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)

Alpha-methyldopa-induced histologic alterations were investigated in 21 patients with hepatic injury after short- and long-term exposure. Seven patients developed liver injury within 6 months and 24 after several years (mean, 5 years) of exposure. Histologic findings and clinical and biochemical data differed significantly in the two groups. Morphologic analysis of the short-term-treated group revealed marked parenchymatous degeneration, focal, confluent and massive necrosis, and inflammation. Fatty accumulation and increased fibrous trabeculae were characteristic for the patients treated for long term. All patients in the short-term-exposed group had acute and severe hepatitis. Four of them had icterus. Two patients died of hepatic coma. Patients in the long-term-treated group had for several months initially mild but increasing discomfort, dyspepsia, nausea, and colics. Liver function tests in these groups revealed differences in serum albumin, bilirubin, and transferase levels. No changes were observed in alkaline phosphatase and Thrombotest. Fat accumulation and fibrous trabeculae suggest that the alterations precede the clinical symptoms and biochemical signs of hepatitis. The findings show that alpha-methyldopa may induce hepatocellular injury after short- and long-term exposure.
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PMID:Morphologic alterations in patients with alpha-methyldopa-induced liver damage after short- and long-term exposure. 732 15

We have administered Isobutyramide as a suspension over a period of 3 months, from a starting dose of 50 mg/kg/day up to 150 mg/kg/day, to four adult sickle cell (SS) anemia patients. The maximum dose was maintained for 3 weeks. The blood counts remained stable and the Hb F levels decreased slightly. The G gamma levels increased at the end of the trial, suggesting activation of the G gamma gene at the highest dose of Isobutyramide. Three patients showed a stable rate of hemolysis, while in one patient, an increase of lactate dehydrogenase occurred. None of the patients experienced pain crisis or organ-specific crisis, but all four complained about mild epigastric burning and a bitter taste. After the first month of treatment one patient complained about intolerable epigastric discomfort which was relieved by Omeprazole. Another patient complained about increasing dyspepsia in the 12th week leading to the termination of the trial. Oral Isobutyramide administration does not qualify as an effective treatment of SS patients.
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PMID:Isobutyramide therapy in patients with sickle cell anemia. 754 4

In patients who present with chronic unexplained upper abdominal pain or discomfort (functional dyspepsia), therapy should ideally be targeted on correcting the individual's disturbed pathophysiology. Here, putative mechanisms implicated in functional dyspepsia and potential approaches to therapy are critically reviewed in order to determine if targeting treatment is of value. Pharmacological therapies reviewed include those that aim to correct disordered gastric emptying (e.g. cisapride, dopaminergic receptor antagonists, macrolides), reduce visceral hypersensitivity (e.g. somatostatin analogues, cholecystokinin antagonists, opioid agonists, serotonin type 3 receptor antagonists), reduce gastric acid secretion (e.g. H2-blockers, acid pump inhibitors), cure Helicobacter pylori infection, enhance muscosal defence (e.g. sucralfate, bismuth) or modify central nervous system processes. It is concluded that the imperfectly understood pathophysiology of functional dyspepsia contributes to the paucity of established efficacious therapies.
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PMID:Review article: functional dyspepsia--should treatment be targeted on disturbed physiology? 760 50

It is widely appreciated that visceral pain differs significantly from pain that arises from cutaneous structures. Visceral pain is difficult for both the patient and physician to localize because it is diffuse in character and is typically referred to cutaneous structures. Further, there are differences between acute, post-operative visceral pain and the altered sensations associated with the so-called functional bowel disorders (e.g. non-ulcer dyspepsia, non-cardiac chest pain and irritable bowel syndrome). A variety of considerations suggests that sensory inputs from the fiscera, like nociceptive inputs from the skin, can be sensitized. Accordingly, inputs from the viscera that are not typically perceived may give rise to discomfort and pain if either visceral afferent fibres are sensitized or central neurones undergo a change in excitability ('central sensitization') after persistent visceral input. The anatomy and potential mechanisms associated with visceral hyperalgesia will be considered as will new information about opioid modulation of visceral inputs to the spinal cord.
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PMID:Visceral nociception: consequences, modulation and the future. 764 39

Alteration in visceral sensation locally at the site of presumed symptom origin in the gastrointestinal tract has been proposed as an important etiopathological mechanism in the so-called functional bowel disorders. Patients presenting with one functional gastrointestinal syndrome, however, frequently have additional symptoms referable to other parts of the gut, suggesting that enhanced visceral nociception may be a panintestinal phenomenon. We measured the sensory thresholds for initial perception (IP), desire to defecate (DD), and urgency (U) in response to rectal balloon distension, and the thresholds for initial perception and for discomfort in response to esophageal balloon distension in 12 patients with irritable bowel syndrome (IBS) and 10 patients with functional dyspepsia (FD), in comparison with healthy controls. As expected, IBS patients exhibited lower rectal sensory thresholds than controls (P < 0.0001), but in addition had significantly lower sensory thresholds for both perception and discomfort evoked by balloon distension of the esophagus (mean +/- SEM: 8.8 +/- 1.3 ml vs 12.1 +/- 1.5 ml (P < 0.05) and 12.2 +/- 1.4 ml vs 16.4 +/- 1.4 ml (P < 0.02) respectively. Patients with FD showed similarly enhanced esophageal sensitivity, with thresholds for perception and discomfort of 8.1 +/- 0.9 ml (P < 0.02), and 10.1 +/- 1.0 ml (p < 0.001), respectively, but were also found to have sensory thresholds for rectal distension similar to those observed in the IBS group, significantly lower than in controls: IP 45.0 +/- 17.6 vs 59.3 +/- 1.5 ml (P < 0.001), DD 98.0 +/- 17.9 vs 298.7 +/- 9.0 ml (P < 0.0001), U 177.2 +/- 25.4 vs 415.1 +/- 12.6 ml (p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heightened visceral sensation in functional gastrointestinal disease is not site-specific. Evidence for a generalized disorder of gut sensitivity. 764 57

Intraduodenal lipid infusion induces symptoms and increases sensitivity to gastric distension in patients with functional dyspepsia. To test whether these effects are specific for lipid, we compared the effects of intraduodenal infusions of either lipid or glucose on symptoms and gastric sensory and motor responses to gastric distension. Eighteen dyspeptic patients and nine controls were studied. The stomach was distended with a flaccid bag during isocaloric infusions (1 kcal/ml) of saline and either 10% Intralipid (nine patients) or 26.7% glucose (nine patients) into the duodenum. Dyspeptic symptoms and sensory thresholds for epigastric fullness and discomfort were assessed. Gastric pressure profiles during distensions were similar during lipid and glucose infusions in patients and controls, but both were significantly lower than during saline infusion. Lower volumes were required to induce fullness and discomfort in the patients compared with the controls. In the controls, the threshold volumes required to induce fullness and discomfort were greater during infusion of lipid and glucose than during saline infusion, but in the patients, the threshold volumes were increased during glucose infusion but further reduced during lipid infusion. Moreover, in the patients, nausea was more common during lipid than glucose infusion and did not occur during saline. The controls did not experience any symptoms during any infusion. In conclusion, intraduodenal lipid but not glucose sensitizes the stomach to distension in patients with functional dyspepsia but not in controls.
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PMID:Nutrient-specific modulation of gastric mechanosensitivity in patients with functional dyspepsia. 764 62

Postprandial bloating and fullness are commonly found both in dysmotility like functional dyspepsia, and after vagotomy but the relation between gastric accommodation and symptom production has not been investigated. Intragastric pressure levels and symptoms developed during controlled distension of the gastric fundus were recorded in nine patients with functional dyspepsia, in seven patients after truncal vagotomy, and in 11 healthy volunteers. The procedure was repeated after ingestion of a liquid nutrient meal (250 ml; 250 kcal). Gastric tone, expressed as the average value of pressure over the distension period was lower in controls (median: 11.3 mm Hg) than in either the dyspeptic patients (median: 16.48 mm Hg) or postvagotomy patients (median: 19.12 mm Hg) (p < 0.05). Meal ingestion reduced gastric tone in controls, but no significant change occurred in either the dyspepsia or the postvagotomy patients. Volumes at which discomfort was elicited by distension during fasting were lower both in dyspeptic patients (median: 210 ml) and in postvagotomy patients (median: 180 ml) than in healthy volunteers (median: 660 ml) (p < 0.05). Discomfort thresholds were unaffected by meal ingestion. These results suggest that a disturbance of gastric relaxation may be related to symptom development in dysmotility like functional dyspepsia, while similarities between dyspeptic patients and postvagotomy patients suggest that the impaired gastric accommodation in functional dyspepsia may be due to an underlying vagal defect.
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PMID:Relations between upper abdominal symptoms and gastric distension abnormalities in dysmotility like functional dyspepsia and after vagotomy. 767 73

The role of Helicobacter pylori infection in the pathogenesis of functional dyspepsia is debated. It is known that a substantial fraction of dyspeptic patients manifest a low discomfort threshold to gastric distension. This study investigated the symptomatic pattern in 27 H pylori positive and 23 H pylori negative patients with chronic functional dyspepsia, and potential relations between infection and gastric hyperalgesia. Specific symptoms (pain, nausea, vomiting, bloating/fullness, early satiety) were scored from 0 to 3 for severity and frequency (global symptom scores: 0-15). The mechanical and perceptive responses to gastric accommodation were evaluated with an electronic barostat that produced graded isobaric distensions from 0 to 20 mm Hg in 2 mm Hg steps up to 600 ml. Gastric compliance (volume/pressure relation) and perception (rating scale: 0-10) were quantified. Standard gastrointestinal manometry and recorded phasic pressure activity at eight separate sites during fasting and postprandially were also assessed. H pylori positive and H pylori negative patients manifested similar severity and frequency of specific symptoms and global symptom scores (mean (SEM)) (severity: 9.5 (2.0) v 9.0 (2.1); frequency: 10.8 (2.0) v 9.7 (2.2)). No differences were seen either in gastric compliance (53 (4) ml/mm Hg v 43 (3) ml/mm Hg) or in gastric perception of distension (slope: 0.50 (0.05) v 0.53 (0.06)). Postprandial antral motility was significantly decreased in H pylori positive patients (two hours motility index: 10.4 (0.6) v 12.6 (0.5); p < 0.05). It is concluded that H pylori infected patients with functional dyspepsia present no distinctive symptoms by comparison with H pylori negative counterparts and H pylori infection is associated with diminished postprandial antral motility but it does not increase perception of gastric distension.
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PMID:Does Helicobacter pylori infection increase gastric sensitivity in functional dyspepsia? 767 80

Symptoms of functional dyspepsia are frequent; the prevalence of dyspepsia (defined as pain or discomfort centred in the upper abdomen) in the general population approaches 25%. By definition, patients with functional dyspepsia do not have a structural or biochemical explanation for their symptoms. Disorders of function (e.g. delayed gastric emptying) are detectable in a proportion of patients but remain poorly understood. Nevertheless, the current rationale for drug treatment is based on altering pathophysiological mechanisms which are believed to be associated with the development of symptoms. Although the placebo response rates approach 60%, prokinetics, acid-suppressing agents and bismuth-containing compounds have been shown to be significantly better than placebo in reducing symptoms. Antacids are widely used, but no controlled study has been able to demonstrate a significant benefit over placebo. The efficacy of sucralfate is uncertain. Rational guidelines on which drug should be used for a given patient are lacking, although approaches based on symptom profiles have been proposed; the duration of treatment needed to achieve long-lasting relief of symptoms is also poorly defined. Identifying optimal treatment for the individual patient, therefore, continues to be largely a trial and error process. Further research efforts are needed to elucidate the pathophysiological basis of functional dyspepsia so that specific therapy can be tailored to underlying pathophysiological disturbances.
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PMID:Functional dyspepsia. Current treatment recommendations. 769 99

Patients with duodenal ulcer or functional dyspepsia do not differ on dyspeptic symptoms. The aim of the present study was to test the hypothesis that functional dyspepsia and duodenal ulcer are two different diagnostic entities by examining the discriminating power of several anamnestic, biological, and psychosocial variables. Ninety-four patients with duodenal ulcer and 86 patients with functional dyspepsia were included. Anamnestic data, global assessment, Helicobacter pylori status, blood group, Lewisa+ phenotype, and several measures of psychological distress and somatic complaints were registered. Compared to patients with functional dyspepsia, the duodenal ulcer patients were more often infected by Helicobacter pylori and had their stomach discomfort more often relieved by eating. Compared to patients with duodenal ulcer, patients with functional dyspepsia had higher scores of depression, trait anxiety, general psychopathology and different somatic complaints (called somatization). They were also less satisfied with the health care system, their disorder had a greater negative impact on their quality of life, and their global assessment of own health was poorer. Discriminant analysis including age, smoking, Helicobacter pylori status, global assessment, and somatic complaint classified 86.1% of the patients correctly (77.9% of the patients with functional dyspepsia and 93.6% of the patients with duodenal ulcer). It is concluded that duodenal ulcer and functional dyspepsia are two separate diagnostic entities. Patients with duodenal ulcer are older, smoke more often, and almost all are infected with Helicobacter pylori, while patients with functional dyspepsia are characterized by somatization and a negative assessment of their own health.
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PMID:Discriminant analysis of factors distinguishing patients with functional dyspepsia from patients with duodenal ulcer. Significance of somatization. 772 72


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