Gastric Hyperplastic Polyps Research Articles

Gastric Xanthoma Associated with Gastric Cancer Development: An Updated Review.

Gastric xanthelasma (GX) is a rare tumor-like lesion customarily found as an incidental finding due to its asymptomatic appearance. Grossly, it is a well-marked yellow-white plaque created in the lamina propria by microscopic clusters of foamy macrophages. Xanthelasma is rarely correlated with gastric hyperplastic polyps; gastric xanthomas are rare benign lesions that appear to be associated with inflammation of the gastric mucosa. Etiopathogenesis is also unclear, but it has been suggested to be involved in chronic gastritis, infection with Helicobacter pylori (H. pylori), diabetes mellitus, and hyperlipidemia. The gastric xanthoma prevalence ranges from 0.23% to 7%. Orth first described the condition in 1887. It has been found that xanthelasmas are associated with chronic gastritis, gastrointestinal anastomosis, intestinal metaplasia, and H. pylori infection. These lesions predispose patients to gastric cancer conditions. Xanthoma (GX) was reported to be a predictive marker for early gastric cancer. However, the effectiveness of these scores and xanthoma (GX) as predictive markers for early gastric cancer detected after H. pylori eradication remains unknown.

Risk factors and clinical correlates of neoplastic transformation in gastric hyperplastic polyps in Chinese patients

Gastric hyperplastic polyps (GHPs) have a potential risk of neoplastic transformation, but the responsible mechanisms have not yet been established. We conducted a study involving 55 patients (33 female) who had undergone endoscopic or surgical resection of GHPs. We compared 16 patients who had GHPs showing neoplastic transformation with 39 patients who had non-neoplastic GHPs. We analyzed differences in serology, gastroscopic manifestations and pathology between the two groups in order to establish risk factors that may be associated with neoplastic transformation. The mean age of the cohort was 61.73 ± 9.024 years. The prevalence of positive serum gastric parietal cell antibody (PCA) was 61.8%. 30 of the GHPs with neoplastic formation had a “strawberry-like” appearance with erosions of polyps (P = 0.000). A history of anaemia was a risk factor for GHPs which demonstrated neoplastic transformation (odds ratio [OR], 3.729; 95% confidence interval [CI], 1.099–12.649; P = 0.035). Although the differences were not significant, our data showed higher prevalences of positive serum PCA (P = 0.057), hypergastrinemia (P = 0.062) and female gender (P = 0.146) in the GHP patients who had neoplastic transformation. Multiple polyps in the corpus (P = 0.024) occurred more frequently in serum PCA positive patients. Hypergastrinemia occurred more frequently in Helicobacter pylori negative patients and of these 20/22 patients had a positive PCA (P = 0.007). GHPs are associated with autoimmune metaplastic atrophic gastritis (AMAG). AMAG is probably one of the risk factors for GHPs to undergo neoplastic transformation.

Associations between gastric histopathology and the occurrence of colonic polyps.

Compromise of the gastric acid barrier may facilitate bacterial invasion of the lower intestinal tract and promote the development of colonic neoplasia. Our study aimed to test the associations between histopathological abnormalities of the upper and lower gastrointestinal tract in patients undergoing bidirectional endoscopy. The Inform Diagnostics database is a national electronic repository of histopathological records of patients distributed throughout the USA. A case-control study of 302061 patients, 163168 of whom had colonic polyps, evaluated whether the occurrence of colonic polyps was influenced by the presence of the following gastro-oesophageal diagnoses: gastric Helicobacter pylori infection, gastric intestinal metaplasia, fundic gland polyps and gastric hyperplastic polyps. The influence of individual diagnoses on the occurrence of colonic polyps was expressed as odds ratios with their 95% confidence intervals. The odds ratio for tubular adenomas being associated with gastric H.pylori was 1.53 (1.49-1.58), with intestinal metaplasia 1.65 (1.59-1.71), with fundic gland polyps 1.49 (1.45-1.54) and with gastric hyperplastic polyps 1.85 (1.75-1.96). The odds ratio for sessile serrated polyps being associated with gastric H.pylori was 1.03 (0.96-1.10), with intestinal metaplasia 1.21 (1.13-1.30), with fundic gland polyps 1.79 (1.69-1.89) and with gastric hyperplastic polyps 1.52 (1.35-1.71. A diminished gastric acid barrier function, which occurs in various upper gastrointestinal diseases associated with lowered gastric acid output, may promote the development of colonic neoplasia.

Helicobacter pylori Eradication Regressed Gastric Hyperplastic Polyp: A Randomized Controlled Trial.

Helicobacter pylori infection and hyperplastic polyp are known to have strong connections, but there are not enough randomized controlled trial data. To evaluate the effect of H. pylori eradication on gastric hyperplastic polyp. This is an open-labeled, single-center, randomized controlled trial. Patients with hyperplastic polyp and current infection of H. pylori were randomly assigned to eradication or non-eradication groups. All participants underwent follow-up endoscopy to investigate the regression of gastric polyps. Gastric polyp regression was defined as the disappearance of polyps or a reduction of more than 50% in size. Thirty-two patients were randomized to eradication (n = 17) and non-eradication groups (n = 15). Final included patients were 14 in eradication group and 13 in non-eradication group. All patients showed polyp regression in eradication group, whereas no regression was observed in non-eradication group (P < 0.001). Disappearance of polyp (n = 7) and decrease in size (n = 7) were observed in eradication group. In non-eradication group, no change (n = 5), increase of size (n = 5), and increase of number (n = 3) were observed. Mean regression time was 6.8months, and disappearance time was 9.8months. In non-eradication group, hyperglycemia was noted in 50% of progression group but not noted in no change group (P = 0.057). H. pylori eradication induced regression of hyperplastic polyp, and persistent H. pylori infection was related to progression of gastric polyp. ClinicalTrials.gov ID: NCT03065868.

Concurrent Gastric Hyperplastic and Fundic Gland Polyps in a Patient Taking Proton-Pump Inhibitor

Concurrent Gastric Hyperplastic and Fundic Gland Polyps in a Patient Taking Proton-Pump Inhibitor

Change in Size of Gastric Hyperplastic Polyps after Helicobacter pylori Eradication: A Prospective Study

Background/Aims Helicobacter pylori (H. pylori) eradication is known to be effective for reducing the size of gastric hyperplastic polyps (HPPs). This study investigated the change in size of gastric HPPs after H. pylori eradication.Materials and Methods This was a prospective study that enrolled 25 H. pylori-positive patients diagnosed as having HPPs at Korea University Guro Hospital between July 2015 and July 2016. If the patient wanted to receive eradication therapy, medication was given. If the patients refused eradication, only clinical follow-up was performed. All patients were subsequently followed up with endoscopic examination to determine any change in polyp size. Results Eighteen of the 25 H. pylori-positive patients diagnosed as having HPPs were given an eradication regimen, and 17 were confirmed to have achieved successful eradication. Twelve (70.8%) of the 17 patients in the eradication group showed ≥50% reduction in size, while two (25.0%) of the eight patients in the non-eradication group showed 50% reduction. The polyp regression rate was significantly higher in the eradication group (P=0.03). A multivariate analysis revealed that H. pylori eradication (OR, 40.047; 95% CI, 1.112~1442.767; P=0.044) and female sex (OR, 12.947; 95% CI, 1.038~161.503; P=0.047) were significant predictive factors of HPP regression. Conclusions H. pylori eradication is an effective therapeutic modality for gastric HPP regression. Key words: Helicobacter pylori; Polyps; Stomach neoplasms

P095 The Very Interesting Small Bowel Lesions of Cronkhite-Canada Syndrome

BACKGROUND: Cronkhite-Canada syndrome (CCS) is a non-hereditary disease characterized by the presence of gastrointestinal polyposis and skin symptoms such as hair loss, nail plate atrophy, and skin pigmentation. Approximately 50% of cases of CCS also have small bowel lesions. However, there have been few image reports of the small intestine lesions. METHODS: We examined the findings of small intestine capsule endoscopy (CE) in 3 cases of CCS in our hospital. RESULTS: Case 1 was of a 64-year-old male whose chief complaint was diarrhea, abnormal taste, and weight loss. He had diarrhea for 2 months and aware of finger pigmentation and nail atrophy. Esophagogastroduodenoscopy (EGD) revealed a collection of reddish polyps that expanded in the stomach and duodenum, and colonoscopy (CS) revealed glossy reddish bumps in the colon. CE showed diffuse reddish, edematous mucosa and villi enlargement in the entire small bowel. From these characteristic endoscopic and skin findings, he was diagnosed with CCS and was started on prednisolone (PSL) treatment. The treatment response was good, and there was no relapse. Case 2 was of a 65-year old female whose chief complaint was skin pigmentation. She had been aware of pigmentation on her back, palms, and upper arms, and loss of fingernails for the last 6 years with repeated disappearances and exacerbations. Furthermore, erosive gastritis and gastric hyperplastic polyps had been detected 4 years ago, and she was followed-up for these symptoms. Gradually, she became aware of nausea and loose stools, which prompted her to visit our hospital. EGD and CS revealed multiple reddish polyps predominantly in the gastric antrum, villous atrophy and reddish polyps in the terminal ileum, and scattered reddish polyps in the entire colon. Mucosal biopsies revealed glandular dilation, mucosal edema, and inflammatory cell infiltration. CE showed diffuse mulberry ridges and villi atrophy throughout the small bowel. She was diagnosed with CCS based on characteristic clinical and endoscopic findings, and was started on steroid treatment. There was no relapse. Case 3 was of a 75-year old male whose chief complaint was diarrhea and hair loss. EGD and CS revealed multiple polyps in the stomach, duodenum, and colon. CE showed reddish edematous mucosa and villi mixed with atrophy and swelling in the small bowel. Of note were that these findings were found in the jejunum. He was diagnosed with CCS and started on PSL and immunomodulator. Four years later, the characteristic findings disappeared in the CE. CONCLUSION(S): All patients had lesions in the entire small bowel, but there they were not associated with clinical findings or steroid response. The mucosa of the small intestine were more likely to have various findings as the period from onset to diagnosis became longer.

Upper Gastrointestinal Disease Influences the Occurrence of Inflammatory Bowel Disease.

Compromise of the gastric acid barrier may facilitate bacterial invasion of the lower intestinal tract and influence the occurrence of inflammatory bowel disease (IBD). Our study tested the associations between histopathologic changes in the upper and lower gastrointestinal tract in patients undergoing bidirectional endoscopy. The Inform Diagnostics database is a national electronic repository of histopathologic records of patients distributed throughout the entire USA. A case-control study among 302,061 patients, of whom 13,943 harbored IBD, evaluated whether the occurrence of Crohn's disease or ulcerative colitis was influenced by the presence of various upper gastrointestinal diagnoses associated with lowered gastric acid output. The influence of individual risk factors on the occurrence of colonic disease was expressed as odds ratios with their 95% confidence intervals. The odds ratio for Crohn's disease being associated with gastric H. pylori was 0.30 (0.24-0.37), with intestinal metaplasia 0.30 (0.24-0.39), with fundic gland polyps 0.42 (0.35-0.50), with gastric hyperplastic polyps 0.35 (0.23-0.51), with Barrett's metaplasia 0.19 (0.14-0.24), and with reflux esophagitis 0.46 (0.42-0.51). The odds ratio for ulcerative colitis being associated with gastric H. pylori was 0.58 (0.50-0.67), with intestinal metaplasia 0.39 (0.32-0.47), with fundic gland polyps 0.61 (0.53-0.71), with gastric hyperplastic polyps 0.64 (0.49-0.84), with Barrett's metaplasia 0.50 (0.43-0.59), and with reflux esophagitis 0.77 (0.71-0.84). A diminished gastric acid barrier function, as evidenced by various upper gastrointestinal diseases associated with lowered gastric acid output, may exert a protective influence against the development of inflammatory bowel disease.

1954 Hyperplastic Polyp: A Rare Case of Recurrent Iron Deficiency Anemia

INTRODUCTION: Hyperplastic polyps are the most common polyps accounting for 17% of all the gastric polyps. Most polyps are asymptomatic but may present with anemia, bleeding or gastric outlet obstruction. Here, we are reporting a case of large benign hyperplastic polyp presenting with iron deficiency anemia. CASE DESCRIPTION/METHODS: A 69-year-old male with a history of chronic back and neck pain and GERD was evaluated for chronic iron-deficiency anemia, treated multiple times with oral and IV iron supplements. The patient had been taking NSAIDs for chronic pain. On labs, patient hemoglobin of 9 with a low iron profile. The patient was scheduled for screening colonoscopy and EGD to further investigate anemia. On EGD patient had a large polypoid lesion about 25 mm in size in the prepyloric antrum extending into the duodenal bulb, likely cause of iron-deficiency anemia. There was also a small superficial clean-based ulcer on the antral lesion. Colonoscopy showed small internal hemorrhoids. Patient was discharged home on PPI and counseled to stop NSAIDs. Pathology report of the biopsies showed fragments of a benign hyperplastic polyp, negative for H pylori. The patient was afterward referred to interventional endoscopist for EUS and polyp excision. DISCUSSION: A hyperplastic gastric polyp is usually an incidental finding on upper endoscopy. With a prevalence of 6.35%, they are seen equally in elderly males and females in their 60s–70s. Hyperplastic polyps are believed to occur as a result of the reactive and inflammatory hyperproliferation of gastric foveolar cells, and Helicobacter pylori are believed to be the precursor. Diagnosis is usually made based on the results of endoscopy and subsequent biopsy of the suspicious area for the histological exam. On endoscopy, they appear as an area of hyperemia with a smooth dome-shaped surface, mostly in the antral area. As the size increases, they become pedunculated and the surface gets eroded resulting in chronic blood loss and anemia. Rarely, gastric outlet obstruction occurs when the large polyps prolapse though the pylorus. Since large polyps (&gt;2 cm) are associated with carcinoma in 0.6%–2% cases, it is important for the pathologist to look carefully for any dysplastic foci and carcinomatous changes in the tissue specimen. Once the diagnosis of hyperplastic polyp is confirmed, treatment consists of endoscopic resection of any polyp measuring &gt;1 cm in size and eradication of H.pylori, when present.

2695 Pedunculated Polyp at the Pyloric Channel Causing Intermittent Gastric Outlet Obstruction

INTRODUCTION: Gastric outlet obstruction (GOO) is the intrinsic or extrinsic obstruction of the pyloric channel or duodenum. The most common cause remains to be peptic ulcer disease which results in inflammation, edema or fibrosis. GOO typically presents with epigastric abdominal pain and postprandial vomiting. While the incidence of GOO is unclear, it has declined since the identification of Helicobacter pylori, H2-receptor antagonists and endoscopic therapy. We present a case of a benign polyp obstructing the pyloric channel. CASE DESCRIPTION/METHODS: 39 year-old female with a history of pulmonary embolism on Eliquis, Diabetes mellitus type 2 who presents for several months of epigastric pain, nausea and intractable vomiting. Prior to arrival, she had endoscopic evaluation at an outside hospital showing evidence of 1.5 cm gastric polyp in the pyloric channel. At the time, the polyp was not excised due to the patient being on anticoagulation. On admission, she underwent CT angiography showing no evidence of clot. She subsequently underwent repeat endoscopic evaluation demonstrating a 15 mm non-bleeding, pedunculated polyp at the pyloric channel obstructing the pyloric opening. The polyp was resected with hot snare. Biopsy showed a hyperplastic gastric polyp negative for malignancy. To prevent bleeding post-intervention, two hemostatic clips were placed. The patients abdominal pain, nausea and vomiting nearly resolved one day after her procedure. DISCUSSION: While the incidence of GOO has declined, it should continue to be considered in patient’s presenting with recurrent epigastric abdominal pain. Recent reviews estimate that, contrary to earlier years, 50 to 80% of cases have been attributable to malignancy such as pancreatic adenocarcinoma and distal gastric cancer. CT scan may show gastric distension or retained material within the gastric lumen. However, identifying the obstruction with upper endoscopy establishes the diagnosis. Treatment should be aimed at the underlying cause.

2144 Gastric Hyperplastic Polyps Are Resistant to Treatment by Endoscopic Submucosal Dissection

INTRODUCTION: Hyperplastic gastric polyps represent a subset of gastric polyps that are known to have malignant potential, with 5-19% harboring focal dysplastic changes, suggesting there would be a benefit to resection. Size &gt; 1.0 cm and pedunculated morphology have been shown as clear risk factors for malignant transformation. Current ASGE recommendations state that any hyperplastic polyp &gt; 0.5 cm be resected. Despite these recommendations, it is unclear how successful current endoscopic techniques are in the long-term management of these polyps. In this study, we sought to better understand if endoscopic submucosal dissection (ESD) would be successful in sustained removal of hyperplastic polyps. CASE DESCRIPTION/METHODS: We conducted a retrospective review of all patients between 2013 and 2019 who underwent ESD at our institution. Those who underwent ESD for treatment of hyperplastic polyps were included. Both the endoscopy reports and pathology reports were analyzed for ESD procedures looking at documented complications, polyp size, and enbloc removal. DISCUSSION: In total, 188 underwent ESD during the time frame studied, and 9 patients met inclusion criteria. In total, 12 ESD procedures were found. On average, each patient underwent 1.6 endoscopies prior to ESD, and 4.9 total for treatment of hyperplastic polyps. When removed by ESD, the average polyp size was 37 mm (range: 15 – 80 mm), and 63.6% were able to be removed enbloc. All polyps were located in the antrum. During ESD, there was intra-procedure bleeding during 83.3% of cases. This was controlled with clips, APC, and overstitching. No patients required hospitalization or emergent surgery. Of the 12 ESD procedures documenting successful polypectomy, 8 had follow up endoscopies within 12 months, with 100% recurrence of hyperplastic polyps. The remaining 4 are awaiting or lost to follow-up. Hyperplastic polyps involving the gastric antrum need removal due to cancer risk and often blood loss. Those resistant to standard resection can be effectively removed by ESD. Although ESD safely and successfully removed polyps, our patient population with follow up suffered a 100% recurrence rate of polyps despite good margins. Thus ESD, while safe, is not successful preventing recurrence. The pathological basis for this recurrence is unclear. We conclude that large gastric polyps recur almost always even after successful removal of by ESD.

3141 Large Gastric Hyperplastic Polyp as a Rare Cause of Iron Deficiency Anemia

INTRODUCTION: Gastric polyps are encountered in approximately 6% of endoscopic procedures. Most of the patients are asymptomatic, some of them can present with complications. We present a rare case of a large hyperplastic polyp resulting in iron deficiency anemia. CASE DESCRIPTION/METHODS: A 57 year-old man with past medical history of diabetes mellitus came in with complaints of 1 week history of dizziness, dyspnea on exertion and fatigue. Associated symptoms included persistent nausea and few episodes of non-bilious, non-bloody emesis. Patient denied melena or hematochezia. He endorsed weight loss of 8 lbs in 4 months. Vitals were grossly stable. Labs significant for Hb 6.7, Hct 23.8, and MCV 62. Patient was subsequently transfused with blood. Iron panel revealed severe iron deficiency with serum Iron 10, TIBC 443, Ferritin 4.6, Transferrin saturation 10. Colonoscopy was unremarkable however EGD revealed a large ulcerated polypoid mass, measuring about 10 to 15 cm in antrum concerning for early carcinoma. Pathology returned positive for hyperplastic polyp with no signs of dysplasia. Based on the large size of polyp, partial gastrectomy was done. On follow up, Hb increased and pt reported clinical improvement. DISCUSSION: Hyperplastic polyps constitute 75% of all the gastric polyps encountered. Hyperplastic polyps result from hyperplasia of epithelium secondary to chronic gastritis. Usually they range from 0.5 to 2 cm. About 1.4% of these polyps can reach a size large enough to cause iron deficiency anemia secondary to chronic bleeding. The risk of malignancy increases with size &gt;1 cm and require surgical resection. Yun et al reported a rare case of 1.5 cm hyperplastic polyp which was a cause of iron deficiency anemia. We describe a case of a large 10-15 cm hyperplastic polyp causing GI bleeding subsequently resulting in iron deficiency anemia. We recommend that physicians should be aware of this rare complication as polypectomy will benefit therapeutically in preventing future complications such as chronic bleeding.

Osseous Metaplasia: An Unusual and Poorly Understood Finding in Gastric Polyps

Abstract Osseous metaplasia (OM) is an uncommon finding in gastrointestinal tract biopsies. Metaplastic bone formation has been predominantly reported in the lower GI tract in a background of benign and malignant neoplasms, as well as nonneoplastic inflammatory conditions. OM in the stomach is extremely rare, with less than 10 cases reported in the English literature to date. We present two cases of gastric OM encountered at one institution among more than 10,000 stomach polyps examined since 1994. The first is a 46-year-old female with spastic quadriplegia, peptic ulcer disease, and a jejunal feeding tube who had multiple gastric hyperplastic polyps removed over a 13-year period. The most recent polypectomy revealed a 3-cm gastric adenoma with benign bone formation in the stroma. The second case is of a 67-year-old asymptomatic male with a remote history of intestinal metaplasia and atrophy of the stomach who underwent upper endoscopy and removal of a 1-cm polyp. Sections consisted of hyperplastic foveolar epithelium with focal ossification. Both polyps showed acute and chronic inflammation and stromal fibrosis, and they lacked Helicobacter infection. Mechanisms driving gastrointestinal OM have been proposed since the first reported cases in the early 1900s. The most widely accepted theory is that osteogenic factors released by the neoplastic or inflammatory tissue induce undifferentiated stromal mesenchymal cells or fibroblasts to undergo transformation to osteoblasts. However, with gastrointestinal biopsies being one of the most common specimens, the picture remains incomplete as only very rare cases show bone formation, warranting further research. Although gastrointestinal OM appears to be clinically insignificant, long-term studies have yet to be performed. Nevertheless, it is crucial for pathologists to be aware of this phenomenon in order to avoid misdiagnosing OM as a primary mesenchymal neoplasm or bone invasion in cases of OM arising in the background of malignancy.

Analysis of serum gastric function and Helicobacter pylori infection in patients with gastric hyperplastic polyps and gastric fundic gland polyps

Objective To analyze the serum gastric function and Helicobacter pylori (HP) infection in patients with gastric hyperplastic polyps and gastric fundic gland polyps. Methods From December 2017 to December 2018, 135 patients with gastric polyps and pathologically confirmed gastric hyperplastic polyps and gastric fundic gland polyps were enrolled in the hospital of Xuzhou Medical University.Among them, 68 patients with hyperplastic polyps, 67 cases of the gastric fundic gland polyps.Serum Hp antibodies (UreA, UreB, VacA, CagA antibodies) were qualitatively detected by immunoblotting.Eighty patients with chronic superficial gastritis were selected as the control group.Three groups of serum pepsinogen-I (PG-I), pepsinogen-Ⅱ (PG-Ⅱ), gastrin were detected by enzyme-linked immunosorbent assay (ELISA). Gastrin-17(G-17) and calculate PGⅠ and PGⅡ ratio(PGR). Results The levels of serum PGⅡ (13.13(8.15, 20.30) μg /L) and G17 (8.44(3.72, 27.17) pmol/L) in the gastric hyperplastic polyp group were higher than those in the control group (9.16(5.56, 15.14) μg/L and 1.83(0.87, 5.95) pmol/L) (P<0.05), and the PGR level was lower than the control group (P<0.05); serum PGI (120.12(86.72, 174.70) μg/L), PGII (11.92(7.27, 22.26) μg/L), G17 (5.68(1.79, 14.65) pmol/L) in the gastric fundic gland polyp group was higher than the control group ((101.32(79.17, 131.33) μg /L, 9.16(5.56, 15.14) μg /L, 1.83(0.87, 5.95) pmol/L)(P均<0.05)) (P<0.05); serum G17 (8.44(3.72, 27.17) pmol/L) level in gastric hyperplastic polyp group was higher than gastric fundus polyp group (5.68(1.79, 14.65) pmol/L) (P<0.05); Hp infection rate in gastric hyperplastic polyp group61.76%(42/68)was higher than that in the gastric fundic gland polyp group40.30%(27/67) (P<0.05), and type I Hp was the main one (P<0.05). The serum PGⅡ and G17 levels in the gastric hyperplastic polyp group were higher than those of Hp negative (all P<0.05). There were no significant differences in serum PGI, PGⅡ, G17, and PGR levels between the HP-positive and negative-positive patients in the gastric fundus polyp group.The serum PGI and PGR levels in the hypertrophic polyp group were higher than those in the HPⅡ type (all P<0.05). There was no significant difference in the levels of serum PGⅠ, PGⅡ, G17, and PGR between the gastric fundic gland polyps group and the type Ⅱ. Conclusion Serum PG and G17 levels in patients with gastric hypertrophic polyps and gastric fundic gland polyps are higher than those in patients with chronic superficial gastritis.Patients with gastric hyperplastic polyps have higher HP infection rate and abnormal gastric function than gastric fundic gland polyps. Key words: Gastric hyperplastic polyp; Gastric fundus polyp; Helicobacter pylori; pepsinogen; Gastrin

Comparative genome-wide analysis of gastric adenocarcinomas with hyperplastic polyp components.

Gastric hyperplastic polyps are common and generally regarded as benign lesions, whereas gastric adenocarcinomas infrequently occur from gastric hyperplastic polyps. Although gastric hyperplastic polyps have received a lot of attention because of their association with malignant transformation, it remains unclear whether gastric hyperplastic polyps are neoplastic lesions that have sporadic genetic changes similar to colorectal hyperplastic polyps. We performed genome-wide analyses of two gastric adenocarcinomas with hyperplastic polyp components. The interface between "adenocarcinoma" and "hyperplastic polyp" components was fairly sharp, and the adenocarcinoma components had copy number alterations and TP53 mutations, whereas the hyperplastic polyp components had only single nucleotide polymorphisms, which were also found in adenocarcinoma components. We did not detect any somatic changes in the hyperplastic polyp components, even in genome-wide analyses, which was in contrast to the adenocarcinoma components. However, due to the small number of cases examined herein, further genetic analyses of more cases are needed.

Magnified Endoscopic Findings of Multiple White Flat Lesions: A New Subtype of Gastric Hyperplastic Polyps in the Stomach

Background/Aims:While the occurrence of multiple whitish flat elevated lesions (MWFL) was first reported in 2007, no studies on MWFL have been published to date. The present retrospective observational study aimed to clarify the endoscopic findings and clinicopathological features of MWFL. Methods:Subjects were consecutive patients who underwent upper gastrointestinal endoscopy as part of routine screening between April 2014 and March 2015. The conventional white-light, non-magnifying and magnifying narrow-band images were reviewed. Clinical features were compared between patients with and without MWFL. Results:The conventional endoscopic findings of MWFL include multiple whitish, flat, and slightly elevated lesions of various sizes, mainly located in the gastric body and fundus. Narrow-band imaging enhanced the contrast of MWFL and background mucosa, and magnifying narrow-band imaging depicted a uniformly long, narrow, and elliptical marginal crypt epithelium with an unclear microvascular pattern. Histopathological findings revealed hyperplastic changes of the foveolar epithelium, and parietal cell protrusions and oxyntic gland dilatations were observed in the fundic glands, without any intestinal metaplasia. The rate of acid-reducing drug use was significantly higher in patients with MWFL than in those without (100% [13/13] vs. 53.7% [88/164], p<0.001). Conclusions:The present study indicated a relationship between the presence and endoscopic features of MWFL and history of acidreducing drug use.

Hyperplastic polyps arising in autoimmune metaplastic atrophic gastritis patients: is this a distinct clinicopathological entity?

Objectives: Gastric hyperplastic polyp (GHP) commonly arises in the abnormal surrounding mucosa, including autoimmune metaplastic atrophic gastritis (AMAG). We aimed to compare clinicopathological features in patients with GHPs associated with AMAG with those in patients with GHPs associated with non-AMAG.Patients and methods: A total of 1170 patients with GHP(s) were enrolled, and their clinical and pathological data were analyzed, retrospectively.Results: The GHP patients were divided into 181 A-GHP (type A GHP, AMAG-associated GHP) participants, 312 B-GHP (type B GHP, Helicobacter pylori infection-associated GHP) participants, and 677 other GHP participants (non-A-GHP and non-B-GHP) based on pathological status of the surrounding non-polypoid mucosa. The A-GHP patients were older and predominantly female (p < .05). Gastroscopically, A-GHPs showed less distal and more multiple-region distribution in the stomach (p < .001). In addition, the A-GHPs were observed to be usually numerous (55.8%), larger (mean maximum diameter 12.3 mm), and more pedunculated or sub-pedunculated (45.3%) (p < .001). Histopathologically, the intestinal metaplasia, intraepithelial neoplasia, and carcinomatous transformation within GHPs were present in 24.3%, 9.9%, and 2.8% of AMAG patients, respectively, which were significantly higher than those in the B-GHPs and other GHPs (p < .05). However, the differences of intraepithelial neoplasia and adenocarcinoma in surrounding non-polypoid mucosa did not reach statistical significance (p > .05).Conclusions: The GHP(s) arising in AMAG patients is a distinct subgroup of GHP(s) and was an important precancerous lesion. The biopsy from surrounding non-polypoid mucosa was essential to evaluate the underlying etiology of the GHPs, and endoscopists should pay attention to these.

Gastric inverted hyperplastic polyp with inflammatory myofibroblastic tumor-like stroma, mimicking GI stromal tumor

A 46-year-old asymptomatic man with no pertinent medical history underwent routine screening EGD, which showed a 2-cm submucosal tumor with central ulceration in the anterior wall of the gastric high body (A). EUS revealed a heterogenous (hypoechoic-hyperechoic) submucosal mass (B). CT of the stomach revealed a solid enhancing mass (C). Because malignant GI stromal tumor could not be completely ruled out, wedge resection of the stomach was performed. On microscopy, the 3.3-cm mass comprised hyperplastic mucosal components growing downward into the submucosa. Focal stroma showed spindle cell proliferations with vimentin and SMA (+), c-kit, CD34, DOG-1, S100, and ALK (−), and Ki-67 index, 2%. The final diagnosis was gastric inverted hyperplastic polyp with inflammatory myofibroblastic tumor (IMT)-like stroma (D). When fluorescence in-situ hybridization for ETV6, RET, and ROS1 were used, gene rearrangements were not observed in the IMT-like stroma. No recurrence was observed during 10 months of follow-up.

Sedated gastroscopy improves detection of gastric polyps.

The detection rate of gastric polyps (GPs) is low, improving the detection rate would be good. The present study aimed to evaluate the role of sedated gastroscopy in GP detection. The data of patients who underwent gastroscopic examination from January 2014 to December 2016 at the First Affiliated Hospital of Wenzhou Medical University (Wenzhou, China) were retrospectively reviewed. Endoscopic records of 6,195 patients diagnosed with GPs were analyzed. The GP detection rate was 3.12 and 5.11% in the unsedated and sedated gastroscopy group, respectively (P<0.05). Also after stratification by sex, the GP detection rate was significantly higher in the sedated gastroscopy group (P<0.05). In addition, patients aged ≥20 years in the sedated gastroscopy group had a higher GP detection rate than those in the unsedated gastroscopy group (P<0.05). The incidence of cardiac, gastric fundus, gastric body and multiple-site GPs was significantly different between the two groups (P<0.05). GPs ≤0.5 and >0.5 cm were more common in the sedated gastroscopy group than in the unsedated gastroscopy group (P<0.05). The common pathologic types of GPs were gastric fundus gland (52.27%) and hyperplastic polyps (34.74%). In conclusion, the GP detection rate may be improved by inhibition of gastric muscle cramping with sedation.

Hyperplastic gastric polyp with foci of ossification.

Key Clinical MessageStromal ossification has been reported in relation with gastrointestinal (GI) cancers. Heterotopic ossification of benign gastric polyps with bone formation is rarely documented and sometimes associated with calcification. Thus, the presence of foci of metaplastic bone (FMB) does not always imply GI cancer.