Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with spinal cord injury (SCI) often suffer from many gastrointestinal (GI) complaints, while delayed GI transit exists in these patients. We are interested in whether the lost sympathetic activity is one of the mechanisms leading to disturbed GI transit in these subjects. Using a noninvasive hydrogen breath test representing orocecal transit time (OCTT) to study GI transit, 36 SCI patients and 12 age- and sex-matched healthy volunteers were enrolled in our study. Meanwhile, electrocardiogram was performed for all subjects. Finally, spectral analysis of heart rate variability (HRV) was then obtained to assess their sympathovagal balance. SCI patients had higher occurrences of GI symptoms, e.g., nausea/vomiting, belching/hiccup, and constipation, compared to controls (P < 0.05). OCTT was delayed in SCI patients compared to controls (180.8 +/- 10.7 vs 98.3 +/- 14.4 min; P < 0.001). The OCTTs of SCI patients were negatively correlated with their low frequencies of HRV (r = -0.384, P = 0.021). In addition, OCTT was further delayed in quadriplegic patients than paraplegic patients (195.8 +/- 14.5 vs 143.6 +/- 19.4 min; P = 0.031). However, neither the SCI etiology, the injury duration, nor the high frequency of HRV had any influence on the delayed OCTT in SCI patients. We conclude that the GI transit of SCI patients is delayed. This transit disturbance is probably due to loss of sympathetic activity, which is one of the essential components in the coordination of GI peristalsis.
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PMID:Loss of sympathetic coordination appears to delay gastrointestinal transit in patients with spinal cord injury. 1686 84

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

Impaired function of the gastrointestinal tract related to diabetes mellitus (DM) results from diabetic autonomous neuropathy, impaired sensory innervation and a direct effect of chronic hyperglycaemia. Another possible connection between DM and the gastrointestinal tract can be infrequent autoimmune diseases associated with type I DM (celiac disease, autoimmune gastropathy, autoimmune chronic pancreatitis). Functional or organic changes resulting from diabetes can be seen in every organ of the gastrointestinal tract. Some of the diabetic gastrointestinal tract difficulties affect almost 60% of patients with long lasting diabetes. On one side, impaired function of individual organs in diabetics can significantly influence level of diabetes compensation and vice versa. On the other side, unsatisfactory diabetes compensation can result in manifestation of digestive problems. The most frequent and the most serious clinical complication is diabetic gastroparesis (DG). The highest incidence of impaired evacuation and motility of the stomach (and the small intestine) is described in diabetics with long lasting unsatisfactory diabetes compensation, microangiopathic complications, and diabetic neuropathy (55-75% in type I diabetes and 15-20% in type II diabetes). Symptoms accompanying impaired motility and emptying of the stomach (feeling of early fullness, eructation, nausea, vomiting and abdominal pains) can be only temporary or can be missing in some patients. Hyperglycaemia accompanied by slowing down evacuation of the stomach is different in patients with an empty stomach--glycaemia over 7.8 mmol/l, and postprandially--antral motility decreases after blood glucose levels get over 9.7 mmol/l. Treatment options for symptomatic diabetic gastroparesis are limited. Achieving normoglycaemia usually improves diabetic gastroparesis but in up to 80% of cases simultaneous administration of prokinetics is necessary.
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PMID:[Gastrointestinal complications in diabetes mellitus]. 1530 28

Functional dyspepsia is a highly prevalent symptom complex and a heterogeneous disorder. Recent studies showed potential associations between specific pathophysiologic disturbances and dyspeptic symptoms. Delayed gastric emptying reported in about 30% of patients with functional dyspepsia is associated with the symptoms of postprandial fullness, nausea, and vomiting. Impaired gastric accommodation present in 40% of functional dyspepsia patients is found to be associated with early satiety. Hypersensitivity to gastric distension is observed in 37% of functional dyspepsia patients and associated with the symptoms of postprandial pain, belching, and weight loss. Psychosocial factors and altered response to duodenal lipids or acid have also been identified as pathophysiologic mechanisms.
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PMID:Pathophysiology of functional dyspepsia. 1532 9

Gastrointestinal (GI) distension by gas expansion may be more of a problem in diving than is usually recognized. In response to a written questionnaire, 2053 scuba divers gave information about GI discomfort such as pain, nausea, and vomiting in connection with diving. One hundred and eleven reports (5.4% of 2053) were considered possible cases of significant GI distension because the majority of divers had their symptoms during ascent and a significant number of them got relief from belching. Difficult middle ear pressure equilibration was a particular problem among divers with GI symptoms. It may have induced frequent swallowing, causing air ingestion and consequent GI problems. Steep, head-first descents appear to have been employed in some dives, leading to GI discomfort presumably be creating large mouth-to-stomach gas-pressure differences. It was concluded that swallowing or any procedure leading to entry of gas into the stomach should be avoided and that belching during diving should be recommended.
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PMID:Nausea and abdominal discomfort--possible relation to aerophagia during diving: an epidemiologic study. 1562 34

Nausea, gastroparesis, and aerophagia are gastrointestinal phenomena that have variable impact on affected patients. The causes of nausea are varied; treatment of these conditions relates to the underlying etiology. Antiemetic agents acting on several distinct receptor subtypes produce benefits in distinct patient subsets. Gastroparesis is characterized by delays in gastric emptying, usually defined scintigraphically. Standard care of gastroparesis relies on dietary modification, antiemetic drug therapy, and initiation of medications that stimulate gastric motor activity. Recent advances include pyloric injection of botulinum toxin and surgical implantation of an electrical neurostimulator. Other surgical therapies are reserved for refractory cases. Aerophagia presents in individuals of normal and impaired cognitive function, most commonly with symptoms of overdistension or eructation. There are no pharmaceutical remedies for this condition; thus, therapy relies on behavioral treatments.
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PMID:Nausea, gastroparesis, and aerophagia. 1579 89

Functional dyspepsia is a highly prevalent symptom complex and a heterogenous disorder. Recent studies showed potential associations between specific pathophysiologic disturbances and dyspeptic symptoms. Delayed gastric emptying reported in about 30% of patients with functional dyspepsia is associated with the symptoms of postprandial fullness, nausea, and vomiting. Impaired gastric accommodation present in 40% of functional dyspepsia patients is found to be associated with early satiety. Hypersensitivity to gastric distension is observed in 37% of functional dyspepsia patients and associated with the symptoms of postprandial pain, belching, and weight loss. Psychosocial factors and altered response to duodenal lipids or acid have also been identified as pathophysiologic mechanisms. Therapeutic options are still limited but targeted therapy directed at the underlying pathophysiology seems desirable. Thus, efforts to further elucidate underlying pathophysiologic mechanisms and identify the appropriate patient population using some type of pathophysiologic testing will be required.
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PMID:Pathophysiology and treatment of functional dyspepsia. 1579 87

Gastroparesis after a pylorus-preserving pancreatoduodenectomy has two main aspects, namely early gastric stasis and subsequent postprandial delayed gastric emptying. Early gastric stasis producing an excessive amount of gastric juice during the immediate postoperative period might be caused by the absence of phase III activity of the gastric migrating motor complex (MMC), and such symptoms usually subside within a month or two. Subsequent postprandial delayed gastric emptying leading to belching, fullness of the stomach, nausea, and vomiting after the resumption of oral intake normally continues for up to 6 months before complete recovery. There are many possible mechanisms to explain these phenomena. The early recovery of phase III of the MMC does not necessarily predict an early relief of postprandial delayed gastric emptying, thus suggesting that these two phenomena are caused by various mechanisms. The phenomena, mechanisms, and treatment strategies for gastroparesis after pylorus-preserving pancreatoduodenectomy are described in this review.
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PMID:Gastroparesis after a pylorus-preserving pancreatoduodenectomy. 1586 14

The purpose of this study was to describe presenting symptoms, diagnostic testing, treatments and outcomes in a group of children with a diagnosis of aerophagia. A computerized diagnostic index was used to identify all children between the age of 1 and 17 years diagnosed with aerophagia at a tertiary care medical centre between 1975 and 2003. Individual medical charts were abstracted for information on the demographics, clinical features, co-morbid diagnoses, diagnostic work up and treatment of children with aerophagia. Information on presenting symptoms was also collected for a group of children who were retrospectively classified as having functional dyspepsia for comparison (n = 40). Forty-five children had a diagnosis of aerophagia. The mean duration of symptoms in children with aerophagia was 16 +/- 5 months. The most common gastrointestinal symptoms were abdominal pain, distention and frequent belching. Children with functional dyspepsia had a higher prevalence of nausea, vomiting, abdominal pain and unintentional weight loss compared to children with aerophagia (all P < 0.05). In conclusion, aerophagia is a disorder that is diagnosed in neurologically normal males and females, who can experience prolonged symptoms. Although many children with aerophagia present with upper gastrointestinal symptoms, the disorder appears to be distinct from functional dyspepsia.
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PMID:Aerophagia in children: characterization of a functional gastrointestinal disorder. 1607 40

A numerically important group of patients with functional gastrointestinal disorders have chronic symptoms that can be attributed to the gastroduodenal region. Based on the consensus opinion of an international panel of clinical investigators who reviewed the available evidence, a classification of the functional gastroduodenal disorders is proposed. Four categories of functional gastroduodenal disorders are distinguished. The first category, functional dyspepsia, groups patients with symptoms thought to originate from the gastroduodenal region, specifically epigastric pain or burning, postprandial fullness, or early satiation. Based on recent evidence and clinical experience, a subgroup classification is proposed for postprandial distress syndrome (early satiation or postprandial fullness) and epigastric pain syndrome (pain or burning in the epigastrium). The second category, belching disorders, comprises aerophagia (troublesome repetitive belching with observed excessive air swallowing) and unspecified belching (no evidence of excessive air swallowing). The third category, nausea and vomiting disorders, comprises chronic idiopathic nausea (frequent bothersome nausea without vomiting), functional vomiting (recurrent vomiting in the absence of self-induced vomiting, or underlying eating disorders, metabolic disorders, drug intake, or psychiatric or central nervous system disorders), and cyclic vomiting syndrome (stereotypical episodes of vomiting with vomiting-free intervals). The rumination syndrome is a fourth category of functional gastroduodenal disorder characterized by effortless regurgitation of recently ingested food into the mouth followed by rechewing and reswallowing or expulsion. The proposed classification requires further research and careful validation but the criteria should be of value for clinical practice; for epidemiological, pathophysiological, and clinical management studies; and for drug development.
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PMID:Functional gastroduodenal disorders. 1667 60


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