Gastroduodenal intussusception is an invagination of a portion of the stomach into the duodenum. It predominately occurs in adults. Case Report: We present a gastroduodenal intussusception in an hypochromic microcytic anemic 2-year-old girl. A large filling defect in the second and third parts of the duodenum, indenting the pyloric antrum, was due to a gastroduodenal intussusception secondary to a cauliflower-like gastric mucosal prolapse polyp, a type of gastric hyperplastic polyp. Conclusion: Anemia may accompany a gastric mucosal prolapse polyp.

In order to improve the efficiency of gastric cancer pathological slice image recognition and segmentation of cancerous regions, this paper proposes an automatic gastric cancer segmentation model based on Deeplab v3+ neural network.

Based on 1240 gastric cancer pathological slice images, this paper proposes a multi-scale input Deeplab v3+ network, _and compares it with SegNet, ICNet in sensitivity, specificity, accuracy, and Dice coefficient.

The sensitivity of Deeplab v3+ is 91.45%, the specificity is 92.31%, the accuracy is 95.76%, and the Dice coefficient reaches 91.66%, which is more than 12% higher than the SegNet and Faster-RCNN models, and the parameter scale of the model is also greatly reduced.

Our automatic gastric cancer segmentation model based on Deeplab v3+ neural network has achieved better results in improving segmentation accuracy and saving computing resources. Deeplab v3+ is worthy of further promotion in the medical image analysis and diagnosis of gastric cancer.

Fundic gland polyps (FGPs) are the most common gastric polyps and have been regarded as benign lesions with little malignant potential, except in the setting of familial adenomatous polyposis. However, in recent years, the prevalence of FGPs has been increasing along with the widespread and frequent use of proton pump inhibitors (PPIs). To date, several cases of FGPs with dysplasia or carcinoma (FGPD/CAs) have been reported. In this review, we evaluated the clinical and endoscopic characteristics of sporadic FGPD/CAs. Majority of the patients with sporadic FGPD/CAs were middle-aged women receiving PPI therapy and without Helicobacter pylori (H. pylori) infection. Majority of the sporadic FGPD/ CAs occurred in the body of the stomach and were sessile and small with a mean size of 5.4 mm. The sporadic FGPs with carcinoma showed redness, irregular surface structure, depression, or erosion during white light observation and irregular microvessels on the lesion surface during magnifying narrow-band imaging. In addition, sporadic FGPs, even with dysplasia, are likely to progress to cancer slowly. Therefore, frequent endoscopy is not required for patients with sporadic FGPs. However, histopathological evaluation is necessary if endoscopic findings different from ordinary FGPs are observed, regardless of their size. In the future, the prevalence of FGPs is expected to further increase along with the widespread and frequent use of PPIs and decreasing infection rate of H. pylori. Currently, it is unclear whether FGPD/CAs will also increase in the same way as FGPs. However, the trends of these lesions warrant further attention in the future.

Diagnostic imaging of pediatric gastric masses often provides a challenge for the practicing radiologist. Radiologists should be aware of this relatively unusual pathology, particularly in cross-sectional imaging findings. We will review pediatric gastric masses and mass-like lesions, focusing on neoplastic and inflammatory etiologies.

We retrospectively studied the clinical and histologic features of pediatric fundic gland polyps (FGPs) in 16 patients. FGPs had an endoscopic prevalence of 0.25% in 8527 pediatric gastric biopsies. Five patients had familial adenomatous polyposis (FAP). The median age of onset was 17.7 years in FAP and 17.3 years in sporadic patients. All syndromic patients were asymptomatic and FGPs were identified during surveillance for existing or concurrent colon polyps. They did not take antacids. In comparison, all 11 sporadic FGPs were identified during evaluation of symptomatic patients who had taken antacids (median duration 21 months). Syndromic FGPs can be multiple at single endoscopy and were more likely to recur, while sporadic FGPs were often single. None of the sporadic patients had recurrence of FGPs or a subsequent diagnosis of FAP during a median follow-up of 20.5 months. The dilated fundic glands were lined by parietal and chief cells only in a majority (22/41, 53.7%) of syndromic FGPs, while additional tall mucinous lining cells were found in all sporadic FGPs. Syndromic FGPs did not have parietal cell hypertrophy in the background oxyntic mucosa. Nuclear immunopositivity for beta-catenin was essentially absent in all the FGPs. In conclusion, FGPs were rare in pediatric patients. In syndromic patients, FGPs are asymptomatic and did not precede colon polyps. Prolonged antacid intake seems to be associated with development of sporadic FGPs. Cellular components of dilated fundic glands and background parietal cell hypertrophy can be useful features to eliminate concern for syndromic polyposis.

There have been increasing numbers of case reports and observational studies of adverse events in patients receiving long-term therapy with proton pump inhibitors (PPIs). The effects of PPI therapy on risks of fundic gland polyps (FGPs) and gastric cancer have received considerable attention. We performed a systematic review with a meta-analysis of randomized controlled trials and observational studies that assessed these risks.

We searched the PUBMED, EMBASE, and Cochrane Central Register of Controlled Trials databases for relevant studies published through July 2015. We calculated pooled odds ratio for FGPs and the risk ratio for gastric cancer in PPI users compared with PPI nonusers using fixed- and random-effects models.

We analyzed data from 12 studies, comprising more than 87,324 patients: 1 randomized controlled trial reporting the effect of PPIs on gastric polyps (location not specified), 6 cohort and 1 case-control studies on FGPs, and 1 cohort and 3 case-control studies on gastric cancer. Pooled odds ratios for FGPs were 1.43 (95% confidence interval, 1.24-1.64) and 2.45 (95% confidence interval, 1.24-4.83) from fixed- and random-effects models, respectively. The pooled risk ratio for gastric cancer was 1.43 (95% confidence interval, 1.23-1.66) from each model. We observed significant heterogeneity among studies reporting on FGPs, but not among studies reporting on gastric cancer.

Based on a systematic review with meta-analysis, long-term use of PPIs (≥12 months) is associated with an increased risk of FGPs. PPI therapy might also increase the risk of gastric cancer, but this association could be biased, because of the limited number of studies and possible confounding factors.

Research in chemoprevention has undergone a shift in emphasis for pragmatic reasons from large, phase III randomized studies to earlier phase studies focused on safety, mechanisms, and utilization of surrogate endpoints such as biomarkers instead of cancer incidence. This transition permits trials to be conducted in smaller populations and at substantially reduced costs while still yielding valuable information. This article will summarize some of the current chemoprevention challenges and the justification for the use of animal models to facilitate identification and testing of chemopreventive agents as illustrated though four inherited cancer syndromes. Preclinical models of inherited cancer syndromes serve as prototypical systems in which chemopreventive agents can be developed for ultimate application to both the sporadic and inherited cancer settings.

Isolated polyps of the upper digestive tract are rarely diagnosed in children, being usually an incidental finding during endoscopic exploration.The diagnostic, therapy, and outcome of these lesions are based on endoscopy and pathology.In a 5-year period, clinical features, topography, size, pathology, therapeutics, and progression of esophagogastric polyps founded in children addressed to our pediatric gastroenterology unit were studied.The authors encountered 3 lesions in teenagers aged 13 to 17 years two males (2M), from a total number of 2140 upper digestive endoscopies (0.14%). All patients presented with pirosis, epigastric pain, and vomits; one of the children had end-stage renal disease and Kabuki syndrome. Endoscopic and pathologic findings were 2 esophageal polyps, an inflammatory one, and another containing goblet cells and a double-headed hyperplastic gastric polyp. Two patients received proton pump inhibitors without any improvement in subsequent endoscopic evaluations.The difficulties related to age group, underlying conditions, debatable response to acid suppression, and limited experience in pediatric therapeutic endoscopy selected significantly the effectiveness of treatment.The rarity of these lesions requires an individualized management, the endoscopic diagnostic, and therapeutic gesture depending on the symptoms, type, location, comorbidities, and team experience.

Although the majority of gastric carcinomas are sporadic, approximately 10% show familial aggregation, and a hereditary cause is determined in 1%-3% cases. Of these, hereditary diffuse gastric cancer is the most recognized predisposition syndrome. Although rare, the less commonly known syndromes also confer a markedly increased risk for development of gastric cancer. Identification and characterization of these syndromes require a multidisciplinary effort involving oncologists, surgeons, genetic counselors, biologists, and pathologists. This article reviews the molecular genetics, clinical and pathologic features, surveillance guidelines, and preventive measures of common and less common hereditary gastric cancer predisposition syndromes.

Gastric carcinoid tumors (GCT) are rare lesions that constitute 2.6-8.7% of all gastrointestinal carcinoids, mostly affect middle-aged females but the incidence in children is unknown. We present a 14-year-old girl, with GCT. She was treated with recombinant human growth hormone (GH) for complete GH deficiency, and endoscopy was performed to identify iron-deficiency anemia. Upper gastrointestinal endoscopy revealed a gastric polyp, and biopsies were compatible with GCT.

Understanding the natural history of Familial Adenomatous Polyposis (FAP) will guide screening and aid clinical management.

Patients with FAP, age ≤20years presenting between 1987 and 2011, were reviewed for presentation, diagnosis, extraintestinal manifestations, polyp burden, family history, histology, gene mutation, surgical intervention, and outcome.

One hundred sixty-three FAP patients were identified. Diagnosis was made by colonoscopy (69%) or genetic screening (25%) at mean age of 12.5years. Most children (58%) were asymptomatic and diagnosed via screening due to family history. Rectal bleeding was the most common (37%) symptom prompting evaluation. Colon polyps appeared by mean age of 13.4years with >50 polyps at the time of diagnosis in 60%. Cancer was found in 1 colonoscopy biopsy and 5 colectomy specimens. Family history of FAP was known in 85%. 53% had genetic testing, which confirmed APC mutation in 88%. Extraintestinal manifestations included congenital hypertrophy of the retinal pigment epithelium (11.3%), desmoids (10.6%), osteomas (6.7%), epidermal cysts (5.5%), extranumerary teeth (3.7%), papillary thyroid cancer (3.1%), and hepatoblastoma (2.5%). Six patients died secondary to FAP.

Clinical presentation and manifestations in pediatric FAP are variable. We suggest an individualized patient-oriented screening algorithm that allows for earlier screening and appropriate management.

Although the exact prevalence of proton pump inhibitor (PPI) use in cancer patients is not known, it is generally perceived to be widespread. PPIs are generally well tolerated and carry an excellent safety profile. However, increasing and longer term PPI use has raised concerns about the risk of pneumonia, bone fractures and enteric infections, and a possible interaction with clopidogrel that could increase the risk of cardiovascular events.

We conducted a PubMed search of English language articles addressing the safety and adverse events associated with PPI use with particular emphasis in cancer patients.

PPIs, frequently used in cancer patients, are generally well tolerated and carry an excellent safety profile. PPI-induced acid suppression may increase the risk of Clostridium difficile or other enteric infections, nutritional deficiencies and community acquired pneumonia, all particularly important in cancer patients. The indications for PPI use in cancer patients should be carefully reviewed prior to use.

We report two cases of a massive fundic gland polyposis associated with protracted proton pump inhibitor (PPI) therapy. Both patients were females aged 51. On repeated endoscopy, the number of fundic gland polyps was increasing steeply, and they resulted in a passage disorder. In the first case, the enormous number of polyps made endoscopic removal impossible, so the patient was treated by total gastrectomy. Although our case is the second one reported in the world, we would like to draw the attention to this rare complication of long lasting PPI therapy.

Proton pump inhibitors have an excellent safety profile and have become one of the most commonly prescribed class of drugs in primary and specialty care. Long-term, sometimes lifetime, use is becoming increasingly common, often without appropriate indications. This paper is a detailed review of the current evidence on this important topic, focusing on the potential adverse effects of long-term proton pump inhibitor use that have generated the greatest concern: B12 deficiency; iron deficiency; hypomagnesemia; increased susceptibility to pneumonia, enteric infections, and fractures; hypergastrinemia and cancer; drug interactions; and birth defects. We explain the pathophysiological mechanisms that may underlie each of these relationships, review the existing evidence, and discuss implications for clinical management. The benefits of proton pump inhibitor use outweigh its risks in most patients. Elderly, malnourished, immune-compromised, chronically ill, and osteoporotic patients theoretically could be at increased risk from long-term therapy.

Proton pump inhibitors (PPI) are very effective drugs used largely in acid related disorders. During the last years concern have been raised regarding their overutilisation in benign condition, such as gastroesophageal reflux disease. The debate focussed also on the risk of adverse events related to long term use of PPI. Apart of the case of Helicobacter Pylori (H. Pylori) positive patients, in whose long term acid suppression lead to the development of corpus predominant atrophic gastritis, precursor of cancer; the other assumed adverse events, have never been demonstrated in prospective studies. The attention should move towards the appropriate prescription of PPI, rather than the fear adverse effects of PPI. In fact, in clinical practise, PPI are often prescribed in patients without a specific acid related disease and continued long term based on their safety profile. This review focus on the main adverse events related to long term PPI use.

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.

Proton pump inhibitors (PPIs) are among the most widely prescribed medications worldwide. Their use has resulted in dramatic improvements in treatment of peptic ulcer disease and gastroesophageal reflux disease. Despite an acceptable safety profile, mounting data demonstrate concerns about the long-term use of PPIs. To provide a comprehensive review regarding the concerns of long-term PPI use, a literature search was performed to identify pertinent original and review articles. Despite study shortcomings, the collective body of information overwhelmingly suggests an increased risk of infectious complications and nutritional deficiencies. Data regarding any increased risk in gastric or colon malignancy are less convincing. PPIs have revolutionized the management and complications of acid-related disorders with a high margin of safety; however, with the data available, efforts to reduce the dosing of or discontinue the use of PPIs must be reassessed frequently.

To use a large pathology database (Caris Diagnostics) to analyze the frequency and associations of gastric polyps in a nationwide US population.

A total of 121,564 esophagogastroduodenoscopy (EGD) procedures from private practices in 36 states in the Caris Diagnostics database from 1 April 2007 to 31 March 2008 were searched for the endoscopic designations of polyp, nodule, and mass, and for the pathological diagnoses that commonly present as gastric polyps. Pertinent demographic data, clinical indications for EGD, and information regarding Helicobacter pylori infection, reactive gastropathy, chronic inactive gastritis, and intestinal metaplasia were also obtained.

A total of 78,909 of the 121,564 patients who underwent EGD had gastric biopsies. The prevalence of gastric polyps in the EGD population was 6.35%; 77% were fundic gland polyps, 17% hyperplastic polyps/polypoid foveolar hyperplasia, 0.69% adenomas, and 0.1% inflammatory fibroid polyps. Malignant neoplasms were slightly >2%. None of the benign gastric polyps had a significant positive association with concurrent H. pylori infection; intestinal metaplasia was detected in the background of 52.2% of carcinoids, 29.6% of adenomas, 20.1% of xanthomas, and 13% of adenocarcinomas and hyperplastic polyps. Adenomas were rarely associated with synchronous adenocarcinomas.

The relative prevalence of fundic gland polyps in this population was much higher than that reported earlier, most likely because of the widespread use of proton pump inhibitors. H. pylori- and atrophy-associated polyps, including adenomas, were less common than in earlier series.

Endoscopy in children has developed along with pediatric gastroenterology over the last four decades. Introduction of endoscopic techniques in adults precedes application in children, and pediatric endoscopists do fewer procedures than their adult counterparts whether routine or as an emergency. Training for pediatric endoscopists therefore needs to be thorough. This article in particular highlights developments in pediatric gastroenterology of importance to emergency procedures.

It is controversial whether proton pump inhibitor use leads to fundic gland polyp development.

To determine whether fundic gland polyp development is due to proton pump inhibitor use and to investigate mechanisms involved.

Proton pump inhibitor use and the presence of fundic gland polyps were assessed in consecutive patients undergoing oesophagogastroduodenoscopy. Biopsies from fundic gland polyps and gastric mucosa were taken. Dysplasia was graded as negative, low or high grade. Prevalence of parietal cell hyperplasia and parietal cell protrusions and the proportional cystic area were assessed.

599 patients participated, 322 used proton pump inhibitors, 107 had fundic gland polyps. Long-term proton pump inhibitor use was associated with an increased risk of fundic gland polyps (1-4.9 years use: OR 2.2, 95% CI: 1.3-3.8; > or =5 years: OR 3.8, 95% CI: 2.2-6.7) while short-term therapy (<1 year) was not (OR 1.0, 95% CI: 0.5-1.8). Low-grade dysplasia was found in one fundic gland polyp. Fundic gland polyps associated with long-term proton pump inhibitor use had a larger proportional cystic area and higher frequency of parietal cell hyperplasia and parietal cell protrusion.

Long-term proton pump inhibitor use is associated with an up to fourfold increase in the risk of fundic gland polyps. Risk of dysplasia is negligible. Aetiologically, these polyps seem to arise because of parietal cell hyperplasia and parietal cell protrusions resulting from acid suppression.

Capsule endoscopy is a revolutionary new diagnostic tool for the detection of small bowel disease. As the name implies, capsule endoscopy makes use of a swallowable video capsule; as such, it is the only technique that allows noninvasive endoscopic examination of the entire small bowel without sedation. Obscure gastrointestinal bleeding is the most common indication for capsule endoscopy, which commonly depicts arteriovenous malformations, small bowel tumors, and ulcers missed at standard endoscopy and imaging examinations. However, capsule endoscopy is not optimal for the localization of small bowel lesions. In addition, lesions can be missed due to poor bowel preparation, rapid or delayed small bowel transit, or orientation of the camera away from a lesion. Computed tomography and barium examinations are useful for detecting these missed lesions and for localizing lesions detected at capsule endoscopy. Other limitations of capsule endoscopy are the inability to treat lesions and its limited use in patients with small bowel strictures or obstruction. Nevertheless, this new technique is easy to perform, is well tolerated by patients, and, for the first time, allows noninvasive endoscopic evaluation of the entire small bowel.

Syndromic and sporadic fundic gland polyps are morphologically indistinguishable but may arise via different pathogenetic mechanisms involving mutations of the adenomatous polyposis coli (APC) and its downstream target beta-catenin genes. Although a higher frequency of dysplasia has been reported in syndromic forms, the risk of developing invasive carcinoma is exceedingly low. The current study was designed to investigate whether syndromic and sporadic fundic gland polyps differ in protein expression of a number of genes that are thought to be important in the control of neoplastic transformation. A total of 262 fundic gland polyps, including 155 syndromic polyps obtained from 35 patients with familial adenomatous polyposis or Gardner's syndrome and 107 sporadic polyps randomly selected from 45 patients with gastroesophageal reflux disease or Barrett's esophagus, were included in this study. Immunohistochemical evaluation showed that loss of immunoreactivity to the antibody against the carboxyl terminus of the APC protein, presumably resulting from APC gene mutations, was more frequent in syndromic than in sporadic cases (40% versus 6.7%, P<0.001). However, immunostaining failed to show aberrant nuclear localization of beta-catenin, a protein regulated by APC, in any of the polyps, irrespective of syndromic or sporadic types. Instead, positive membranous staining for beta-catenin was observed in all the cases. In addition, the expression characteristics of 2 other proteins, c-Myc and cyclin D1, whose genes have been reported to be transcriptionally regulated by the APC/beta-catenin pathway, were similar in these two types of polyps. Furthermore, all cases, including those harboring dysplasia, showed negative nuclear staining for p53 and positive nuclear staining for retinoblastoma (RB). Taken together, these data show a lack of dysregulation in the APC/beta-catenin signaling pathway and in the expression of p53 and RB in fundic gland polyps despite a high frequency of somatic mutations of the APC and beta-catenin genes reported in these polyps. These findings may explain at least in part why fundic gland polyps show a negligible malignant potential even in the presence of dysplasia.

Familial adenomatous polyposis (FAP) is a hereditary cancer syndrome that includes gastro-duodenal involvement, polyposis, and a propensity to adenocarcinoma necessitating endoscopic surveillance. There are few data describing pediatric upper gastrointestinal FAP resulting in conflicting screening recommendations.

To characterize pediatric gastroduodenal FAP and to investigate the association between symptoms at endoscopy and APC mutation analysis with endoscopic-histologic findings warranting surveillance.

A retrospective chart review was performed, including all children with FAP who underwent upper endoscopy (EGD) at two institutions; (UNMC: 1992-2002, JHH: 1983-2002), all biopsies were reviewed and the APC mutations present in the cohort of patients were correlated to the pattern of severity of endoscopic findings and the frequency of APC mutations identified through commercially available testing for FAP (Labcorp: 1998-2002).

Twenty-four patients from 21 families underwent 49 EGDs. Eighty-three percent were asymptomatic at the time of endoscopy. The most common finding was fundic gland polyposis (FGP) (51%), of which 42% and 15% harbored dysplasia and changes indefinite for dysplasia, respectively. Periampullary duodenal adenomata were present in 41% of patients with one patient necessitating ampullectomy. Symptoms at endoscopy were not predictive of premalignant changes. In 15 patients where the APC mutation was known patients with dysplastic FGP, gastric, or duodenal adenoma were more likely to harbor a mutation between codons 1225-1694 than the reference population (p= 0.006).

All pediatric patients with FAP warrant upper gastrointestinal screening and surveillance endoscopy from the time of initial colonoscopy irrespective of referable symptoms. Patients with APC mutation between codon 1225-1694 may be more susceptible to aggressive gastroduodenal involvement in FAP.

Inflammatory fibroid polyp (IFP) is a rare benign lesion that may occur throughout the digestive tract. IFP is more commonly found in the antrum of the stomach in particular. It mostly affects adults at the average age of 60 years. These polyps are able to cause abdominal pain, gastrointestinal bleeding, intestinal obstruction or intussusception. In this paper we report a case of gastric IFP with unusual presenting features.

A child with gastric IFP was described and the literature was reviewed.

A 4-year-old girl presented with fever for 2 months, arthralgia of knees and ankles, iron deficiency anemia, and hypoalbuminemia. Her stool examination was positive for occult blood. The upper gastrointestinal study demonstrated a large lobulated mass at the upper part of gastric body. Partial gastrectomy en bloc with this 5 cm x 8 cm mass was subsequently performed. Pathological examination was consistent with IFP. Following the mass excision, her fever abruptly declined and disappeared together with anemia and arthralgia. She remained asymptomatic and the abdominal ultrasonography performed at the 24-month follow-up demonstrated no recurrence of the tumor.

The etiopathogenesis of IFP still remains unclear. The presence of IFP throughout the gastrointestinal tract and its variable clinical appearances make it difficult to diagnose. The inflammatory symptoms found in this patient support the hypothesis of inflammatory benign lesions of IFP.

We present a case of fundic gland polyps (FGPs) containing high-grade dysplasia in a 68-year-old man. High-grade dysplasia, and even gastric adenocarcinoma, associated with FGPs have been described in patients with familial adenomatous polyposis (FAP) and attenuated familial adenomatous polyposis (AFAP) but never in non-FAP patients. Two colonoscopies in the past six years virtually rule out FAP and AFAP in our patient. Dysplasia in FGPs from non-FAP patients is extremely rare, and until now only cases of low-grade dysplasia have been described. The literature on dysplasia in FGPs is reviewed briefly. Additional immunohistochemical investigations in this case showed nuclear staining of beta-catenin, increased proliferation and apoptosis in the dysplastic areas of the FGPs. Our case suggests that the malignant potential of FGPs is not limited to FAP-associated FGPs.