Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 42 patients (25 men, 17 women, mean age 62 years) with severe erosive or ulcerative oesophagitis not responding to H2-receptor antagonist treatment over at least 3 months and ineligible for surgery, omeprazole was administered at an initial dose of 40 mg/day, subsequently reduced to 20 mg after healing of the lesions. Patients had monthly clinical, endoscopic, histological and laboratory assessment over the healing period, then were reevaluated 3-monthly over one year, then 6-monthly, during the maintenance treatment. Stages of oesophagitis were based on the Savary-Miller classification, modified for stage I (erosions must be present). With 40 mg omeprazole, healing was observed in 71%, 83% and 90% of the patients after 1, 2 and 3 months of treatment, respectively. After one month of treatment, a complete healing was less frequently observed in patients with stage IV oesophagitis pre-trial (55%) than in the patients with stages I, II and III pre-trial (90%) (p less than 0.05). Ninety per cent of the patients healed at one month were asymptomatic whereas 50% of the patients with incomplete healing still had symptoms, most often dysphagia, rarely heartburn. Maintenance treatment with 20 mg was sufficient in most patients, with a probability of remaining healed of 69% from 9 to 24 months after starting this dosage. In 9 patients with Barrett's oesophagus, the lengths of the circumferential metaplasia were found to be reduced after one year of treatment compared to pre-trial lengths (p less than 0.005). There was no further significant reduction of length after 2 years of treatment. Fasting gastrin was increased in most of the patients, although great inter-patient variability was observed; 50% of the patients had levels not exceeding 5 times the upper limit of normal. There was no consistent increase of enterochromaffin-like cell density in 29 patients investigated up to nearly 2 years of omeprazole administration. The treatment was well tolerated. By inducing a profound and sustained inhibition of acid secretion, as confirmed by pH monitoring, omeprazole promotes healing of the lesions of severe oesophagitis and prevents recurrence of lesions and symptoms. Omeprazole is therefore a valuable treatment for patients ineligible for surgery, particularly in the elderly.
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PMID:Omeprazole in the treatment of patients with severe reflux oesophagitis not responding to H2-receptor antagonists and ineligible for surgery. 213 May 87

We have found 20 cases of ectopic gastric mucosa in the proximal esophagus. Five patients had symptoms, usually a burning sensation in the neck and/or dysphagia. We report the results of immunoperoxidase staining of this tissue for gastrin, somatostatin, vasoactive intestinal peptide, and bombesin. In 85% of biopsy specimens tested, one or more polypeptides were present. Gastrin and bombesin were found more frequently in symptomatic patients, and somatostatin in asymptomatic patients. Chronic inflammatory changes were more frequent in symptomatic patients.
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PMID:Ectopic gastric mucosa in proximal esophagus. Its clinical significance and hormonal profile. 287 20

The effect of pentagastrin on oesophageal motility was studied in six subjects with idiopathic diffuse oesophageal spasm (IDOS). Pentagastrin was administered by continuous intravenous infusion in doses of 1 microgram/kg/h, 5 micrograms/kg/h, and 10 micrograms/kg/h. Saline infusion was used as a control. No subject experienced pain during pentagastrin infusion. Two developed dysphagia and repetitive contractions with 'wet' swallows during the saline infusion and the lowest pentagastrin infusion. Contraction amplitude was increased only with 'dry' swallows during the 10 micrograms/kg/h infusion period. Contraction duration was increased with both 'wet' and 'dry' swallows during the 1 microgram/kg/h infusions, and with 'dry' swallows during the 10 micrograms/kg/h infusion. Propagation velocity was not altered by pentagastrin. We conclude that gastrin released physiologically by eating probably does not contribute to symptom production in IDOS. Moreover, it seems unlikely that pentagastrin, at least in these doses, can be exploited for diagnostic purposes.
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PMID:Pentagastrin in diffuse oesophageal spasm. 722 56

Thyroid disease is common, and its effects on the gastrointestinal system are protean, affecting most hollow organs. Hashimoto disease, the most common cause of hypothyroidism, may be associated with an esophageal motility disorder presenting as dysphagia or heartburn. Dyspepsia, nausea, or vomiting may be due to delayed gastric emptying. Abdominal discomfort, flatulence, and bloating occur in those with bacterial overgrowth and improve with antibiotics. Reduced acid production may be due to autoimmune gastritis or low gastrin levels. Constipation may result from diminished motility, leading to an ileus, megacolon, or rarely pseudoobstruction. Ascites in myxedema is characterized by a high protein concentration. Graves' disease accounts for 60% to 80% of thyrotoxicosis. Hyperthyroidism is accompanied by normal gastric emptying with low acid production, partly due to an autoimmune gastritis with hypergastrinemia. Transit time from mouth to cecum is accelerated, resulting in diarrhea. Steatorrhea is due to hyperphagia and stimulation of the adrenergic system. Diarrhea in medullary carcinoma of the thyroid (MCT) may be due to elevated calcitonin, prostaglandins, or 5-hydroxyindoleacetic acid. Ileal or colonic function may be abnormal. The esophagus may be compressed by benign processes, but more often by malignancies. MRI and CT scans are the best diagnostic modalities. The gastrointestinal manifestations of thyroid disease are generally due to reduced motility in hypothyroidism, increased motility in hyperthyroidism, autoimmune gastritis, or esophageal compression by a thyroid process. Symptoms usually resolve with treatment of the thyroid disease.
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PMID:The thyroid and the gut. 2035 69

We present a case of a gastric neuroendocrine carcinoma in a patient with a history of long-term proton pump inhibitor (PPI) use. A 49-year-old man using PPI for the last 15 years due to gastroesophageal reflux disease developed progressive dysphagia, dyspepsia and weight loss. Upper gastrointestinal endoscopy, endoscopic ultrasonography and abdominal CT diagnosed a malignant tumor localized to a hiatal hernia. Fasting serum chromogranin A and gastrin concentrations were elevated (32 nmol/l and 159 pmol/l, respectively). Helicobacter pylori PCR analysis of antral biopsies was negative. Biopsies from endoscopically normal oxyntic mucosa showed enterochromaffin-like (ECL) cell hyperplasia. Tumor biopsies revealed a poorly differentiated neuroendocrine carcinoma. Sevier-Munger staining, immunohistochemistry and electron microscopy indicated ECL cell as origin of the tumor cells. Concerns have previously been raised about the safety of long-term PPI use due to a possible increased risk of cancer. This case illustrates a patient with a poorly differentiated neuroendocrine carcinoma with ECL cell characteristics probably induced by hypergastrinemia secondary to long-term PPI use.
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PMID:Gastric neuroendocrine carcinoma after long-term use of proton pump inhibitor. 2208 94