Treatment of helicobacter pylori infection in atrophic gastritis

Helicobacter pylori (Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis (AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows: (1) Cure of infection, resolution of inflammation and normalization of gastric functions; (2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and (3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric pH, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroup of patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG

Common Pitfalls in the Management of Patients with Micronutrient Deficiency. Keep in Mind the Stomach

Micronutrient deficiencies are relatively common, in particular iron and cobalamin deficiency, and may potentially lead to life-threatening clinical consequences when not promptly recognized and treated, especially in elderly patients. The stomach plays an important role in the homeostasis of some important hematopoietic micronutrients like iron and cobalamin, and probably in others equally important such as ascorbic acid, calcium, and magnesium. A key role is played by the corpus oxyntic mucosa composed of parietal cells whose main function is gastric acid secretion and intrinsic factor production. Gastric acid secretion is necessary for the digestion and absorption of cobalamin and the absorption of iron, calcium, and probably magnesium, and is also essential for the absorption, secretion, and activation of ascorbic acid. Several pathological conditions such as Helicobacter pylori-related gastritis, corpus atrophic gastritis, as well as antisecretory drugs, and gastric surgery may interfere with the normal functioning of gastric oxyntic mucosa and micronutrients homeostasis. Investigation of the stomach by gastroscopy plus biopsies should always be considered in the management of patients with micronutrient deficiencies. The current review focuses on the physiological and pathophysiological aspects of gastric acid secretion and the role of the stomach in iron, cobalamin, calcium, and magnesium deficiency and ascorbate homeostasis

Time trend occurrence of duodenal intraepithelial lymphocytosis and celiac disease in an open access endoscopic population

Background: Duodenal intraepithelial lymphocytosis (DIL) is a histological finding characterized by the increase of intraepithelial CD3T-lymphocytes over the normal value without villous atrophy, mostly associated to coeliac disease (CD), Helicobacter pylori (Hp) gastritis and autoimmune diseases. Objective: To assess the occurrence of DIL, CD and Hp gastritis in an endoscopic population over a 13 year period. Methods: From 2003 to 2015 we included adult patients who consecutively underwent oesophago-gastro-duodenoscopy (OGD) with duodenal biopsies assessing the overall and annual occurrence of DIL and CD and the prevalence of Hp gastritis. Results: 160 (2.3%) patients with DIL and 275 (3.9%) with CD were detected among 7001 patients. CD occurrence was higher from 2003 to 2011, while since 2012 DIL occurrence gradually increased significantly compared to CD (p = 0.03). DIL patients were more frequently female (p = 0.0006) and underwent OGD more frequently for dyspepsia (p = 0.002) and for indications not related to gastrointestinal symptoms than CD patients (p = 0.0003). Hp gastritis occurred similarly in CD and DIL patients but the latter had higher frequency of atrophic body gastritis (p = 0.005). Conclusions: DIL is a condition increasing in the general endoscopic population mainly diagnosed by chance. Concomitant gastric histological evaluation is able in one third of DIL patients to identify associated possible causes of DIL, such as Hp and atrophic gastritis

Mapping of ionomic traits in Mimulus guttatus reveals Mo and Cd QTLs that colocalize with MOT1 homologues

Peer reviewedPublisher PD

Relationship between Persistent Gastrointestinal Symptoms and Duodenal Histological Findings after Adequate Gluten-Free Diet. A Gray Area of Celiac Disease Management in Adult Patients

A gluten-free diet (GFD) leads to a rapid improvement in gastrointestinal (GI) symptoms, biochemical alterations and duodenal histological damage in the majority of celiac disease (CD) patients. This study aimed to assess the frequency and factors associated with the persistence of GI symptoms/malabsorption signs and their relationship with duodenal histological findings among CD patients on an adequate GFD (mean duration 16 months, range 12-28 months). This longitudinal cohort study included 102 adult CD patients (median age 38.5 years, range 18-76 years, F = 71.6%) diagnosed between 2012 and 2018. A total of 36.3% of the included patients had persistent GI symptoms and/or malabsorption signs (Group 1), while the remaining patients had complete GI well-being without malabsorption signs (Group 2) at the time of histological re-evaluation. The persistence of GI symptoms/signs was associated with a long duration of symptoms/signs before CD diagnosis (>= 5 years) (OR 5.3; 95% CI 1.3-21.8) and the presence of constipation at the time of CD diagnosis (OR 7.5; 95% CI 1.3-42) while for other variables, including age at CD diagnosis, sex, duration of GFD, comorbidities, CD serology positivity and severity of duodenal damage at histological re-evaluation, no association was found. According to our results, the persistence of symptoms/signs is not associated with histological findings, and their relationship could be a gray area in CD management

Iron deficiency anemia caused by nonspecific (idiopathic) small bowel ulceration: an uncommon presentation of an uncommon disease.

Ulcers of the small bowel are rare, and in most cases are due to infections, inflammatory bowel diseases, malignancies or drugs. When none of these causes is recognized, they are classified as 'nonspecific' or idiopathic. Such lesions are uncommon, and in most cases present with occlusion. A case of a middle-aged woman with iron deficiency anemia due to occult bleeding, with negative gastroscopy and colonoscopy is presented. The diagnosis of a small bowel pathology resembling Crohn's disease was made by small bowel follow through and small intestine contrast ultrasonography. An ileal ulcer was identified at surgery, and after resection the patient experienced a stable recovery from the anemia without ulcer recurrence. Neither histology nor clinical or biochemical features suggested the diagnosis of an inflammatory bowel disease. Other possible causes were unlikely and the lesion was therefore diagnosed as idiopathic. This report also focuses on the need and the modality to investigate the small bowel in iron deficiency anemia patients

Mutations in Arabidopsis \u3ci\u3eYellow Stripe-Like1\u3c/i\u3e and \u3ci\u3eYellow Stripe-Like3\u3c/i\u3e Reveal Their Roles in Metal Ion Homeostasis and Loading of Metal Ions in Seeds

Here, we describe two members of the Arabidopsis (Arabidopsis thaliana) Yellow Stripe-Like (YSL) family, AtYSL1 and AtYSL3. The YSL1 and YSL3 proteins are members of the oligopeptide transporter family and are predicted to be integral membrane proteins. YSL1 and YSL3 are similar to the maize (Zea mays) YS1 phytosiderophore transporter (ZmYS1) and the AtYSL2 iron (Fe)-nicotianamine transporter, and are predicted to transport metal-nicotianamine complexes into cells. YSL1 and YSL3 mRNAs are expressed in both root and shoot tissues, and both are regulated in response to the Fe status of the plant. β-Glucuronidase reporter expression, driven by YSL1 and YSL3 promoters, reveals expression patterns of the genes in roots, leaves, and flowers. Expression was highest in senescing rosette leaves and cauline leaves. Whereas the single mutants ysl1 and ysl3 had no visible phenotypes, the ysl1ysl3 double mutant exhibited Fe deficiency symptoms, such as interveinal chlorosis. Leaf Fe concentrations are decreased in the double mutant, whereas manganese, zinc, and especially copper concentrations are elevated. In seeds of double-mutant plants, the concentrations of Fe, zinc, and copper are low. Mobilization of metals from leaves during senescence is impaired in the double mutant. In addition, the double mutant has reduced fertility due to defective anther and embryo development. The proposed physiological roles for YSL1 and YSL3 are in delivery of metal micronutrients to and from vascular tissues

Root Suberin Forms an Extracellular Barrier That Affects Water Relations and Mineral Nutrition in Arabidopsis

Though central to our understanding of how roots perform their vital function of scavenging water and solutes from the soil, no direct genetic evidence currently exists to support the foundational model that suberin acts to form a chemical barrier limiting the extracellular, or apoplastic, transport of water and solutes in plant roots. Using the newly characterized enhanced suberin1 (esb1) mutant, we established a connection in Arabidopsis thaliana between suberin in the root and both water movement through the plant and solute accumulation in the shoot. Esb1 mutants, characterized by increased root suberin, were found to have reduced day time transpiration rates and increased water-use efficiency during their vegetative growth period. Furthermore, these changes in suberin and water transport were associated with decreases in the accumulation of Ca, Mn, and Zn and increases in the accumulation of Na, S, K, As, Se, and Mo in the shoot. Here, we present direct genetic evidence establishing that suberin in the roots plays a critical role in controlling both water and mineral ion uptake and transport to the leaves. The changes observed in the elemental accumulation in leaves are also interpreted as evidence that a significant component of the radial root transport of Ca, Mn, and Zn occurs in the apoplast.</p

Cell Blood Count Alterations and Patterns of Anaemia in Autoimmune Atrophic Gastritis at Diagnosis: A Multicentre Study

Background: Autoimmune atrophic gastritis (AAG) leads to iron and/or vitamin B12 malabsorption, with subsequent haematological alterations which could represent the sole clinical manifestation. We aimed to assess patterns of anaemia and micronutrient deficiencies in patients with AAG at the time of diagnosis. Methods: Observational, multicentre, cross-sectional study including consecutive adult patients diagnosed with AAG within the last ten years. Cell blood count, red cell distribution width, serum vitamin B12, and ferritin were collected. Multivariate analysis for predictive factors of anaemia was computed. Results: 654 AAG patients (mean age 59.2 \ub1 13.8 years, female (F): male (M) ratio = 2.3:1) were included. Anaemia was present in 316 patients (48.3%; mean age 60.1 \ub1 15.8 years, F:M ratio = 2.3:1). Pernicious anaemia (132/316 cases, 41.7%) was more common in males (27.1% versus 12.4%; p = 0.001) and in older patients (63.0 \ub1 14.6 versus 58.9 \ub1 14.9 years; p = 0.014), while iron deficiency anaemia (112/316 cases, 35.4%) was more common in females (16.9% versus 10.0%; p = 0.039) and in younger patients (56.8 \ub1 16.6 versus 60.2 \ub1 14.6 years; p = 0.043). The prevalence of iron deficiency was equally distributed between anaemic and non-anaemic patients (p = 0.9). Anisocytosis (odds ratio: 10.65, 95% confidence interval: 6.13-18.50, p &lt; 0.0001) was independently associated with anaemia. Conclusions: Anaemia is a common manifestation in AAG patients, mostly due to micronutrient deficiencies. Scant haematologic alterations and micronutrient deficiencies may precede overt anaemia