. Mesenteric angiography was subsequently performed to identify any other source of GI bleed for IR embolization, but no contrast extravasation was observed to suggest one. The patient's clinical status improved during the procedure, suggesting that the hemorrhage had ceased. DISCUSSION: The development of FGPs is a rare phenomenon. When they do form, they may form sporadically, or may be associated with hypergastrinemia seen in patients taking proton pump inhibitors, in those with Zollinger-Elison syndrome, and in those with autoimmune metaplastic atrophic gastritis (AMAU). Interestingly, our patient was found to have AMAU on pathology and there have been multiple reports of a bidirectional association between lymphocytic malignancies, like DLBCL, and autoimmune manifestations. Our patient's GI bleed was likely the result of a combination of factors, including his AMAU and his DVT prophylaxis (enoxaparin), but the most significant of these factors is the gastrointestinal side effects of his chemotherapeutic R-EPOCH (Rituximab, Etoposide, Prednisone, Oncovin, Cyclophosphamide and Doxorubicin Hydrochloride) regimen. Many of the drugs used in this regimen are known to cause mucositis, and prednisone in particular has been historically associated with GI bleeds due to mechanisms such as impaired wound healing. As seen in this case, when his chemotherapeutic regimen was stopped, his bleeding also ceased.Figure 1.: Endoscopic photograph of the fundic gland polyp.Figure 2.: The biopsy of the fundic gland polyp demonstrates cystically dilated glands arising in oxyntic-type mucosa.Figure 3.: The biopsy of the background fundic mucosa shows atrophic mucosa with loss of oxyntic glands, pseudopyloric metaplasia, and chronic inflammation in the lamina propria, compatible with autoimmune gastritis.

Relative risk factors associated with the development of fundic gland polyps.

The prevalence of fundic gland polyps (FGPs) is increasing. Some researchers consider this increase to be associated strongly with the long-term use of proton-pump inhibitors (PPIs); however, not all researchers share this belief. There are minimal data on the development of FGPs in China. Therefore, we aimed to investigate the prevalence of FGPs and risk factors associated with the development of this disease. We studied 10 904 consecutive patients who underwent gastroduodenal endoscopies at our digestive endoscopy center between February 2011 and January 2013. Information on sex, age, Helicobacter pylori infection, PPIs intake, and the pathological results of the polyps were collected in the FGPs group and in the control group. The use of PPIs, sex, and H. pylori infection were statistically evaluated as dichotomous variables using a χ-test; age was evaluated as a continuous variable using a t-test. Finally, these factors were evaluated using a multiple logistic regression analysis. Gastric polyps were found in 759 (7.0%) patients, and 213 (2.0%) of these patients had FGPs. FGPs accounted for 28.1% of the gastric polyps. In the FGPs group, the percentage of H. pylori infection was 66.8% and the percentage of PPIs intake for at least 12 months was 23.1%. In the control group, the percentage of H. pylori infection was 77.4% and the percentage of PPIs intake for at least 12 months was 2.3%. The difference in the long-term use of PPIs was statistically significant between these two groups [χ=33.98, P<0.05, odds ratio (OR)=12.83, 95% confidence interval (CI): 4.47-36.80]. The results of the logistic regression were as follows: long-term use of PPIs (P<0.01, OR=14.11, 95% CI: 4.15-47.93); age (P<0.01, OR=1.69, 95% CI: 1.31-2.18). The P-values for sex and H. pylori infection were higher than 0.05. Age and the long-term use of PPIs were risk factors for the presence of FGPs; the long-term use of PPIs was a particularly strong risk factor.

W1083 The Development of Fundic Gland Polyps Associated With Chronic Proton Pump Inhibitor Therapy Involves in Increased Expression of Aquaporin 4

W1083 The Development of Fundic Gland Polyps Associated With Chronic Proton Pump Inhibitor Therapy Involves in Increased Expression of Aquaporin 4

Safety of the long-term use of proton pump inhibitors

The proton pump inhibitors (PPIs) as a class are remarkably safe and effective for persons with peptic ulcer disorders. Serious adverse events are extremely rare for PPIs, with case reports of interstitial nephritis with omeprazole, hepatitis with omeprazole and lansoprazole, and disputed visual disturbances with pantoprazole and omeprazole. PPI use is associated with the development of fundic gland polyps (FGP); stopping PPIs is associated with regression of FGP. In the absence of Helicobacter pylori infection, the long-term use of PPIs has not been convincingly proven to cause or be associated with the progression of pre-existing chronic gastritis or gastric atrophy or intestinal metaplasia. Mild/modest hypergastrinemia is a physiological response to the reduction in gastric acid secretion due to any cause. The long-term use of PPIs has not been convincingly proven to cause enterochromaffin-like cell hyperplasia or carcinoid tumors. PPIs increase the risk of community acquired pneumonia, but not of hospital acquired (nosocomial) pneumonia. There is no data to support particular care in prescribing PPI therapy due to concerns about risk of hip fracture with the long-term use of PPIs. Long-term use of PPIs does not lead to vitamin B12 deficiencies, except possibly in the elderly, or in persons with Zollinger-Ellison Syndrome who are on high doses of PPI for prolonged periods of time. There is no convincingly proven data that PPIs increase the risk of Clostridium difficile-associated diarrhea in persons in the community. The discontinuation of PPIs may result in rebound symptoms requiring further and even continuous PPI use for suppression of symptoms. As with all medications, the key is to use PPIs only when clearly indicated, and to reassess continued use so that long-term therapy is used judiciously. Thus, in summary, the PPIs are a safe class of medications to use long-term in persons in whom there is a clear need for the maintenance of extensive acid inhibition.

Chronic Proton Pump Inhibitor Therapy Associated with Increased Development of Fundic Gland Polyps

Fundic gland polyps (FGP) have been implicated with long-term proton pump inhibitor (PPI) use. We attempted to investigate the impact of length and dosage of PPI therapy on the development of FGP. A retrospective cohort study of all patients who had gastric polyps removed during elective upper endoscopy between March and September 2007 as part of a prior prospective study protocol was carried out. FGP were determined histologically. Prior to endoscopy, all patients completed a questionnaire regarding PPI use and length of therapy (no PPI use, 1-48 months, >48 months). The dosage of PPI was obtained via a thorough chart review of electronic medical records. Three hundred and eighty-five patients completed upper endoscopy and a questionnaire reporting PPI use (252 [65.4%] patients on PPI). On endoscopy, 55 patients had polyps, with the majority (43/55, 78%) being FGP, resulting in an overall prevalence of 11.1% (43/385). On univariate analysis, FGP were associated with Caucasian race (15 vs. 6%; P=0.009) and chronic PPI therapy (>48 months) (31.9 vs. 7.5%, P<0.001). There was a significant linear-by-linear association between PPI dosage and FGP prevalence (no PPI use, 7.5%; once daily, 10.8%; twice daily 17.4%, P=0.026). On logistic regression, the only independent predictor of FGP was duration of PPI use >48 months (P=0.001, odds ratio [OR] 4.7 [2.0-12.9]). The only independent predictor of FGP development in our study was duration of PPI therapy greater than 48 months. Increased dosage of therapy did not significantly impact the development of FGP.

Fundic gland polyps (retrospective analysis of two-year endoscopic records)

Background: Long-term use of proton-pump inhibitors (PPI) has a hypothetical role in the development of fundic gland polyps (FGP) what are the most common hyperplastic, non-dysplastic type of gastric polyps. Clinical importance of FGP remained controversial. Moreover the extensive use of PPIs in GERD and Barrett metaplasia indicate to pay more attention to this pathologic condition.

532 Incidence and Risk Factors for Development of Fundic Gland Polyps and Hyperplastic Polyps During Long-Term Proton Pump Inhibitor Therapy: A Prospective Multicenter Study in Japan

532 Incidence and Risk Factors for Development of Fundic Gland Polyps and Hyperplastic Polyps During Long-Term Proton Pump Inhibitor Therapy: A Prospective Multicenter Study in Japan

DEVELOPMENT OF SPORADIC GASTRIC FUNDIC GLAND POLYP AFTER ERADICATION OF HELICOBACTER PYLORI

The pathogenesis of sporadic gastric fundic gland polyps (FGP) without familial adenomatous polyposis remains unclear. However, development of FGP is associated with normal gastric mucosa without Helicobacter pylori infection. We report two cases of FGP newly developed after successful eradication therapy of H. pylori infection. H. pylori-associated gastric ulcers occurred in the two patients; H. pylori eradication was performed in the patients and was successful. The patients have not received medication of long-term proton pump inhibitors. Follow-up gastrointestinal endoscopy demonstrated a FGP in the fundus of the stomach of each patient after eradication therapy. Regression of sporadic FGP can be observed to coincide with the acquisition of H. pylori infection. Conversely, the present cases demonstrated that the curing of H. pylori infection could lead to the development of FGP.