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)

A preliminary dose-range finding study and a 13-week toxicity study were performed in male cynomolgus monkeys with catena-(S)-[mu-[N a-(3-aminopropionyl) histidinato (2-)-N1,N2,O:N tau]-zinc] (Z-103, CAS 107667-60-7), a novel anti-peptic ulcer agent, as part of a safety evaluation program. In the preliminary ascending dose study emesis was observed in animals treated at 625 mg/kg and transient reductions in food intake with associated body weight loss in a male treated at 625 or 312.5 mg/kg. Plasma zinc levels were also increased in all animals treated at 625 or 312.5 mg/kg. As a result dosages of 0, 20, 63 and 200 mg/kg/day were selected for the 13-week toxicity study. In this study, treatment-related changes were confined to the 200 mg/kg/day dosage and consisted of emesis, piloerection and transient body weight loss in one animal, increased plasma zinc concentrations, and zinc and copper deposition in the liver and kidneys without any associated morphological change. The no observed effect level was estimated to be 63 mg/kg/day in this study.
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PMID:Toxicity of the novel anti-peptic ulcer agent catena-(S)-[mu-[Na- (3-aminopropionyl)histidinato(2-)-N1,N2,Q:N tau]-zinc in male cynomolgus monkeys. 832 1

The role played by Helicobacter pylori in the pathogenesis of peptic ulcer disease (PUD) is discussed, and the epidemiology, identification, diagnosis, eradication, and treatment of H. pylori infection are reviewed. Isolation of H. pylori from up to 100% of patients with duodenal ulcer and 80% of patients with gastric ulcer establishes a strong association between H. pylori and idiopathic PUD, although other factors also may be essential for the development of PUD. Invasive procedures for diagnosis of H. pylori infection include upper endoscopy and biopsy of gastroduodenal tissues followed by culture or the rapid urea test; noninvasive tests include the urea breath tests and serology. Although H. pylori is susceptible to a number of antimicrobials, eradication (as opposed to suppression) of this organism has been a major challenge. The most important predictive factor for clinical and microbiological efficacy is the pretreatment susceptibility of H. pylori to nitroimidazoles. Triple therapy with bismuth, metronidazole, and either amoxicillin or tetracycline has resulted in better clinical and microbiological outcomes than either monotherapy or dual therapy. Possible adverse effects of this regimen include nausea, vomiting, taste disturbance, and diarrhea. Anti-H. pylori therapy should be reserved for those patients who have recurrent symptomatic or intractable PUD. Currently, the regimen of choice includes bismuth, metronidazole, and either amoxicillin or tetracycline given for at least two weeks.
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PMID:Helicobacter pylori and peptic ulcer disease. 842 32

Infection due to Helicobacter pylori may be associated with gastritis and peptic ulcer disease in children. The aim of this study was to compare the presentation of gastritis due to H pylori with that of gastritis not associated with H pylori infection. The medical records of 296 children who had esophagogastroduodenoscopy were reviewed; 23 (8%) had H pylori gastritis, and 51 had primary gastritis without H pylori infection. Of patients with H pylori, 43% had antral nodularity and 17% had duodenal ulcers. The incidence of epigastric pain, nocturnal pain, postprandial pain, family history of peptic ulcer disease, water brash, vomiting, weight loss, fecal occult blood, and hematemesis was similar between both groups. Periumbilical pain was less common in children with gastritis than epigastric pain, and pain in the periumbilical region was present in only 4% of children with H pylori infection, compared with 31% of patients who had gastritis without H pylori infection. The presence of H pylori should be sought in children having endoscopy for evaluation of upper gastrointestinal mucosal disease.
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PMID:Symptoms of gastritis due to Helicobacter pylori in children. 860 56

Milk-alkali syndrome is characterized by progressive hypercalcemia, systemic alkalosis, and renal insufficiency. After calcium carbonate is ingested with diary products, hypercalcemia and alkalosis may develop in susceptible persons, particularly those with underlying renal insufficiency. We describe a young woman who neither drank milk nor had peptic ulcer disease, yet who ingested enough calcium carbonate to require admission to an intensive care unit for acute renal failure. Chronically bulimic, she was taking Rolaids (Warner-Lambert Co, Morris Plains, NJ), which contained calcium carbonate, and was eating yogurt daily to prevent osteoporosis. We discuss the characteristics and complex metabolic interactions of the milk-alkali syndrome, a critical but generally reversible electrolyte disorder. Early recognition of coincident hypercalcemia and alkalosis and prompt cessation of calcium carbonate ingestion are essential for successful recovery. Finally, we suggest that nephrologists should discourage patients with renal insufficiency and chronic vomiting from consuming calcium-containing antacids and excessive dietary calcium.
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PMID:Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome. 865 5

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

We have experienced a case who showed the gastric tube-right main bronchus fistula. A 51-year-old male complained cough and vomiting suddenly. He underwent esophagectomy and radio-chemotherapy for advanced esophageal cancer 19 months ago. Chest X-ray showed severe pneumonia, and gastroscopy, bronchoscopy and CT scan showed the fistula between the whole stomach esophageal substitute and right main bronchus. After recovery from the pneumonia with the treatment by continuous suction through the naso-gastric tube, operation was performed. The fistula was repaired with transposition of a pedicled pectralis major muscle successfully. After the operation, respiration was performed independently with two ventilators for right and left lung to avoid increasing air way pressure. His postoperative course was uneventful, and he discharged on the 66th postoperative day. The cause of the fistula was considered to be a peptic ulcer due to residual secretion of gastric acid.
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PMID:[Repair of the gastric tube-right main bronchus fistula after operation for esophageal cancer--treatment by transposition of pedicled pectoralis major muscle flap]. 891 Oct 50

Intramural duodenal hematoma is rarely seen in adults and may occur as an iatrogenic complication of endoscopic injection for peptic ulcer treatment. In the appropriate clinical setting, the diagnosis is easy with its ultrasonography and computed tomography characteristic findings. In one of our patients, UGI study revealed duodenal obstruction, bowel related lesion in sonography and hyperdense mass lesion in computed tomography. Clinical presentation of severe vomiting and epigastralgia were noted. Laparoscopy confirmed the location of the hematoma and subsequent evacuation was performed. The symptoms were relieved after the operation and a follow-up sonography demonstrated the regression of the duodenal hematoma.
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PMID:Laparoscopic finding and imaging of the iatrogenic duodenal intramural hematoma. 905 32

Postemetic spontaneous rupture of the esophagus is an intrathoracic disaster which is generally lethal if untreated. The tragedy seems to strike more often than commonly suspected. The current literature review focuses on publications since 1980 and includes the retrospective review of 18 additional patients treated in our hospital for spontaneous rupture of the esophagus. Frequently, a wide variety of unspecific symptoms has led to the mistaken diagnosis of an acute abdomen, pancreatitis or cardiac arrest. About 40% of the patients with spontaneous rupture of the esophagus presented a history of alcoholism or heavy drinking and 41% suffered from gastroduodenal ulcer disease. Pain (83%) and vomiting (79%) often associated with dyspnea (39%) and shock (32%) are the major symptoms. This unspecific symptomatology delayed the correct diagnosis of the Boerhaave's syndrome and resulted in a significant complication rate. The mortality rate associated with Boerhaave's syndrome was 50% from the first successful surgical repair in 1947 by Barrett to 1980. After 1980, however, the mortality rate dropped to 31%, because of earlier diagnosis, surgical repair and improvement in intensive care. When surgery is delayed, the prognosis of patients with spontaneous rupture of the esophagus is in general severe.
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PMID:Boerhaave's syndrome: analysis of the literature and report of 18 new cases. 907 78

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

Nausea, vomiting, and abdominal pain are common symptoms that suggest many diagnoses. The patient's symptoms may be related to an anatomical defect such as a peptic ulcer or a mechanical small bowel obstruction. However, no anatomical abnormality may be identified despite radiological, endoscopic, or laboratory studies. The cause of the patient's symptoms may have significant impact on the patient's quality of life (nonulcer dyspepsia) and life span (intestinal pseudo-obstruction). Abnormal antroduodenal motility may be the underlying cause of the patient's symptoms. Normally, coordinated phasic contractions in the stomach and small intestine maintain digestion and absorption of food. A prolonged set of phasic contractions (phase 3 of the migrating complex) begins in the stomach and propagates down the small intestine to excrete nondigestible foods, bacteria, and dead cells. Any disturbance in the normal motility pattern can lead to maldigestion and symptoms of upper intestinal dysfunction. Objective tests of motility disturbances in the stomach and small intestine include measurement of gastric emptying, intestinal transit, contractions of the stomach and duodenum, and electrogastrography. Abnormal antroduodenal motility may be secondary to an abnormality in the smooth muscle (myopathy) or the nerves in controlling smooth muscle contractions (neuropathy). Antroduodenal motility measurements may help identify a partial small bowel obstruction, the cause of small intestinal overgrowth, and the cause of chronic abdominal visceral pain. Motility studies may suggest useful drugs for correcting the underlying pathophysiology and relieving symptoms.
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PMID:Role of motility measurements in managing upper gastrointestinal dysfunction. 953 Nov 16


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