Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 1 035 routine serum gastrin investigations was undertaken with a commercially available kit. Levels in 49 normal subjects were similar to those found in 200 patients with duodenal ulcertaion, in 42 patients with gastric ulcers, in 9 patients with carcinoma of the stomach, in 55 patients with chronic alcohol-induced pancreatitis, and in 27 with iron deficiency anaemia. Significantly raised levels of serum gastrin were found in 32 patients with megaloblastic anaemias, where the rise in serum gastrin concentration correlated with a fall in maximal acid output, and in 14 patients with complete vagotomies. It is suggested that a level of less than 2 mEq/h of acid after insulin and a raised serum gastrin level are useful criteria of completeness of vagotomy.
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PMID:Basal serum gastrin levels in normal subjects and in various gastro-intestinal conditions. 122 75

A 51 year-old woman with vomitus, intermittent epigastric pain and heartburn had chronic sideropenic anemia. Gastroscopy revealed a subcardial, submucosal tumor. The tumor was removed totally by endoscopic polypectomy. Histologically it was identified as a carcinoid. The endocrinologic examination showed hypergastrinemia caused by chronic atrophic gastritis. The association of this gastric carcinoid with chronic atrophic gastritis type A, hypergastrinemia, hyperplasia of the gastrin-producing antral cells and micronodular hyperplasia of endocrine cells in the gastric fundus, confirms the hypothesis about the pathogenesis of these extremely rare gastric tumors.
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PMID:[Gastric carcinoid in chronic atrophic gastritis with hypergastrinemia]. 203 30

Pseudo-Zollinger--Ellison syndrome appears to very rarely afflict young children. Hypergastrinemia, regardless of the etiology, presents with signs and symptoms of nonhealing or multiple gastric or duodenal ulcers, or both. We present a 7-yr-old boy with fasting hypergastrinemia (serum gastrin 200-500 pg/ml) who had mild to moderate iron deficiency anemia, but was asymptomatic. Stool guaiac was positive and gastric acid secretion was almost 40-fold above normal. Endoscopy showed multiple small gastric fundal ulcerations and severe gastritis. Workup for Zollinger--Ellison syndrome was negative. Changes in serum gastrin levels after secretin injection and after ingestion of a protein meal were compatible with those noted in adults with pseudo-Zollinger--Ellison syndrome. This child may be the first case of pseudo-Zollinger--Ellison syndrome under the age of 17 yr.
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PMID:Pseudo-Zollinger--Ellison syndrome in a child presenting with anemia. 379 86

Antral gastrin cell hyperfunction (AGCH) is a rare syndrome characterized by persistent hypergastrinemia and important peptic symptoms in the absence of a gastrin-producing tumor. The pathogenesis of AGCH is still unknown and debated. Helicobacter pylori (Hp) infection has been reported as a possible cause of sustained hypergastrinemia. To assess the relevance of Hp infection in pediatric AGCH patients, Hp status, G cell function, acid secretion, and antral G and D cell populations were investigated in six children presenting with gastrointestinal bleeding of unknown origin, sideropenic anemia, and variable abdominal symptoms. All patients had moderate high basal gastrinemia with abnormally increased peak values after meals and elevated values of basal acid output (BAO), maximal acid output (MAO), and pentagastrin-stimulated acid output (PAO). Circulating pepsinogen I was also significantly increased. Three children had Hp infection, as assessed by enzyme-linked immunosorbent assay, urease test, and histology. Endoscopy showed duodenal erosions in three children, with ulcer in two Hp-positive cases. At histology, moderate gastritis was observed only in the three Hp-positive cases. In all patients, quantitative assessment of antral gastrin and somatostatin cells gave significantly elevated G cell counts; D cells were at the lower reference limit and the G/D cell ratio was significantly elevated. These data indicated a diagnosis of AGCH, possibly due to the elevated G/D cell ratio, and suggest HP infection as an overlapping factor complicating the clinical picture in some cases.
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PMID:Helicobacter pylori infection in children with antral gastrin cell hyperfunction. 791 67

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.
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PMID:Variable hematologic presentation of autoimmune gastritis: age-related progression from iron deficiency to cobalamin depletion. 1700 59

Pernicious anemia is a megaloblastic anemia caused by vitamin B12 deficiency, and is the end-stage of autoimmune gastritis that typically affects persons older than 60 years. It is the most common cause of vitamin B12 deficiency. Pernicious anemia can also be diagnosed concurrently with other autoimmune diseases. We report the occurrence of megaloblastic anemia in a 22-year-old woman with chronic autoimmune thyroiditis for 10.5 years. Recently, she presented with microcytic anemia, and iron deficiency anemia was diagnosed initially. After administration of ferrous sulfate, macrocytic anemia was revealed and vitamin B12 deficiency was detected. Pernicious anemia was highly suspected because of the endoscopic finding of atrophic gastritis, and high titer of antigastric parietal cell antibody, as well as elevated serum gastrin level. After intramuscular injections of hydroxycobalamine 100 microg daily for 10 days, and monthly later, her blood counts returned to normal.
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PMID:Coexistence of megaloblastic anemia and iron deficiency anemia in a young woman with chronic lymphocytic thyroiditis. 1705 Jan 98

Despite elegant regulatory mechanisms, iron deficiency anemia (IDA) remains one of the most common nutritional deficiencies of mankind. Iron deficiency is the result of an interplay between increased host requirements, limited external supply, and increased blood loss. When related to increased physiologic needs associated with normal development, iron deficiency is designated physiologic or nutritional. By contrast, pathological iron deficiency, with the exception of gross menorrhagia, is most often the result of gastrointestinal disease associated with abnormal blood loss or malabsorption. If gastroenterologic evaluation fails to disclose a likely cause of IDA, or in patients refractory to oral iron treatment, screening for celiac disease (anti-tissue transglutaminase antibodies), autoimmune gastritis (gastrin, anti-parietal or anti-intrinsic factor antibodies), and Helicobacter pylori (IgG antibodies and urease breath test) is recommended. Recent studies indicate that 20-27% of patients with unexplained IDA have autoimmune gastritis, about 50% have evidence of active H. pylori infection, and 4-6% have celiac disease. The implications for abnormal iron absorption of celiac disease or autoimmune gastritis are obvious. In patients with unexplained IDA and H. pylori infection, cure of refractory IDA by H. pylori eradication offers strong evidence for a cause-and-effect relation between H. pylori infection and unexplained IDA. Stratification by age cohorts in autoimmune gastritis implies a disease presenting as IDA many years before the establishment of clinical cobalamin deficiency. It is likely caused by an autoimmune process triggered by antigenic mimicry between H. pylori epitopes and major autoantigens of the gastric mucosa. Recognition of the respective roles of H. pylori and autoimmune gastritis in the pathogenesis of iron deficiency may have a strong impact on the diagnostic workup and management of unexplained, or refractory IDA.
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PMID:Iron deficiency, Helicobacter infection and gastritis. 1990 46

The peptide hormone gastrin has been identified as a major regulator of acid secretion and a potent mitogen for normal and malignant gastrointestinal cells. The importance of gastric acid in the absorption of dietary iron first became evident 50 years ago when iron deficiency anemia was recognized as a long-term consequence of partial gastrectomy. This review summarizes the connections between circulating gastrins, iron status and colorectal cancer. Gastrins bind two ferric ions with micromolar affinity and, in the case of non-amidated forms of the hormone, iron binding is essential for biological activity in vitro and in vivo. The demonstration of an interaction between gastrin and transferrin by biochemical techniques led to the proposal that gastrins catalyze the loading of transferrin with iron. Several lines of evidence, including the facts that the concentrations of circulating gastrins are increased in mice and humans with the iron overload disease hemochromatosis and that transferrin saturation positively correlates with circulating gastrin concentration, suggest the potential involvement of gastrins in iron homeostasis. Conversely, recognition that ferric ions play an unexpected role in the biological activity of gastrins may assist in the development of useful therapies for colorectal carcinoma and other disorders of mucosal proliferation in the gastrointestinal tract. This article is part of a Special Issue entitled: 11th European Symposium on Calcium.
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PMID:Gastrins, iron homeostasis and colorectal cancer. 2132 May 35

A 50-year-old woman was admitted because of severe sideropenic anemia. The gastrin levels were within normal ranges. Esophagogastroduodenoscopy showed diffuse gastric polyposis with signs of diffuse oozing. Colonoscopy showed the presence of a 3-cm wide pedunculated polyp of the ascending colon, which was removed by diathermy. The patient was treated by total gastrectomy with Roux-Y esophagojejunostomy. Histological examination showed the presence of diffuse gastric polyposis with the contemporary occurrence of hyperplastic polyps and mixed hyperplastic and adenomatous polyps, with a tubular pattern and the focal aspect of serrate adenoma. This is the first case report of sporadic diffuse hyperplastic and adenomatous polyposis of the stomach.
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PMID:Sporadic diffuse gastric polyposis: Report of a case. 2192 71

H. pylori is a gram-negative pathogen, etiologically associated with atrophic and non-atrophic gastritis, peptic ulcer, primary gastric B-cell lymphoma and gastric carcinoma. Several observations demonstrated a correlation between H. pylori and malabsorption of essential nutrients; epidemiological studies have shown an association between H. pylori infection and iron deficiency anemia, while the absorption of some vitamins such as vitamin B12, vitamin A, vitamin C, folic acid and Vitamin E may be affected by the infection. The main mechanism related to malabsorption of this components is the modified intragastric pH (hypo- achlorhydria) due to H. pylori infection. Moreover H. pylori is also able to determine a modification of gastrointestinal hormones by reducing plasma levels of ghrelin and increasing those of leptin and gastrin, thus affecting appetite and promoting the occurrence of dyspeptic symptoms. On the other hand, H. pylori eradication has been shown to improve serum level of iron and vitamin B12, has some effects on Vitamin A and Vitamin E absorption and has a late effects on ghrelin levels. As a consequence of those effects, H. pylori is also associated with childhood malnutrition in developing countries either for the occurrence of malabsorption or for an increased susceptibility to enteric infections caused by hypochlorhydria.
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PMID:Nutritional aspects of Helicobacter pylori infection. 2210 25


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