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)

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

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

Chronic autoimmune atrophic gastritis (CAAG) is an organ-specific autoimmune disease, which affects the corpus-fundus gastric mucosa. Although it has been described for several years, the real pathophysiological mechanisms, the natural history and the possible neoplastic complications are not completely known. Atrophy of the gastric mucosa is the endpoint of the chronic processes, with the loss of glandular cells and their replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue. As a consequence, hydrochloric acid, pepsin and intrinsic-factor is impaired resulting in pernicious anemia. The exact causal agent is not yet known, but both genetic and environmental factors seem to play a decisive role. Moreover, the clinical onset may assume different characteristics; differently from what previously observed, recent evidence has reported the onset of CAAG at a younger age, frequently with iron deficiency anemia or upper gastro-intestinal symptoms. The diagnosis of CAAG might be challenging and usually requires the combination of clinical, serological and histopathologic data; moreover, CAAG patients are often misdiagnosed as refractory to HP eradication therapy, probably because achlorhydria might allow urease-positive bacteria other than H pylori to colonize the stomach, causing positive 13C-urea breath test results. However, biopsy is the most reliable method to evaluate the presence of metaplastic atrophic gastritis. In order to assess the severity of gastric atrophy and intestinal metaplasia, OLGA and OLGIM staging systems have been proposed and seem to correlate with the risk of developing gastric adenocarcinoma. Indeed, CAAG represents a pre-neoplastic condition, as patients with CAAG are very likely to develop either type-1 gastric neuroendocrine tumors and gastric adenocarcinomas, as well as several other neoplastic diseases. To date, the need, the intervals and cost-effectiveness of endoscopic/histological surveillance for patients with CAAG/pernicious anemia are yet to be established.
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PMID:The changing face of chronic autoimmune atrophic gastritis: an updated comprehensive perspective. 3063 39

Children differ from adults regarding Helicobacter pylori (H. pylori) infection in many terms. H. pylori infection represents a key factor in the pathogenesis of duodenal ulcer and chronic gastritis in children. H. pylori infection causes some extraintestinal diseases as well as gastrointestinal diseases. Although, among these illnesses in children, symptoms like recurrent abdominal pain are not specific. Moreover, the role of the pathogen in the growth faltering, iron deficiency anemia, and asthma still remains controversial. A reliable method to detect H. pylori infection is a crucial issue, sand is still a matter of active debate. The tests applied for H. pylori diagnosis are grouped as either invasive or non-invasive methods. Invasive methods consist of endoscopic evaluation, the rapid urease test (RUT), histology, and bacterial culture. Non-invasive tests include the urea breath test (UBT), stool antigen test (SAT), serology, and molecular diagnostic approaches. Use of endoscopy is a pre-requisite for all invasive methods and poses difficulties in children as it is a difficult procedure and requires patient's cooperation. For this reason, the non-invasive tests have been commonly used in children, although their accuracy is not very reliable in some cases. Invasive tests may be opted to confirm the diagnosis as and when needed. This review presents the diagnostic tests used to detect H. pylori infection in children.
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PMID:Helicobacter pylori infection in children: an overview of diagnostic methods. 3073 29

Brunner's gland adenoma is a rare benign tumor of small bowel, often incidentally discovered during endoscopy or radiological imaging. Mostly they are asymptomatic or often present with nonspecific symptoms such as nausea, vomiting, gastrointestinal hemorrhage, iron deficiency anemia. We reported a 76 years old male case presented with chief complaints of vomiting and black tarry stool. General physical examination was normal except mild tenderness over epigastrium. Esophagogastroduodenoscopy revealed a pedunculated polypoid tubular structure with blind end distally of length approximately 10-12* 3.5*1.5 cm in the second section of the duodenum with multiple skipped ulcers on the exposed surface of it. Additionally, there were few erosions in the duodenum proximally and multiple superficial ulcerations in the antrum, associated with helicobacter pylori confirmed by rapid urease test kit. Surgical or endoscopic excision is the treatment of choice. We consider our case is the eldest case among Brunner's gland adenoma case in literature. Keywords: Brunner's gland adenoma; Brunner's gland hamartoma; Brunner's gland hyperplasia; case report.
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PMID:Giant Brunner's Gland Adenoma Presenting as Upper Gastrointestinal Bleeding in 76 Years Old Male: A Case Report. 3108 Feb 46