Systematic review and meta-analysis: Artificial intelligence for the diagnosis of gastric precancerous lesions and Helicobacter pylori infection.

BACKGROUND: The endoscopic diagnosis of Helicobacter-pylori(H.pylori) infection and gastric precancerous lesions(GPL), namely atrophic-gastritis and intestinal-metaplasia, still remains challenging. Artificial intelligence(AI) may represent a powerful resource for the endoscopic recognition of these conditions. AIMS: To explore the diagnostic performance(DP) of AI in the diagnosis of GPL and H.pylori infection. METHODS: A systematic-review was performed by two independent authors up to September 2021. Inclusion criteria were studies focusing on the DP of AI-system in the diagnosis of GPL and H.pylori infection. The pooled accuracy of studies included was reported. RESULTS: Overall, 128 studies were found (PubMed-Embase-Cochrane Library) and four and nine studies were finally included regarding GPL and H.pylori infection, respectively. The pooled-accuracy(random effects model) was 90.3%(95%CI 84.3-94.9) and 79.6%(95%CI 66.7-90.0) with a significant heterogeneity[I2=90.4%(95%CI 78.5-95.7);I2=97.9%(97.2-98.6)] for GPL and H.pylori infection, respectively. The Begg's-test showed a significant publication-bias(p = 0.0371) only among studies regarding H.pylori infection. The pooled-accuracy(random-effects-model) was similar considering only studies using CNN-model for the diagnosis of H.pylori infection: 74.1%[(95%CI 51.6-91.3);I2=98.9%(95%CI 98.5-99.3)], Begg's-test(p = 0.1416) did not show publication-bias. CONCLUSION: AI-system seems to be a good resource for an easier diagnosis of GPL and H.pylori infection, showing a pooled-diagnostic-accuracy of 90% and 80%, respectively. However, considering the high heterogeneity, these promising data need an external validation by randomized control trials and prospective real-time studies.

Efficacy of Lactobacillus paracasei sub. paracasei F19 on abdominal symptoms in patients with symptomatic uncomplicated diverticular disease: a pilot study.

AIM: The standard therapeutic approach for symptomatic uncomplicated diverticular disease (DD) remains to be defined, and only a few studies have tested the efficacy of probiotics in these patients. METHODS: Patients with symptomatic uncomplicated DD were randomized to a control arm, i.e., (group A, [N.=16], high-fibre diet alone), or to Group B ([n=18], twice daily 1 sachet of probiotic + high-fibre diet), or group C ([N.=16], twice daily 2 sachets of probiotic + high-fibre diet). The probiotic Genefilus F19© containing Lactobacillus paracasei sub. paracasei F19 was administered for 14 days/month for 6 months. The primary endpoint under consideration was a decrease in abdominal pain and bloating intensity after treatment. RESULTS: Bloating decreased significantly in Groups B and C VAS score group B: 4.6 ± 2.6 vs. 2.3 ± 2.0, P<0.05, group C: 3.9 ± 2.9 vs. 1.8 ± 2.1, P<0.05). The decrease in abdominal pain within 24 hours in these groups did not reach statistical significance. During treatment, none of the group B (N.=4) or group C patients (N=3) with abdominal pain >24 hours reported the recurrence of this symptom, while the 3 group A patients reported at least one episode (P=0.016). No significant difference regarding abdominal pain <24 hours and bloating was observed between the two groups of patients treated with a low or high probiotic dose. CONCLUSION: Lactobacillus paracasei F19, in association with a high-fibre diet, is effective in reducing abdominal bloating and prolonged abdominal pain in symptomatic uncomplicated diverticular disease, and could thus be a promising option in the treatment of these patients.

Diagnostic Accuracy of EndoFaster® and Narrow-Band Imaging Endoscopy in Patients with Impaired Gastric Acid Secretion: A Real-Time Prospective Study.

BACKGROUND: EndoFaster® analyzes gastric juice in real time during gastroscopy allowing the detection of hypo-achlorhydric conditions, like corpus atrophic gastritis. Narrow-band imaging (NBI) endoscopy allows to accurately detect and perform target biopsies in areas of intestinal metaplasia, a histological change often associated to corpus atrophic gastritis. AIMS: To compare the diagnostic accuracy of EndoFaster® with histological evaluation for corpus atrophic gastritis through high-resolution (HR) NBI targeted biopsies. METHODS: Prospective study on consecutive adult patients undergoing gastroscopy between April and November 2018. Patients in therapy with proton pump inhibitors, previous gastric surgery, and/or known gastric neoplasia were excluded. At the beginning of gastroscopy, gastric juice was aspirated and analyzed by EndoFaster® in 15 seconds. Endoscopists were blinded to the report of EndoFaster®. Evaluation of gastric mucosa in HR-white light was firstly performed, then with HR-NBI allowing to perform targeted biopsies on areas suspected for intestinal metaplasia; otherwise, biopsies were performed according to the updated Sydney System protocol and sent for histopathological evaluation. RESULTS: Overall, 124 patients were included [64% F; 56 (18-85) years]. Corpus atrophic gastritis was present in 41.9% of patients. EndoFaster® showed an accuracy for corpus atrophic gastritis diagnosis, compared to histopathological evaluation as gold standard, of 87.1% and a sensitivity, specificity, PPV, and NPV of 78.8%, 93.1%, 89.1%, and 85.9%, respectively. pH showed a positive correlation with the severity score of atrophy (r = 0.67, 95% CI: 0.73-0.81, and p < 0.0001). EndoFaster® allowed to diagnose corpus atrophic gastritis in 3.7% of patients negative to NBI (corpus atrophic gastritis without intestinal metaplasia). CONCLUSION: EndoFaster® seems a promising tool to diagnose corpus atrophic gastritis. The evaluation of hypo-achlorhydria during gastroscopy can address bioptic sampling in corpus atrophic gastritis patients without intestinal metaplasia.

Upper and lower gastrointestinal causes of iron deficiency anemia in elderly compared with adult outpatients.

AIM: In the elderly, prevalence of bleeding- and/or iron malabsorption-related gastrointestinal (GI) causes of iron deficiency anemia (IDA) has not been addressed yet. The aim of this study was to assess the occurrence of malabsorptive diseases and bleeding lesions of the upper and lower GI tract in early (65-74 year-old) and late (over 75 year-old) elderly group compared with adult (50-64 year-old) outpatients. METHODS: The study enrolled 136 consecutive adult (N.=31), early (N.=48) and late elderly (N.=57) IDA outpatients who were referred to the Gastroenterology Department for IDA evaluation and underwent gastroscopy/histology and colonoscopy. RESULTS: Bleeding lesions were significantly less frequent in adult patients than in elderly patients (29% vs. 49.5%, P=0.0252). The most common bleeding lesions were large hiatal hernia (14.7%) and colon cancer (12.5%). Iron malabsorption diseases (Hp-related pangastritis, atrophic body gastritis and celiac disease) were more frequent in the adult group than in the early elderly group (80.6% vs. 56.2%, P=0.0367). In elderly patients, the observed prevalence of bleeding and iron malabsorption IDA causes was similar, whereas in adult patients iron malabsoptive diseases were more frequently detected (P<0.0001). The occurrence of concomitant IDA causes was not different among the three age-groups. CONCLUSION: In the early and late elderly, almost half of GI IDA causes are related to bleeding lesions which are more frequently observed respect to the adult patients. Iron malabsorption diseases affect almost 60% of early and late elderly groups. As for adult patients, an accurate upper and lower endoscopical/histological evaluation diagnoses IDA causes in the vast majority of the elderly outpatients.

Cameron lesions: A still overlooked diagnosis. Case report and systematic review of literature.

Cameron lesions are erosive-ulcerative alterations of gastric mucosa occurring in patients with large hiatal hernia, potentially causing gastrointestinal bleeding and iron deficiency anaemia. Diagnosis may be challenging, and not infrequently erosions are overlooked at endoscopy, so that repeated and unnecessary diagnostic procedures are performed, particularly in those patients with chronic anaemia. We described two peculiar cases of patients with iron deficiency anaemia in whom Cameron lesions were either overlooked or misinterpreted. By reviewing data of 22publications reporting endoscopic and clinical data of 140patients, we noted a large prevalence of females (75%). The most frequent presenting symptoms were anaemia (62%) and overt gastrointestinal bleeding (36%). Noteworthy, as many as 69% of patients underwent one or more previous upper endoscopy before diagnosis of Cameron lesion was achieved. Patients were mainly treated with proton pump inhibitor (PPI) therapy and iron supplementation. Moreover, endoscopic haemostasis was performed in 10% of case, blood transfusion was required in one third of cases, and a similar quote of patients underwent a surgical approach for hiatal hernia repair. The observation that as many as 60% patients were already receiving standard PPI therapy when diagnosis was performed would suggest that either long-term treatment with adequate dose PPI or surgical approach for hiatal hernia repair is required. In conclusion, Cameron lesion is still an overlooked diagnosis in patients with iron deficiency anaemia in whom a 5-9.2% prevalence has been reported.

Corpus-predominant gastritis as a risk factor for false-negative 13C-urea breath test results.

BACKGROUND: Urea breath test sensitivity seems affected by increased intragastric acidity during therapy with antisecretory drugs. Intragastric pH is increased in patients with corpus gastritis with/without atrophy. AIM: To test the hypothesis that urea breath test results may also be affected by this gastritis phenotype. METHODS: 123 untreated patients underwent gastroscopy plus biopsies and intragastric pH measurement. The study included 82 endoscopically proven Helicobacter pylori-positive patients who were offered urea breath test with an acidic meal. Histological findings, urea breath test results and intragastric pH were compared in 66 of the subjects. RESULTS: 21 of 66 (31.8%) patients had a false-negative urea breath test. In these patients corpus-predominant gastritis (85.7% vs. 37.7%; P = 0.0004) and fundic atrophy (66.6% vs. 17.7%; P = 0.0001) were more frequent than in patients with true-positive urea breath test. Intragastric pH was higher in false-negative patients (mean 6.3 vs. 4.4; P = 0.001). In a multivariate analysis, the only risk factor for a false-negative urea breath test was the presence of corpus-predominant gastritis (OR = 5.6; 95% CI: 1.1-27). There was a negative correlation between the intragastric pH and the delta over baseline values (r = -0.378; P = 0.0023). CONCLUSIONS: Our results support the hypothesis that the pattern of gastritis can affect the sensitivity of urea breath test, and suggest that patients with corpus-predominant gastritis have a high risk of false-negative urea breath test results.

Long-term follow-up in atrophic body gastritis patients: atrophy and intestinal metaplasia are persistent lesions irrespective of Helicobacter pylori infection.

BACKGROUND: Long-term outcome of atrophic body gastritis has not yet been defined. AIM: To investigate at long-term follow-up the behaviour of atrophy and intestinal metaplasia and the occurrence of neoplastic lesions in atrophic body gastritis patients. METHODS: Overall 106 atrophic body gastritis patients with > or = 4-year follow-up were studied; 38 were Helicobacter pylori-positive at histology + serology and cured of infection (group A), 36 were positive at serology and not treated (group B) and 32 were H. pylori-negative (group C). Patients underwent gastroscopy with antral (n = 3) and body (n = 3) biopsies for histology according to the Sydney System. RESULTS: At 6.7-year follow-up body atrophy and intestinal metaplasia remained unchanged in all 106 patients irrespective of H. pylori status. Antral atrophy was significantly increased at follow-up only in group C, whereas antral intestinal metaplasia was unchanged in all three groups. During follow-up eight (8%) patients developed neoplastic lesions (one adenocarcinoma, one adenoma with low-grade dysplasia and six low-grade dysplasia without endoscopic lesions). Antral atrophic gastritis was present at baseline in all but one (88%) of the eight patients with neoplastic lesions, but only in 15 (15%) of the 98 patients without (P < 0.0001, RR = 26.7). CONCLUSIONS: Atrophy and intestinal metaplasia persist at 6.7-year follow-up and atrophic body gastritis patients with panatrophic gastritis are at increased risk of developing neoplastic lesions.

Occurrence and risk factors for benign epithelial gastric polyps in atrophic body gastritis on diagnosis and follow-up.

BACKGROUND: Benign epithelial gastric polyps have been reported to be more common in atrophic body gastritis. The role of Helicobacter pylori infection in the induction of gastric atrophy is well-known. The development of hyperplastic polyps may be in relation to H. pylori infection. AIM: To investigate occurrence of benign epithelial gastric polyps in atrophic body gastritis patients at diagnosis and follow-up, and the role of H. pylori and other risk factors for the development of benign epithelial gastric polyps. METHODS: A total of 259 consecutive atrophic body gastritis patients included in a follow-up programme, of whom 202 were followed up for median period of 4 years (range: 2-11). At baseline and follow-up gastroscopies, the presence of benign epithelial gastric polyps was evaluated. Biopsies for histology were obtained from all detected benign epithelial gastric polyps. RESULTS: Frequency of benign epithelial gastric polyps in atrophic body gastritis patients were 4.6% at baseline and 5.9% at follow-up. About 91.7% were hyperplastic polyps. H. pylori infection was detected in 79.2% atrophic body gastritis patients with benign epithelial gastric polyps, and in 70.8% without benign epithelial gastric polyps. Smoking was more frequent among patients with benign epithelial gastric polyps [42% vs. 20%, OR 2.8 (95% CI: 1.2-6.9)]. CONCLUSIONS: Benign epithelial gastric polyps occur in about 5% of atrophic body gastritis patients, and the vast majority are hyperplastic polyps. Smoking habit, but not H. pylori infection, increases the risk for benign epithelial gastric polyps in atrophic body gastritis patients.

The long-term effects of cure of Helicobacter pylori infection on patients with atrophic body gastritis.

BACKGROUND: Helicobacter pylori infection induces atrophic body gastritis, but the long-term effect of its cure on body atrophy is unclear. AIM: To investigate the long-term effects of H. pylori cure on gastric morpho-functional parameters in patients with atrophic body gastritis. METHODS: Forty patients with atrophic body gastritis were cured of H. pylori infection. Gastroscopy with biopsies, gastrin and pepsinogen I levels and basal and stimulated acid secretion were evaluated before and 6-12 months after treatment. RESULTS: At eradication assessment (6-12 months), in eight of the 40 patients, body atrophy was no longer observed, whereas in 32 of the 40 it remained substantially unchanged (2.03 +/- 0.12 vs. 1.83 +/- 0.15). In the eight patients with reversed body atrophy, gastrinaemia decreased significantly with respect to pre-treatment values (265 +/- 59.9 pg/mL vs. 51.8. +/- 6.04 pg/mL), and basal and stimulated acid secretion increased significantly after cure. In the 32 patients still presenting body atrophy, gastrinaemia was similar topre-treatment values (457 +/- 76.04 pg/mL vs. 335.1 +/- 58.8 pg/mL). At follow-up (21-25 and 32-70 months), the eight patients with reversed body atrophy continued with normal gastrinaemia (35.3 +/- 10.1 pg/mL vs. 38.5 +/- 8.8 pg/mL), but in the 19 patients with continued atrophy, both corporal atrophy and intestinal metaplasia remained substantially unchanged. CONCLUSIONS: Following successful treatment in patients with atrophic body gastritis and H. pylori infection, long-term histological investigations are crucial in order to detect reversed body damage or to confirm continued body atrophy.

Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection.

BACKGROUND: Helicobacter pylori infection, gastric acid hypersecretion and NSAID consumption may cause peptic ulcer. AIM: To investigate the respective roles of H. pylori and acid secretion in bleeding duodenal ulcer. PATIENTS AND METHODS: A total of 99 duodenal ulcer patients were referred for evaluation of acid secretion: seven with Zollinger-Ellison Syndrome; 14 with hypersecretory duodenal ulcer, defined by the coexistence of elevated basal acid output and pentagastrin acid output; and 78 duodenal ulcer patients with normal acid output. All non-Zollinger-Ellison Syndrome patients were H. pylori-positive and cured of infection. All patients were followed-up for a 36-month period, to assess the occurrence of bleeding episodes. RESULTS: Twenty-nine patients had at least one bleeding episode in the 4 years before the study. Bleeding was more frequent in males and in patients on NSAIDs. The mean basal acid output was not higher among bleeders. In the 21 patients (14 hypersecretory duodenal ulcer, seven Zollinger-Ellison Syndrome) with basal acid output > 10 meg/h and pentagastrin acid output > 44.5 meg/h, the risk of bleeding was higher (OR 6.5; 95% CI: 2-21). In the follow-up period, three out of 83 (3.3%) non-Zollinger-Ellison Syndrome patients had a H. pylori-negative duodenal ulcer with bleeding. The risk of bleeding after H. pylori cure was not higher in hypersecretory duodenal ulcer patients (P > 0.3), nor among patients with previous bleeding episodes (P > 0.2). CONCLUSIONS: In H. pylori-positive duodenal ulcer patients, the coexistence of elevated basal acid output and pentagastrin acid output leads to a sixfold increase in the risk of bleeding. After H. pylori cure, gastric acid hypersecretion is not a risk factor for bleeding. However, duodenal ulcer recurrence with bleeding may occasionally occur in patients cured of H. pylori, even if acid output is normal.

Role of Helicobacter pylori serology in atrophic body gastritis after eradication treatment.

BACKGROUND: It has been reported that 50% of patients with atrophic body gastritis have positive Helicobacter pylori antibody titres only. In atrophic body gastritis, a decrease in H. pylori antibodies after eradication treatment has been reported, suggesting that serology may indicate an active H. pylori infection. AIM: To investigate the time course of H. pylori antibodies and gastric inflammation after eradication treatment in patients with atrophic body gastritis, and to determine whether serology alone can be considered as a valid tool to assess the efficacy of eradication treatment in patients with atrophic body gastritis. METHODS: Twenty-seven patients with atrophic body gastritis (12 serologically H. pylori-positive only, ABG-S+; 15 H. pylori-positive at histology and serology, ABG-H+) were included in the treatment group, and 17 patients (all ABG-S+) in the no treatment group. All patients had gastroscopy plus biopsies evaluated according to the updated Sydney system and H. pylori immunoglobulin G determination: in the treatment group, at baseline and 6 and 24 months after eradication (bismuth-based triple regimens); in the no treatment group, at baseline and after 3 years. RESULTS: In the treatment group, in ABG-S+ patients, H. pylori antibodies decreased significantly 6 months after treatment [37.5 U/mL (16-100 U/mL) vs. 15 U/mL (0--100 U/mL), P < 0.01], but 2 years after treatment no further decrease occurred. In addition, in ABG-H+ patients, a significant decrease in H. pylori antibodies occurred 6 months after treatment [45 U/mL (12.5-100 U/mL) vs. 31 U/mL (0-65 U/mL), P < 0.01], but a further decrease was also observed 2 years after treatment [20 U/mL (0-56 U/mL), P < 0.01]. In ABG-S+ patients, no correlation was observed between the H. pylori antibodies and gastric inflammation score, whereas, in the ABG-H+ group, this correlation was extremely significant (r=0.5991, P < 0.0001). In the no treatment group, at follow-up, a significant decrease in H. pylori antibodies was observed [26 U/mL (15-100 U/mL) vs. 22 U/mL (0-53 U/mL), P < 0.05], but the gastric body inflammation remained unchanged. CONCLUSIONS: This study shows that, in ABG-S+ patients after eradication treatment, serology does not keep in step with gastric inflammation. This suggests that, in patients with atrophic body gastritis, serology alone may not be valid for the assessment of the efficacy of eradication treatment.

Involvement of the corporal mucosa and related changes in gastric acid secretion characterize patients with iron deficiency anaemia associated with Helicobacter pylori infection.

BACKGROUND: Recent studies have reported an association between iron deficiency anaemia and Helicobacter pylori. Helicobacter pylori could cause iron deficiency anaemia by altering iron absorption. We observed that most patients with Helicobacter pylori infection and iron deficiency anaemia present a chronic superficial pangastritis. AIM: To investigate whether Helicobacter pylori-positive patients with iron deficiency anaemia have peculiar histological and functional features when compared with non-anaemic Helicobacter pylori-positive subjects. PATIENTS: Fifty-one patients with iron deficiency anaemia, in whom chronic superficial Helicobacter pylori gastritis was the only gastrointestinal finding, and 103 non-anaemic Helicobacter pylori-positive controls were included in the study. Thirty-seven patients were randomly matched with 37 controls of the same sex and age. METHODS: Gastroscopy, with antral (n=3) and body (n=3) biopsies, was performed. Gastrin and pepsinogen I levels and antiparietal cell antibodies were evaluated. Intragastric pH was also measured. RESULTS: Gastritis involved the corporal mucosa in 90% of patients compared to 42.7% of controls (P < 0.0001). The mean inflammatory score in the gastric body was significantly higher among patients than in controls (2.2 vs. 0.6; P=0.012). Gastrin was significantly higher in patients than in controls (mean 60.2 vs. 29 pg/mL; P=0.0069). Intragastric pH was higher in patients than in controls (median 5.7 vs. 2; P=0.0026). CONCLUSIONS: These data suggest that patients with iron deficiency anaemia and Helicobacter pylori infection have a peculiar pattern of gastritis with corporal involvement and related changes in intragastric pH.

Endoscopic Evaluation of the Upper Gastrointestinal Tract is Worthwhile in Premenopausal Women with Iron-Deficiency Anaemia Irrespective of Menstrual Flow.

BACKGROUND: In premenopausal women, iron-deficiency anaemia is common and menstrual flow is often held responsible, but it is not clear whether these women should be submitted to gastrointestinal (GI) evaluation. We aim to prospectively investigate whether premenopausal women with iron-deficiency anaemia benefit from GI evaluation regardless of menstrual flow. METHODS: The study population comprised 59 consecutive premenopausal women with iron-deficiency anaemia. Excluded were women with obvious or suspected causes of anaemia and those ≤21 years. Heavy menstrual loss was not considered an exclusion criterion. All subjects had: complete blood count, ferritin, non-invasive testing by faecal occult blood (FOB), 13C-urea breath test (13C-UBT), anti-tissue transglutaminase antibodies (tTG) and gastrin levels. Gastroscopy with antral (n = 3), corporal (n = 3) and duodenal (n = 2) biopsies was performed in women with positive 13C-UBT or tTG titre or hypergastrinaemia. RESULTS: Heavy menstrual loss was present in 50.8%. Non-invasive tests were positive in 40/59 (67.8%): 30 had positive 13C-UBT, 12 had hypergastrinaemia, 7 had positive tTG and 3 had positive FOB. Women tested positive were similar to those tested negative as far as concerned age, haemoglobin and ferritin levels and heavy menstrual flow (55% versus 42.1%). All 40 women tested positive underwent gastroscopy with biopsies. Four (10%) had bleeding-associated lesions and 34 (85%) had non-bleeding-associated lesions. As regards upper GI findings, no differences were observed between women with normal and those with heavy menstrual flow. No lower GI tract lesions were detected in the three women with positive FOB. CONCLUSIONS: Our data suggest that premenopausal women with iron-deficiency anaemia benefit from endoscopic evaluation of the upper GI tract irrespective of menstrual flow.

Role of Helicobacter pylori infection in pernicious anaemia.

BACKGROUND: Pernicious anaemia is associated with atrophic body gastritis and considered an autoimmune disease. Whether Helicobacter pylori is involved in the induction of pernicious anaemia is uncertain. AIMS: To investigate the prevalence of Helicobacter pylori infection in pernicious anaemia patients and to ascertain whether the Helicobacter pylori-positive patients had distinctive clinical and gastric morphofunctional characteristics. PATIENTS AND METHODS: A series of 81 consecutive pernicious anaemia patients underwent serological, functional and endoscopic/histological investigations. RESULTS: A total of 49 (60.5%) patients were Helicobacter pylori-positive (males 61.2% vs females 38.8%). No difference was observed in clinical and morphofunctional characteristics between Helicobacter pylori-positive and negative patients, whereas distinctive functional/histological features between histologically Helicobacter pylori-positive (n=8) and serologically Helicobacter pylori-positive (n=41) cases were detected. In the histologically Helicobacter pylori-positive group, Pepsinogen I was higher [13 (058) vs 5 (0-26) ng/ml; p=0.0025)] and positivity for anti-parietal cell antibodies was lower [42.9% vs 76.9, p=0.0867]. Antral histological variables of the gastritis score were significantly higher in the histologically Helicobacter pylori-positive than in the serologically Helicobacter pylori-positive patients, but this latter group had a higher score of body atrophy (2.63+/-0.12 vs 1.71+/-0.29; p=0.0051). Body inflammation was also significantly higher in the histologically Helicobacter pylori-positive group (chronic inflammation: 1.43+/-0.2 vs 1.05+/-0.06; p=0.0271; inflammation acitivity: 0. 57+/-0.3 vs 0.15+/-0.06, p=0.0220). Antral mucosa was normal in 24/41 (58.5%) of the serologically Helicobacter pylori-positive patients, but only in 1/8 (12.5%) of the histologically Helicobacter pylori-positive patients (p=0.0232). CONCLUSIONS: Almost two thirds of pernicious anaemia patients have evidence of Helicobacter pylori, but only those with an active Helicobacter pylori infection have distinctive functional and histological features. These findings support the hypothesis that Helicobacter pylori infection could play a triggering role in a subgroup of pernicious anaemia patients.

Role of small bowel investigation in iron deficiency anaemia after negative endoscopic/histologic evaluation of the upper and lower gastrointestinal tract.

BACKGROUND: The usefulness of small bowel investigation in iron deficiency anaemia (IDA) patients is controversial. AIM: To evaluate the presence of small bowel lesions likely to cause IDA in patients with unexplained IDA after negative gastroscopy with biopsies and colonoscopy (CS). METHODS: A total of 117 outpatients, referred for unexplained IDA, underwent gastroscopy with biopsies and colonscopy. In 17 (14.5%) patients, endoscopic/histological investigations were negative. Of these patients, 13 underwent small bowel follow-through (SBFT) and if necessary to confirm the diagnosis, further gastrointestinal (GI) investigations. RESULTS: Small bowel lesions likely to cause IDA were found in five (38%) patients. Four of these lesions were detected by SBFT, two of them were malignant. These findings, confirmed at surgery and ileoscopy (IS), led to the final diagnoses ofjejunal and ileal adenocarcinoma, idiopathic ileal ulcers and ileal Crohn's disease. In one case, after negative SBFT, jejunal angiodysplasia was detected by video capsule endoscopy (VCE). Faecal occult blood test (FOBT) was positive in four (31%) patients, all of whom presented lesions likely to cause IDA, detected in three cases by SBFT and in one case by VCE. CONCLUSIONS: This study shows the importance of investigating the small bowel in IDA patients after negative upper and lower GI endoscopy, particularly if FOBT is positive.

Histological recovery and gluten-free diet adherence: a prospective 1-year follow-up study of adult patients with coeliac disease.

BACKGROUND: Adequate gluten-free diet (GFD) is the only treatment for coeliac disease (CD). However, no agreement has been reached on either how and when to assess patient adherence to GFD or its effectiveness on villous atrophy. AIM: To assess, in a prospective study, patient adherence to and efficacy of GFD on histological recovery after 1-year of GFD. METHODS: Between 2009 and 2012, we enrolled 65 consecutive newly-diagnosed adult patients (median age 38 years, 18-70) with biopsy-proven atrophic CD. Patients were re-evaluated after 1 year of GFD with duodenal histology, serological assays, symptoms and a dietary interview based on a validated questionnaire. Complete histological recovery was defined as the absence of villous atrophy and ≤30/100 intraepithelial lymphocytes. RESULTS: Overall, 81.5% of patients had adequate adherence (ADA) to GFD, whereas 18.5% had an inadequate adherence (IADA); 66% of ADA patients and no IADA patients achieved complete histological recovery (P < 0.00001). Among ADA patients, antibody seroconversion and symptoms were not significantly different between patients who achieved complete histological recovery and those who achieved partial histological recovery with P = 0.309 and P = 0.197, respectively. Multivariate analysis showed that Marsh 3C was a risk factor for incomplete histological recovery in ADA patients (OR 8.74, 95% CI: 1.87-40.83). CONCLUSIONS: This study shows that complete histological recovery after 1-year of GFD in adult patients, who are assessed as adherent to the GFD, can be obtained in 66% of patients. Patients with severe histological damage at diagnosis are at risk for incomplete histological recovery 1 year later.

Systematic review: gastric cancer incidence in pernicious anaemia.

BACKGROUND: Pernicious anaemia (PA) has an increased risk for gastric cancer (GC). It is not established whether PA patients need to undergo endoscopic/histological follow-up. AIM: To provide a systematic overview of the literature on PA and the development of gastric cancer, to estimate the gastric cancer incidence-rate. METHODS: According to PRISMA, we identified studies on PA patients reporting the incidence of gastric cancer. Quality of studies was evaluated using the Newcastle-Ottawa Quality Assessment Scale. Meta-analysis on annual gastric cancer incidence rates was performed. RESULTS: Twenty-seven studies met eligibility criteria. 7 studies were of high, 6 of medium, 10 of low and 4 of very low quality. Gastric cancer incidence-rates ranged from 0% to 0.2% per person-years in 7 American, from 0% to 0.5% in 2 Asiatic, from 0% to 1.2% in 11 Northern European studies and from 0% to 0.9% in 7 studies from other European countries. The incidence-rates of gastric cancer ranged from 0% to 1.2% per person-years in studies which used gastroscopy, from 0.1% to 0.9% in those based on International Classification of Disease. Heterogeneity between studies was not statistically significant at the 5% level (Chi-squared test = 17.9, P = 0.08). The calculated pooled gastric cancer incidence-rate was 0.27% per person-years. Meta-analysis showed overall gastric cancer relative risk in PA as 6.8 (95% CI: 2.6-18.1). CONCLUSIONS: This systematic review shows a pooled gastric cancer incidence-rate in pernicious anaemia of 0.27% per person-years and an estimated nearly sevenfold relative risk of gastric cancer in pernicious anaemia patients. Further high quality studies are needed to confirm this higher risk.

Development of type I gastric carcinoid in patients with chronic atrophic gastritis.

BACKGROUND: Long-term observational studies assessing the incidence of type I gastric carcinoid (typeIGC) in patients with chronic atrophic gastritis are few. AIM: To evaluate the occurrence of typeIGC at diagnosis and during follow-up and to identify patient features associated with the presence of typeIGC in a cohort of chronic atrophic gastritis patients. METHODS: Three hundred and sixty-seven chronic atrophic gastritis patients [245 women, age 54 (18-79) years] underwent regular follow-up by gastroscopy. The incidence of typeIGC was determined in chronic atrophic gastritis patients with at least 2 years of follow-up (n = 214). Baseline clinical and histological features were analysed as factors associated with the presence of typeIGC by univariate analysis. RESULTS: Type I gastric carcinoid was diagnosed in nine (2.4%) patients at the moment when chronic atrophic gastritis was diagnosed. After 1463 person-years, six patients developed typeIGC with an annual incidence rate (person-year) of 0.4%. Patients with typeIGC had significantly higher levels of gastrin, chromogranin A and more frequently the presence of body polyps and ECL-dysplasia compared with chronic atrophic gastritis patients without typeIGC. CONCLUSIONS: This cohort study shows that typeIGC is a rare complication in patients with chronic atrophic gastritis, and the presence of body polyps and ECL-dysplasia at gastroscopic/histologic evaluation is strongly associated with the presence of typeIGC.