Gastric biopsies are recommended in patients with iron deficiency anaemia to identify atrophic gastritis. However, in practice, only duodenal biopsies are routinely performed. The aim of our study was to determine the value of gastric biopsies in iron deficiency anaemia.

A prospective study including all patients referred for gastrointestinal endoscopy for iron deficiency anaemia from May 2008 to September 2014 was performed. All patients having endoscopic lesions which may explain occult bleeding were excluded, as well as patients using non-steroidal anti-inflammatory drugs or anticoagulation treatment. Two fundic biopsies, two antral biopsies, and one biopsy from the lesser curve were taken in all patients. Following entities were particularly looked for: chronic gastritis, Helicobacter pylori infection, intestinal metaplasia, endocrine hyperplasia and villous atrophy. In cases where intestinal metaplasia was present in the fundus and associated with endocrine hyperplasia and glandular atrophy, immunohistochemical study was performed to confirm autoimmune gastritis.

One hundred seventy-seven patients (mean age 50 years, range: 15-90) were included. Chronic gastritis was found in 149 cases (84%). Infection by Helicobacter pylori was found in 107 cases (60%). Fundic intestinal metaplasia was observed in 25 patients (14%) and was associated with Helicobacter pylori infection in 52% of cases. Atrophic gastritis was observed in 14 cases (8%) and autoimmune gastritis was confirmed in 5 cases by immunohistochemical study. One patient had on gastric biopsy a carcinoma with signet ring cells.

Intestinal metaplasia was frequently observed and was mostly related to Helicobacter pylori infection. These patients require monitoring, especially if they are young because it represents a pre neoplastic condition. However, in our study autoimmune gastritis often described in the literature in case of iron deficiency anaemia was rarely seen raising the question of relative cost-efficiency of fundic biopsies during iron deficiency anaemia.

Plummer-Vinson syndrome (PVS), a rare clinical condition, is characterized by a triad of dysphagia, iron deficiency anemia and esophageal web in the post-cricoid region. It was first described over a century ago. However, literature on this condition remains scanty, and its prevalence appears to be declining worldwide, possibly due to improvements in nutrition over time. The condition has been reported most commonly in thin-built, middle-aged, white women. The esophageal webs in PVS are thin mucosal folds, which are best seen either in lateral views at barium swallow or at esophagoscopy. These are usually semilunar or crescentic, being located most often along the anterior esophageal wall, but can be concentric. The exact cause and pathogenesis of PVS remain unclear, though iron and other nutritional deficiencies, genetic predisposition and autoimmunity have all been implicated in formation of the webs. Treatment includes correction of iron deficiency and endoscopic dilation of the esophageal webs to relieve dysphagia. PVS is associated with an increased risk of hypopharyngeal and esophageal malignancies. Correction of iron deficiency may arrest and reverse the mucosal changes and possibly reduces this risk.

Chronic atrophic autoimmune gastritis (CAAG) is an organ-specific autoimmune disease characterized by an immune response, which is directed towards the parietal cells and intrinsic factor of the gastric body and fundus and leads to hypochlorhydria, hypergastrinemia and inadequate production of the intrinsic factor. As a result, the stomach's secretion of essential substances, such as hydrochloric acid and intrinsic factor, is reduced, leading to digestive impairments. The most common is vitamin B12 deficiency, which results in a megaloblastic anemia and iron malabsorption, leading to iron deficiency anemia. However, in the last years the deficiency of several other vitamins and micronutrients, such as vitamin C, vitamin D, folic acid and calcium, has been increasingly described in patients with CAAG. In addition the occurrence of multiple vitamin deficiencies may lead to severe hematological, neurological and skeletal manifestations in CAAG patients and highlights the importance of an integrated evaluation of these patients. Nevertheless, the nutritional deficiencies in CAAG are largely understudied. We have investigated the frequency and associated features of nutritional deficiencies in CAAG in order to focus on any deficit that may be clinically significant, but relatively easy to correct. This descriptive review updates and summarizes the literature on different nutrient deficiencies in CAAG in order to optimize the treatment and the follow-up of patients affected with CAAG.

We re-evaluated the old hypothesis that gastritis-induced achlorhydria is a cause of iron deficiency anemia (IDA) in humans. First, we analyzed the currently available research on the association between achlorhydria and IDA. When gastric acid secretion was measured after maximal stimulation, the frequency of achlorhydria (or severe hypochlorhydria) was 44% in patients with idiopathic IDA and 1.8% in healthy controls. In some patients with pernicious anemia, presumed achlorhydria preceded the development of IDA in time. However, we found no credible evidence that IDA caused gastritis or that IDA preceded the development of achlorhydria. Thus, correlational results favor achlorhydria as the causal factor in the association between achlorhydria and IDA. Second, we sought to determine whether gastritis and achlorhydria cause negative iron balance. When biosynthetic methods were used to isotopically label iron in food, achlorhydric patients were found to have severe malabsorption of nonheme iron, which persisted after the development of IDA. In 1 study, achlorhydria reduced the normal increase in heme-iron absorption from hemoglobin in response to iron deficiency. After an injection of isotopic iron into normal men, the physiologic loss of iron from the body was found to be 1 mg/d. Patients with chronic gastritis had excess fecal loss of isotopically tagged plasma iron. Calculations based on these results indicate that the absorption of iron from a typical Western diet by achlorhydric patients would be less than physiologic iron losses, creating a negative iron balance that could not be overcome by the adaptive increase in duodenal iron absorptive capacity that occurs in response to iron deficiency. The combination of results from these correlational and pathophysiologic studies supports the hypothesis that gastritis-induced achlorhydria can be an independent cause of IDA.

We report the case of a 54-year-old patient presenting with a typical pernicious anaemia. His mother was diagnosed with unquestionable pernicious anaemia 5 years previously. Serum ferritin was strongly increased (1,160 microg/l, normal range 29-380), with a transferrin saturation of 95%. We found a homozygous C282Y mutation of the HFE gene in our patient, his mother being heterozygous. The son of our patient was compound C282Y/H63D heterozygous without detectable pernicious anaemia. This seems to be the first report of an association between familial pernicious anaemia and hereditary haemochromatosis. The simultaneous occurrence of the 2 diseases in the same patient helps to delineate the relative contribution of each of them to iron metabolism and erythropoiesis: iron overload was only moderately increased and responded rapidly to phlebotomies, whereas haemochromatosis did not modify the cytologic presentation of pernicious anaemia.

Iron deficiency is a known complication of achlorhydria and may precede the development of pernicious anemia. Among 160 patients with autoimmune gastritis identified by hypergastrinemia and strongly positive antiparietal antibodies, we explored the overlap between 83 subjects presenting with iron deficiency anemia (IDA), 48 with normocytic indices, and 29 with macrocytic anemia. Compared with macrocytic patients, patients with IDA were 21 years younger (41 +/- 15 years versus 62 +/- 15 years) and mostly women. All groups had a high prevalence of thyroid disease (20%) and diabetes (8%) suggestive of the autoimmune polyendocrine syndrome. Stratification by age cohorts from younger than 20 years to older than 60 years showed a regular and progressive increase in mean corpuscular volume (MCV) from 68 +/- 9 to 95 +/- 16 fl, serum ferritin levels from 4 +/- 2 to 37 +/- 41 microg/L, gastrin level from 166 +/- 118 to 382 +/- 299 pM/L (349 +/- 247 to 800 +/- 627 pg/mL), and a decrease in cobalamin level from 392 +/- 179 to 108 +/- 65 pg/mL. The prevalence of Helicobacter pylori infection was 87.5% at age younger than 20 years, 47% at age 20 to 40 years, 37.5% at 41 to 60 years, and 12.5% at age older than 60 years. These findings challenge the common notion that pernicious anemia is a disease of the elderly and imply a disease starting many years before the establishment of clinical cobalamin deficiency, by an autoimmune process likely triggered by H pylori.

Important implications for the recognition of iron deficiency anaemia include diagnosis and correction of underlying causes, most of which are identifiable, in the older patient, by means of conventional upper gastrointestinal endoscopy, and by colonoscopy. The aetiological search may, however, have to be widened to include enteroscopic examination of the jejunum and ileum and, in some instances, investigation of potential non-gastrointestinal foci of chronic blood loss. A substantial minority may defy even the most thorough search for the underlying cause.

An up to date review of our knowledge of human iron metabolism is given including problems of iron balance, internal transport, and intracellular mechanisms. Current knowledge of the iron proteins is summarized and this background is used in discussing the pathophysiology of iron deficiency and overload, together with the internal derangements such as sideroblastic anemia which form much of the clinical practice associated with disorders of iron metabolism. The therapeutic approach to these problems will be described.

The incidence of parietal cell antibodies (P.C.A.) in patients with various diseases was investigated by complement fixation test (C.F.T.). The relationship between the incidence of P.C.A. and clinical and pathological findings was also investigated. The incidence of P.C.A. with simple atrophic gastritis was 34.8% in total cases, 29.0% in male and 48.1% in female, respectively. The difference between the sexes was statistically significant (p less than 0.05). The incidence of P.C.A. in superficial gastritis was 37.5%, showing the same incidence as atrophic gastritis. The difference between the two groups was not statistically significant (p less than 0.05). The incidence in patients with hypo- and hyperactivity was 43.0% and 11.8%, respectively. The difference was statistically significant, but that between hypo- and normoacidity was not significant (p less than 0.05). The author postulated the conclusion that the superficial gastritis could be included in the category of atrophic gastritis. The dissociation of correlation of titer of C.F.T. with acidity and histological findings was found. The correlation was more significantly observed with acidity than with histological findings. The relatively high incidences of P.C.A. were noted in patients with peptic ulcer, gastric carcinoma and chronic thyroiditis. The incidence of P.C.A. in other diseases showed the nearly equal incidence to that of other investigators. Three cases of postgastrectomy patients were noted, in which the P.C.A. disappeared four to six months after total or subtotal gastrectomy.

Hemoglobin iron absorption in patients with treated prenicious anemia (PA) and concomitant iron deficiency was low compared to absorption in patients with iron deficiency alone. Crude and purified hog intrinsic factor (IF) concentrates doubled the absorption of hemoglobin iron in these patients as did normal (neutralized depepsinized) human gastric juice. Hemoglobin iron absorption was not significantly enhanced by PA gastric juice. Absorption of heme iron, like that of hemoglobin iron, was enhanced by normal neutralized depepsinized gastric juice. No enhancement of hemoglobin iron absorption by these substances was obtained in the normal or iron-deficient non-PA control subjects. Preincubation of the hog IF concentrate with antisera to IF significantly reduced the enhancement of hemoglobin iron absorption due to the concentrate. In vitro studies suggest that heme complexes with a substance present in IF-containing materials. Whether a gastric glycoprotein similar to IF serves as an intestinal transport factor for heme, similar to transport of vitamin B(12), or whether normal gastric juice acts by another mechanism cannot be determined at this time.