Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical features of the Mallory-Weiss syndrome were prospectively documented in 130 of 1 667 patients submitted to endoscopy for gastro-intestinal haemorrhage, an incidence of 7,8%. The important clinical features found in these patients were: alcohol abuse (21%); retching or vomiting (38%); salicylate ingestion (36%); dyspepsia (39%). The correct clinical diagnosis was therefore often difficult to make. Additional lesions were found in 40% of patients at endoscopy. Blood loss was relatively small, and surgery was not required in any patient. The 2 deaths that occurred were not attributable to haemorrhage. A high index of suspicion and early endoscopy are required to establish the diagnosis.
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PMID:The Mallory-Weiss syndrome. A prospective study in 130 patients. 30 21

The association of chronic obstructive pulmonary disease (COPD) with esophageal-gastric and duodenal disease is very common. In our experience 21.8% of patients with COPD were affected by peptic ulcer and 50.9% by inflammatory disease of upper digestive tract. This association appears independent from smoking and alcohol abuse. Dyspepsia and corticosteroid therapy were associated with endoscopic lesions (dyspepsia was present in 75.6% of patients with abnormal endoscopy vs 42.8% without endoscopic lesions, p less than 0.01 and corticosteroid therapy in 43.9% vs 0, p less than 0.001). On the contrary therapy with theophylline and beta 2-adrenoceptor-agonists is not associated with digestive disease. Spirometric parameters and blood gas analysis were not different among patients with and without endoscopic lesions. We suggest endoscopy of upper digestive tract in patients affected by COPD with dyspepsia and/or corticosteroid therapy.
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PMID:[Association of chronic obstructive bronchitis and upper digestive pathology. A clinical study]. 176 30

The most common toxicities of nonsteroidal anti-inflammatory drugs (NSAIDs) are gastropathy, renal dysfunction, and liver function abnormalities. We outline an approach to monitoring patients on long-term NSAID therapy, focusing on the early detection of complications. Gastropathy caused by NSAID use is more common in elderly patients or those with a history of dyspepsia, peptic ulcer disease, or alcohol abuse. Fecal occult blood testing and hemograms are less accurate in detecting gastropathy than direct visualization but are convenient and relatively inexpensive. We recommend the periodic use of these tests to detect NSAID-induced acute or chronic blood loss. Renal toxicity is seen in patients with preexisting renal disease or functional volume depletion and in the elderly. Complications include renal insufficiency, hyponatremia, hyperkalemia, and protein-uria. Renal function should be monitored during the first few weeks of NSAID therapy, especially in high-risk patients, with periodic testing thereafter. Hepatic toxicity is less common but warrants occasional determinations of alanine aminotransferase levels. Elderly patients and those with renal insufficiency or alcohol abuse have a higher risk of complications. Nonsteroidal anti-inflammatory drugs should be used cautiously in those patients at high risk for complications. Strategies can be used to limit toxicity. Patients taking these drugs long term should be monitored periodically for signs of blood loss, renal dysfunction, and hepatic dysfunction.
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PMID:Nonsteroidal anti-inflammatory drugs. Proposed guidelines for monitoring toxicity. 187 28

Ulcer-like epigastric symptoms constitute the most common presentation in acute abdominal complaints. A prospective study of such patients attending a surgical emergency unit is presented. Among the patients with dyspepsia, the numbers per thousand population varied between different parts of the city from 0 to 45. Most of the patients with dyspepsia were seen early in the week. Men, unmarried persons and immigrants were overrepresented in the dyspepsia group, and the relative figures for low educational status, history of alcohol abuse and smoking were higher than expected from city averages. Sick-listing during the preceding year exceeded 90 days in 17% of this group. The observed associations indicated the advisability of preventive measures.
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PMID:Social and demographic characteristics of 20-29-year-olds attending the emergency room for dyspepsia. 360 21

The causes of functional dyspepsia remain unclear. Research has linked other functional gastrointestinal disorders, particularly irritable bowel syndrome, to a history of physical or sexual abuse, psychosocial distress and certain psychiatric disorders. In functional dyspepsia, there is a possibility of certain psychiatric disorders, particularly alcohol abuse and eating disorders, indirectly influencing the development of functional dyspepsia-like symptoms. However, the literature on possible psychosocial correlates in functional dyspepsia is not as mature as the literature on irritable bowel syndrome. This paper critically reviews the psychosocial dimensions and implications for the psychotherapeutic treatment of functional dyspepsia.
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PMID:Are psychosocial factors of aetiological importance in functional dyspepsia? 989 88

The intake of larger quantities of alcoholic beverages leads to manifold functional disturbances and organ injury in the upper gastrointestinal tract. These damaging effects of alcohol are frequently the cause of complaints, such as heart burn, symptoms of dyspepsia and diarrhoea. Examples of more pronounced organ injury which can occur even following a single episode of heavy drinking are tears in the mucosa at the junction of the esophagus and the stomach (Mallory-Weiss-lesion) and hemorrhagic erosions in the stomach and/or the duodenum which may lead to massive bleeding. In the small intestine alcohol abuse interferes with the absorption of glucose, amino acids, lipids, water, sodium and vitamins (especially thiamine and folic acid). This inhibition of absorption of nutrients may contribute to nutritional deficiencies frequently observed in alcoholics. Acute alcohol ingestion can also damage the mucosa in the upper region of the small intestine and may lead to the disruption of the tips of the villi. Chronic alcohol abuse increases markedly the prevalence of bacterial overgrowth in the small intestine. The findings of human and animal studies suggest that the mucosal injury together with bacterial overgrowth favour the following sequence of events: Alcohol induced mucosal injury in the small intestine increases the permeability of the mucosa to macromolecules, such as endotoxin and/or other bacterial toxins, into the blood or lymph. This results in the release of potentially toxic cytokines and other mediators like Kupfer cells and other phagocytes. These cytokines and other mediators, in turn, exert multiple injurious effects on the microcirculation and membranes. The result is cell damage and even cell death (apoptosis, necrosis) in the liver and other organs. Chronic alcohol abuse is one of the most important risk factors for the development of cancers of the tongue, larynx, pharynx and esophagus. In many countries alcohol abuse is the most important cause for the development of chronic pancreatitis. In the initial phase the disease is frequently characterised by episodes of 'acute' pancreatitis. These episodes develop only on the basis of prolonged alcohol abuse leading to subclinical damage of the gland. The latter is found in about 20-50% of patients with chronic alcohol abuse while the clinically overt pancreatitis is observed in only 1%-3% of alcoholics. Despite numerous studies performed in animal experiments and man the pathogenesis of alcoholic pancreatitis until now has not been clarified.
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PMID:[Alcohol, the gastrointestinal tract and pancreas]. 1080 79