Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cases of Mallory-Weiss syndrome aged over 75 year were analyzed with regard to their clinical features. In a 5-year period, there were 9 such cases, representing 19% of the total number of Mallory-Weiss syndrome cases. Four patients had a history of retching or vomiting, but in the other 5 patients, Mallory-Weiss tears occurred during endoscopic examination with slight vomiting reflex or even almost vomiting reflex. The latter cases had a spindle-shaped tear which was located on the lesser curvature at the cardia of the stomach. All patients were managed conservatively by observation without endoscopic hemostatic procedure, because the amount of bleeding was small. The 5 patients were thin and three of them had chronic atrophic gastritis. Mucosal weakness is an important etiologic factor in aged patients who develop Mallory-Weiss syndrome.
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PMID:[Clinical study of Mallory-Weiss syndrome in the aged patients over 75 year--mainly five cases induced by the endoscopic examination]. 807 8

Sarcoidosis is a systemic granulomatous disease of unknown etiology, characterized by an immunological disorder with accumulation of activated lymphocytes and macrophages in all the organs and apparatus. The intrathoracic lymphnodes and the lung remain the most common sites of such disease. The gastrointestinal sarcoidosis, particularly of the stomach, is very rare. The stomach may be the primitive or the secondary (systemic sarcoidosis) site of sarcoid granuloma. The endoscopic aspects of the gastric mucosa are variable: localized or diffused hyperemia, single or multiple ulcers, aspects of atrophic gastritis with easy bleeding during contact, rigid mucosa and so on. Generally asymptomatic, the disease may show symptoms as pain in the epigastrium, nausea, vomiting, haematemesis and so on. The wide range of gastric pathologies resembling sarcoidosis both on a histological level and on a clinic-endoscopical one (syphilis, histoplasmosis, Crohn's disease, stomach cancer) require an extremely accurate diagnosis above all for the setting out of the therapy with steroids which are the most appropriate drugs (prednisone). Three out of thirty-two patients observed for respiratory problems, already affected by cutaneous and pulmonary sarcoidosis, started suffering from gastric symptoms of different kind: pain in the epigastrium, haematemesis, weight loss, nausea and post-prandial vomiting. Gastroscopy and biopsy, with histopathologic examination of gastric mucosal specimens taken from the most suspicious sites, confirmed the diagnosis of sarcoidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Gastric localization of sarcoidosis]. 829 Jul 86

It is now recognised that Helicobacter pylori, like most enteric infections, is mainly acquired in childhood. Adults rarely become infected, with seroconversion rates varying between 0.33and 0.5% per person year. The age at which children are most likely to become infected is still unclear, but findings in a number of cross-sectional studies suggest that infection is acquired before the age of five. The prevalence of infection is highest in children in the developing world where up to 75% of children may be infected by the age of 10. In the developed world the prevalence of infection is noticeably increased among socially deprived children. The diagnosis of H pylori infection in childhood is most often made at endoscopy, for which there are many indications. Symptoms such as abdominal pain, vomiting, and haematemesis may be associated with duodenal ulcer and H pylori infection. However, in the case of children undergoing endoscopy for assessment of oesophagitis, failure to thrive, coeliac disease, Crohn's disease, or portal hypertension, the finding of H pylori infection is likely to be incidental. How should we manage these children with a diagnosis of H pylori infection? Currently, there are no consensus guidelines for the management of H pylori infected children. In 1994 the National Institutes of Health consensus statement recommended that adults with gastric or duodenal ulcer disease, who are infected with H pylori, should receive antimicrobial treatment. The European Maastricht Consensus Report suggested broader indications for treatment of infected adults. It states that treatment is advisable for all H pylori infected dyspeptic patients diagnosed non-invasively under 45 years of age at a primary care level. Patients older than 45 years with dyspeptic symptoms should be treated for H pylori infection but only after endoscopy to rule out any other underlying pathology. The European guidelines also recommend treatment for infected patients with mucosa associated lymphoid tissue lymphoma and patients who are found to have intestinal metaplasia and gastric atrophy.
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PMID:How should Helicobacter pylori infected children be managed? 1045 35

Helicobacter pylori infection of the gastric mucosa can be found in approximately 50% of the world's population and is associated with a range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer. To explore immunization as a strategy for preventing and treating H. pylori-associated disease, we assessed the safety and immunogenicity in healthy adults of a formalin-inactivated, oral H. pylori whole-cell (HWC) vaccine, administered with or without mutant Escherichia coli heat-labile toxin (LT(R192G)) as a mucosal adjuvant. In a dose-response study, 23 subjects with or without H. pylori infection were vaccinated with either 2.5 x 10(6) HWC, 2.5 x 10(8) HWC, or 2.5 x 10(10) HWC, plus 25 microg of LT(R192G). Thereafter, a randomized study was conducted in which 18 H. pylori-infected subjects were assigned, in a double-blind fashion, to receive either 2.5 x 10(10) HWC plus placebo-adjuvant, placebo-vaccine plus 25 microg of LT(R192G), placebo-vaccine plus placebo-adjuvant, or 2.5 x 10(10) HWC plus 25 microg of LT(R192G). Diarrhea (six subjects), low-grade fever (five subjects), and vomiting (two subjects) were observed, usually after the first dose. Significant rises in geometric mean mucosal (fecal and salivary) anti-HWC immunoglobulin A antibodies occurred among H. pylori-infected and uninfected subjects following inoculation with 2.5 x 10(10) HWC plus 25 microg of LT(R192G). Moreover, among H. pylori-negative volunteers, this regimen induced significant lymphoproliferative responses in 5 of 10 subjects and gamma interferon production responses to H. pylori sonicate in 7 of 10 subjects. There was no evidence that vaccination eradicated H. pylori in infected volunteers. These results suggest that it is possible to stimulate mucosal and systemic immune responses in humans to H. pylori antigens by using an HWC vaccine.
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PMID:Safety and immunogenicity of oral inactivated whole-cell Helicobacter pylori vaccine with adjuvant among volunteers with or without subclinical infection. 1134 17

A 19-month-old, male, Labrador retriever was presented with a history of chronic vomiting. Blood analysis and abdominal ultrasononography could not rule out the possibility of gastrointestinal inflammation. Histologic examination of endoscopic gastrointestinal biopsies confirmed severe lymphocytic-plasmacytic and atrophic gastritis, as well as, predominantly eosinophilic, severe enteritis.
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PMID:Severe lymphocytic-plasmacytic and atrophic gastritis, as well as, predominantly eosinophilic, severe enteritis, in a 19-month-old Labrador retriever. 1588 51

Scientific evidence based on controlled clinical research confirm substantial benefits resulting from the eradication of H. pylori infection in such pathologies of the alimentary tract as: gastric peptic and duodenal ulcer (active or confirmed in the future and ulcer disease complications), MALT (Mucosa Associated Limphoid Tissue) lymphoma, atrophic gastritis, past stomach resection, gastric cancer in the family. The above group of indications is strongly recommended for eradicative treatment. During the last several years there have been many guidelines made by international and national specialist groups. "Test and treat" strategy of undiagnosed dyspepsia treatment is based on possibility to carry out non-invasive tests confirming H. pylori infection. First symptoms of dyspepsia in people over 45 years of age constitute recommendation for endoscopy, as well as symptoms assumed to be "alarming" (loss of weight, anaemia, bloody vomiting, tarry stool, dysphagia) regardless of patient age. An individual approach to eradication is proposed in gastroesophageal reflux disease, and use of non-steroid anti-inflammatory drugs. Antibacterial activity towards H. pylori is shown by many antibiotics (amoxicillin, macrolides, tetracyclines) and some other chemotherapeutic agents (nitroimidazoles) and bismuth. PPIs are recommended, because through increase of pH in stomach they create conditions to act for antibiotics. During the stage of first line triple therapy, it is advised to apply PPI and two antibacterial medicines at the same time (PPI + amoxicillin+metronidazole or clarithromycin). Such therapeutic action ensures achievement of eradication of H. pylori infection in 80-90% of cases. In case of lack of treatment efficiency in the first-line therapy, 7-14 day treatment may be repeated using triple therapies (PPI + 2 antibiotics) substituting the antibiotic with the metronidazole or tetracycline, or quadruple therapies (PPI + bismuth citrate + 2 antibiotics). Side effects during eradicative treatments occur quite rarely (from 15 to 30%).
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PMID:Guidelines in the medical treatment of Helicobacter pylori infection. 1703 12

We describe a case of recurrent deterioration of renal function in a 54-year-old man who was found to have metabolic alkalosis, with a maximum PaCO(2) of 73.9 mmHg and a bicarbonate concentration of 55.3 mmol/l. He had a gradual exacerbation of nausea and vomiting due to atrophic gastritis, with a scarred, deformed pyloric part of the stomach and a duodenal bulb secondary to chronic peptic ulcer. His metabolic alkalosis and deteriorated renal function were corrected by intravenous saline with or without potassium chloride. However, his recovered creatinine clearance was at most 60 l/day (41.6 ml/min). A renal biopsy revealed cellular infiltration of mononuclear cells and atrophic change in the tubulointerstitium, suggesting chronic interstitial nephritis. Latent renal insufficiency and dehydration induced by protracted vomiting may easily induce a rapid and recurrent deterioration of renal function, and control of vomiting seemed to be the cardinal measure. Initially, his nausea and vomiting seemed to be successfully controlled by medication, however, they later became persistent and surgical correction of the stomach was carried out. Postoperative recovery was smooth, and the patient's vomiting and recurrent deterioration of renal function finally settled.
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PMID:A case of recurrent renal failure associated with metabolic alkalosis induced by protracted vomiting. 1718 33

The rarely described gastric micropneumatosis is caused by accumulating air in the mucus membrane. It may associate mainly with Helicobacter pylori positive atrophic gastritis or with pneumatosis due to gas producing bacteria or non-infectious causes. In our case the disorder was diagnosed in a 69 years old patient, taking clopidogrel, living in a nursing home, with history of hypertension, general arteriosclerosis, cerebral infarction, who was admitted to our department because of melaena and hematemesis. Upper endoscopy revealed a map-like, slightly raised, palm-sized area with yellowish spots on the posterior wall of the markedly inflamed stomach at the level of fundus - corpus border. Based on histology findings, that showed empty spaces among corpus glands, 10-20 microm in diameter, with no epithelial lining, the diagnosis was gastric micropneumatosis. The impaired mucosal integrity caused by mesenteric ischaemia and repeated vomiting were supposed as possible etiological factors, because 72 hours after the patient had stopped vomiting, control endoscopy showed regression, and the empty spaces were no more detectable in the histology samples. By this case report the authors would like to draw attention to a seldom diagnosed gastric injury, and discuss the factors that may predispose the development of gastric micropneumatosis.
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PMID:[Gastric micropneumatosis: a rare endoscopic entity]. 1745 10

Norwegian Lundehunds are often affected by gastrointestinal disease, the most common clinical signs of which are intermittent diarrhea, vomiting, weight loss, lethargy, ascites, and subcutaneous edema of the hind legs. The most frequent laboratory changes include hypoalbuminemia (with or without hypoglobulinemia), hypocalcemia, a decrease in the serum cobalamin concentration, and an increase or decrease in the serum folate concentration, reflecting microbial synthesis or malabsorption, respectively. Histopathologic abnormalities can include chronic atrophic gastritis, intestinal lymphangiectasia, and lymphoplasmacytic enteritis. Because the underlying cause of gastroenteropathy in Norwegian Lundehunds has not been identified, treatment is symptomatic.
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PMID:Gastroenteropathy in Norwegian Lundehunds. 1784

Type 1 diabetes mellitus (T1DM) results from autoimmune destruction of insulin-producing beta cells and is characterised by the presence of insulitis and &and beta-cell autoantibodies. Up to one third of patients develop an autoimmune polyglandular syndrome. Fifteen to 30% of T1DM subjects have autoimmune thyroid disease (Hashimoto's or Graves' disease), 5 to 10% are diagnosed with autoimmune gastritis and/or pernicious anaemia (AIG /PA), 4 to 9% present with coeliac disease (CD), 0.5% have Addison's disease (AD), and 2 to 10% show vitiligo. These diseases are characterised by the presence of autoantibodies against thyroid peroxidase (for Hashimoto's thyroiditis), TSH receptor (for Graves' disease), parietal cell or intrinsic factor (for AIG /PA), tissue transglutaminase (for CD), and 21-hydroxylase (for AD). Early detection of antibodies and latent organ-specific dysfunction is advocated to alert physicians to take appropriate action in order to prevent full-blown disease. Hashimoto's hypothyroidism may cause weight gain, hyperlipidaemia, goitre, and may affect diabetes control, menses, and pregnancy outcome. In contrast, Graves' hyperthyroidism may induce weight loss, atrial fibrillation, heat intolerance, and ophthalmopathy. Autoimmune gastritis may manifest via iron deficiency or vitamin B12 deficiency anaemia with fatigue and painful neuropathy. Clinical features of coeliac disease include abdominal discomfort, growth abnormalities, infertility, low bone mineralisation, and iron deficiency anaemia. Adrenal insufficiency may cause vomiting, anorexia, hypoglycaemia, malaise, fatigue, muscular weakness, hyperkalaemia, hypotension, and generalised hyperpigmentation. Here we will review prevalence, pathogenetic factors, clinical features, and suggestions for screening, follow-up and treatment of patients with T1DM and/or autoimmune polyglandular syndrome.
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PMID:Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. 2000 14


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