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 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

Alkaline reflux (bile) gastritis and esophagitis result from mucosal injury by duodenal contents. Bile gastritis occurs after gastric surgery, cholecystectomy, ampullary sphincteroplasty, and, rarely, in nonoperated patients. Diagnostic features include chronic, continuous epigastric pain, exacerbated by eating, bilious vomiting, weight loss, iron deficiency anemia, achlorhydria, gastritis, and intragastric bile. The pathophysiology probably relates to excess enterogastric reflux and bile-induced mucosal damage. There is no perfect diagnostic test, but chemical and scintigraphic documentation of enterogastric reflux, as well as provocative testing with alkali solutions, are promising new techniques. Medical therapy with antacids, H2 antagonists, bile salt absorbants, and metoclopramide has been without significant benefit. Prostaglandins and sucralfate are now being evaluated. Surgical therapy that diverts duodenal contents away from the stomach is usually of benefit in appropriately selected patients. Alkaline reflux esophagitis shares many features with alkaline gastritis.
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PMID:Alkaline reflux gastritis and esophagitis. 637 64

The development of adenocarcinoma or carcinoid tumors in atrophic gastritis is widely documented. We report the simultaneous occurrence of gastric adenocarcinoma and carcinoid (composite tumor) in atrophic gastritis, a finding reported only twice before in the literature. This 52-yr-old man with rectal bleeding, epigastric pain, and iron deficiency anemia was noted to have multiple polypoid masses on upper endoscopy. Biopsy revealed features of both adenocarcinoma and carcinoid tumor in a background of atrophic gastritis, leading to a total gastrectomy, lymph node dissection, and liver biopsy. The gastrectomy specimen was characterized by a 6 cm pedunculated polyp and multiple sessile nodular masses between 0.4 and 2.5 cm in the background of a granular mucosa. On microscopic examination, the large polypoid mass corresponded to a well-differentiated adenocarcinoma, intestinal type, infiltrating the wall. The smaller nodules were composed of carcinoid tumors, restricted to the mucosa, or infiltrating the gastric wall. Carcinoid tumor was also seen in the large polypoid mass closely intermingled with adenocarcinoma. The carcinoid tumor metastasized to the liver. Lymph nodes showed both adenocarcinoma and carcinoid tumor. The gastric mucosa was characterized by atrophic gastritis with intestinal metaplasia, neuroendocrine hyperplasia, and microcarcinoids. The adenocarcinoma stained strongly for CK7, CK 20, MIB-1, and focally for chromogranin and synaptophysin. The carcinoid tumor was negative for CK7, CK 20 and MIB-1, and was positive for chromogranin and synaptophysin. Overexpression of p53 was noted only in the adenocarcinoma. Electron microscopy revealed neurosecretory granules in the carcinoid characteristic of a neuroendocrine tumor. Composite tumor can occur in the setting of atrophic gastritis. The findings in this patient reinforce the concept that the epithelial and neuroendocrine cells of the gastrointestinal tract both result from multidirectional differentiation of a primitive cell.
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PMID:Combined adenocarcinoma and carcinoid tumor in atrophic gastritis. 1245 98

A 50-year-old female was referred to our hospital because of postprandial epigastric pain and pancreatic head mass. On admission, an elastic hard mass with tenderness was palpable in the epigastric region. Laboratory findings showed no abnormalities, except for a slightly elevated C-reactive protein value and iron deficiency anemia. Serum levels of pancreatic enzymes and tumor markers were also within the reference range. Computed tomography (CT) demonstrated a 5-cm heterogenous mass at the head of the pancreas. Angiography showed that gastroduodenal artery was transformed and narrowed by the mass. Smooth stenosis of portal vein was also observed. Fusion CT-positron emission tomography with 2-deoxy-2-[F]fluoro-D-glucose demonstrated a focus of increased uptake in the pancreatic head mass. We suspected the mass of malignancy but, surprisingly, tumor size was gradually decreased without any therapies. Biopsy specimens from the mass of the pancreas showed marked inflammatory cell infiltration and marked interstitial fibrosis without malignant cells. Thereafter, we could isolate Corynebacterium coyleae from the biopsy specimen. We diagnosed the mass as a pancreatic abscess caused by C. coyleae and started with the intravenous antibiotics therapy. Subsequent follow-up CT and ultrasonography showed dramatic improvement in pancreatic mass. We present here a case of pancreatic abscess which was difficult to differentiate from malignant lesion by various imaging studies. Moreover, we could culture and identify C. coyleae which had never been reported to be the source of pancreatic abscess.
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PMID:Pancreatic abscess caused by Corynebacterium coyleae mimicking malignant neoplasm. 1707 50

Helicobacter pylori infection is recognised as a cause of gastritis and peptic ulcer disease (PUD) and usually acquired during the first years of life. While there is a decline in the prevalence of H. pylori infection in northern and western European countries, the infection is still common in southern and eastern parts of Europe and Asia. Symptoms of H. pylori-related PUD are nonspecific in children and may include epigastric pain, nausea and/or vomiting, anorexia, iron deficiency anaemia and hematemesis. Besides, only a small proportion of children develop symptoms and clinically relevant gastrointestinal disease. H. pylori infection can be diagnosed either by invasive tests requiring endoscopy and biopsy or non-invasive tests including the (13)C-urea breath test, detection of H. pylori antigen in stool and detection of antibodies in serum, urine and saliva. The aim of treatment is at least 90 % eradication rate of the bacteria, and a combination of two antibiotics plus a proton pump inhibitor has been recommended as first-line treatment. However, frequent use of antibiotics during childhood is associated with a decline in eradication rates and the search for new treatment strategies as well. This is an overview of the latest knowledge and evidence-based guidelines regarding clinical presentation, diagnosis and treatment of H. pylori infection in childhood.
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PMID:Clinical practice: Helicobacter pylori infection in childhood. 2301 42

Eosinophilic gastrointestinal disorders or eosinophilic digestive disorders encompass a spectrum of rare gastrointestinal disorders that includes eosinophilic esophagitis, eosinophilic gastroenteritis, and eosinophilic colitis. Eosinophilic gastroenteritis is a rare inflammatory disease characterized by eosinophilic infiltration of the gastrointestinal tract. The clinical manifestations include anemia, dyspepsia, and diarrhea. Endoscopy with biopsy showing histologic evidence of eosinophilic infiltration is considered definitive for diagnosis. Corticosteroid therapy, food allergen testing, elimination diets, and elemental diets are considered effective treatments for eosinophilic gastroenteritis. The treatment and prognosis of eosinophilic gastroenteritis is determined by the severity of the clinical manifestations. We describe a 24-year-old woman with eosinophilic gastroenteritis presenting as epigastric pain with a history of severe iron deficiency anemia, asthma, eczema, and allergic rhinitis, and we review the literature regarding presentation, diagnostic testing, pathophysiology, predisposing factors, and treatment recommendations.
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PMID:Eosinophilic gastroenteritis presenting with severe anemia and near syncope. 2313 32

Clinical vignette: A 38-year-old man consults you in the GI clinic because of frequent episodes of epigastric pain, nausea, and tiredness. His blood count shows signs of mild iron deficiency anemia. Upper GI endoscopy was normal, but antral and corpus biopsy specimens show evidence of gastric atrophy and Helicobacter pylori infection. Colonoscopy and capsule endoscopy showed no evidence of lesions in the large or small bowel. He receives a standard one-week course eradication therapy consisting of a proton pump inhibitor (PPI), amoxicillin, and clarithromycin. His symptoms improve, but his infection persists and he remains mildly anemic. He asks you whether the infection must be eradicated, as he read on the Internet that it can cause stomach cancer. He is also concerned about the anemia.
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PMID:Iron deficiency and Helicobacter pylori-induced gastric cancer: too little, too bad. 2325 61

We present a case of primary malignant pylorus neoplasia, emphasizing its rarity, the difficulty of diagnosis and the importance of an adequate prepare before the endoscopic procedure. Literature shows that tumors compromising the first, third and fourth segments of duodenum are rare, especially those of the pyloric area, representing only 0.35% of all malignant tumors of the gastrointestinal tract. Adenocarcinoma is the most common histological type, representing 50% of all malignant neoplasias at this site. The most common symptoms are weight loss, nausea, vomiting, abdominal pain, abdominal mass, sudden changes in intestinal habits and iron deficiency anemia secondary to chronic intestinal hemorrhage. Survival after five years is only 18%. We report a case of a seventy-one year-old male referring early satiety, epigastric pain, retrosternal burning and dyspepsia, with unspecific results in complementary exams, since complete gastric emptying was not achieved. As symptoms worsened, the patient was submitted to laparotomy, with identification of gastric dilation and severe pyloric stenosis, macroscopically suggesting malignancy. The chosen procedure was a subtotal gastrectomy. Adjuvant radiotherapy and chemotherapy were not used. The patient is been followed-up without tumor recurrence so far.
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PMID:[Pyloric stenosis due to adenocarcinoma of the pylorus]. 2457 95

Median arcuate ligament syndrome is an anatomic and clinical entity characterized by dynamic compression of the proximal celiac artery by the median arcuate ligament, which leads to postprandial epigastric pain, vomiting, and weight loss. These symptoms are usually nonspecific and are easily misdiagnosed as functional dyspepsia, peptic ulcer disease, or gastropathy. In this report, we presented a 72-year-old male patient with celiac artery compression syndrome causing recurrent abdominal pain associated with gastric ulcer and iron deficiency anemia. This association is relatively uncommon and therefore not well determined. In addition, we reported the CT angiography findings and three-dimensional reconstructions of this rare case.
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PMID:Clinical and radiologic review of uncommon cause of profound iron deficiency anemia: median arcuate ligament syndrome. 2505 2

We report here the case of a young man suffering from a rare germ cell tumour. The patient was a 25-year-old man who was referred to our centre for asthenia, stinging epigastric pain, and an iron deficiency anaemia. Gastroscopy revealed a circumferential vegetating lesion on the second portion of the duodenum. The lesion was indurated at the third portion of the duodenum, responsible for a tight stenosis. A computerized tomography-scan of the chest, abdomen and pelvis, and a pancreatic MRI showed a circumferential lesion with a bi-ductal dilatation (i.e., of the common bile duct and Wirsung's duct) without metastatic localisation. The patient underwent a pancreaticoduodenectomy with lymph node dissection including all cellular adipose tissues of the hepatic pedicle from the hepatic common artery and of the retroportal lamina. Histological findings were suggestive of a duodenal embryonal carcinoma with pancreatic infiltration. This is the second published case highlighting the duodenal primitive localisation of an embryonal carcinoma with pancreatic infiltration.
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PMID:Real case of primitive embryonal duodenal carcinoma in a young man. 2821 81


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