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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In light of the lack of any prior systematic evaluations of the prevalence and types of pain syndromes and treatments found in patients with AIDS, a chart review study was undertaken to evaluate this issue. Fifty-two of 96 charts reviewed (54%) had at least one note on nonprocedural pain or analgesic prescription. Although chest pain was the most prevalent pain location (22%), presumably because of the high incidence of Pneumocystis carinii pneumonia, other possible AIDS-related entities, such as peripheral neuropathy and thrombophlebitis, were also found. No specific AIDS syndromes could be identified that were related to a higher incidence of pain. Nearly one-third of patients with pain received codeine (31%), others received acetaminophen (27%), and 17% of patients received acetaminophen and oxycodone HCl. Specific pain management interventions must be evaluated and applied to control the nontrivial occurrence of pain in patients who have AIDS symptoms that may be overlooked by the physician given the overwhelming disease process.
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PMID:The prevalence and management of pain in patients with AIDS: a review of 134 cases. 252 Apr 10

Sixty consecutive patients referred for evaluation of non-cardiac chest pain had oesophageal manometry. Motility was assessed basally, after edrophonium 80 micrograms/kg iv and during oesophageal perfusion with 0.1 N HCl at 6 and 14 ml/min for eight and seven minutes respectively. A positive response, defined as symptom reproduction with or without abnormal motility, was present in 21 patients (35%) after acid perfusion and 12 (20%) after edrophonium. Eleven of the 12 patients responding to edrophonium also responded to acid perfusion, including most of the patients with primary motility disorders. Significantly greater increases in peristaltic duration, but not amplitude, were recorded after edrophonium (p less than 0.01) and acid perfusion (p less than 0.05) in positive responders, compared with non-responders. Results indicate that acid perfusion during oesophageal manometry may be a more useful stress test than edrophonium and that the mechanism of symptom production may be similar.
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PMID:Comparison of intravenous edrophonium and oesophageal acid perfusion during oesophageal manometry in patients with non-cardiac chest pain. 341 Mar 28

The effect of hypertonic glucose as a provocative test was studied in 51 patients with noncardiac chest pain, 15 patients with esophagitis, and 16 asymptomatic controls. It was compared to esophageal perfusion with 0.1 N HCl and saline and intravenous administration of 10 mg edrophonium. Continuous esophageal manometric recordings were performed at the time of testing. The patients' symptoms were monitored every minute. The effect of these solutions and edrophonium on lower esophageal sphincter (LES) pressure and amplitude of esophageal contractions was also evaluated. Esophageal perfusion with hypertonic glucose, saline, or acid had no significant effect on LES pressure or amplitude of esophageal contractions in most patients. Edrophonium, however, resulted in a significant rise in the amplitude of esophageal contractions and the LES pressure in all groups studied. Hypertonic glucose resulted in chest pain in 13.6% of patients with noncardiac chest pain and 20% of those with esophagitis, whereas edrophonium reproduced the pain in 38.7 and 37%, respectively. Our results indicate that hypertonic glucose is not effective as a provocative test for noncardiac chest pain nor does it contribute to the chest pain in esophagitis. They also had no significant effect on the amplitude of esophageal contractions or LES pressure. Edrophonium continues to be a relatively sensitive test for noncardiac chest pain.
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PMID:Comparison of hypertonic glucose to other provocative tests in patients with noncardiac chest pain. 357 20

Concern about upper respiratory tract irritation and other symptoms among workers at a glass bottle manufacturing plant led to an epidemiologic and an industrial hygiene survey. Questionnaire responses from 35 hot end and 53 cold end workers indicated that the incidence of wheezing, chest pain, dyspnea on exertion, and cough was significantly elevated among hot end workers. Among both smokers and nonsmokers, hot end workers reported higher, but not significantly higher, rates of wheezing and chest pain. Among smokers, hot end workers reported significantly higher rates of dyspnea on exertion and cough than did cold end workers. Data suggest that reported exposure to stannic chloride solution likely caused these symptoms. The industrial hygiene survey, conducted when stannic chloride use had been reduced, cleaning had been done, and ventilation improved, focused on measuring air contaminants that might possibly cause symptoms. Levels of hydrogen chloride, which apparently was formed by the combination of stannic chloride and water in the presence of heat, were elevated. The finding of increased prevalence of respiratory symptoms among hot end workers was consistent with this exposure. Recommendations were made to reduce hazardous exposures at this plant. Individuals responsible for occupational health should be aware that relatively benign substances, such as stannic chloride and water, can combine spontaneously to form hazardous substances.
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PMID:Respiratory symptoms among glass bottle makers exposed to stannic chloride solution and other potentially hazardous substances. 399 80

Thirty-four consecutive patients referred to a gastroenterology clinic with suspected esophageal motility abnormality as a cause of their chest pain or dysphagia, or both, were prospectively studied in an 18-mo period. Peristaltic response to 10 wet (5 ml H2O) swallows was recorded in all studies with a low-compliance infusion system. To provoke symptoms and motility abnormalities after baseline evaluation, all patients had acid infusions (0.1 N HCl) and administration of edrophonium (80 micrograms/kg i.v.), pentagastrin (6 micrograms/kg s.c.), and bethanechol (40 micrograms/kg s.c.). Tracings were coded, read, and interpreted blindly. Baseline tracings were abnormal in 23 of 34 patients (68%), including increased amplitude peristaltic contractions ("nutcracker esophagus") in 10 and nonspecific esophageal motor disorders in 13. Acid infusion produced substernal burning in 3 of 33 patients, in motility change in 1 patient. Edrophonium produced chest pain with manometric changes in 6 of 34 (18%) patients. Pentagastrin produced chest pain with manometric change in 1 patient. Bethanechol produced chest pain with manometric change in 2 patients. One patient with low amplitude had elevation of esophageal baseline and multiple simultaneous contractions but no chest pain (subsequently developed achalasia). It was concluded that (a) abnormal motility is a common finding in a symptomatic group of patients with presumed esophageal motility disorder, (b) the "nutcracker" esophagus is the most frequent defect, and (c) attempted provocation of symptoms with acid or drugs is not generally effective; however, edrophonium is the best tolerated and most effective of currently available drugs.
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PMID:Prospective manometric evaluation with pharmacologic provocation of patients with suspected esophageal motility dysfunction. 683 64

In order to differentiate the cardiac or oesophageal origin of chest pain, 55 patients with chest pain, normal coronary arteriogram and normal left ventricular function, were studied. Patients were evaluated with ergonovine test to induce coronary artery spasm and oesophageal function study (including basal manometry in all cases, ClH acid instillation in 53, manometry during ClH instillation in 32 and edrophonium test in 9). There was coronary artery spasm following ergonovine test in 8 patients (group 1) and negative results in 47 (group 2). There was oesophageal disfunction in 50% patients in group 1 and in 62% patients in group 2 (p = NS). The incidence of motor disorders or chest pain following acid instillation was not significatively different in both groups. Nevertheless, in group 1 a tendency to a greater incidence of oesophageal spasm was observed while in group 2 unspecified disorders were more frequent. Thus, in patients with chest pain and normal coronary arteriogram, we always must discard coronary artery spasm and oesophageal disfunction, because, due to a probably common cause, association between both disorders is frequent.
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PMID:[Chest pain of esophageal origin in patients with a normal coronary angiogram and ergonovine-induced coronary spasm]. 843 Feb 34

Esophageal hypersensitivity is one of the most common causes of noncardiac chest pain in patients. In this study, we investigated whether exposure of the esophagus to acid and other chemical irritants affected activity of thoracic spinal neurons responding to esophageal distension (ED) in rats. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital sodium-anesthetized, -paralyzed, and -ventilated male rats. ED (0.2 or 0.4 ml, 20 s) was produced by water inflation of a latex balloon placed orally into the middle thoracic region of the esophagus. The chemicals were administered via a tube that was passed through the stomach and placed in the thoracic esophagus. To irritate the esophagus, 0.2 ml of HCl (0.01 N), bradykinin (10 microg/ml), or capsaicin (10 microg/ml) were injected for 1-2 min. Only neurons excited by ED were included in this study. Results showed that intraesophageal instillation of HCl, bradykinin, and capsaicin increased activity in 3/20 (15%), 7/25 (28%), and 9/20 (45%) neurons but enhanced excitatory responses to ED in 9/17 (53%), 8/15 (53%), and 7/11 (64%) of the remaining spinal neurons, respectively. Furthermore, intraesophageal chemicals were more likely to enhance the responsiveness of low-threshold neurons than high-threshold neurons to the esophageal mechanical stimulus. Normal saline (pH 7.4, 0.2 ml) or vehicle instilled in the esophagus did not significantly affect activity or ED responses of neurons. We conclude that enhanced responses of thoracic spinal neurons to ED by the chemically challenged esophagus may provide a possible pathophysiological basis for visceral hypersensitivity in patients with gastroesophageal reflux and/or esophagitis.
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PMID:Intraesophageal chemicals enhance responsiveness of upper thoracic spinal neurons to mechanical stimulation of esophagus in rats. 1818 15

Distal oesophageal acid exposure has been shown to increase visceral sensitivity of the proximal oesophagus via central sensitization. Here we evaluated whether acidification of the distal oesophagus also affects the sensorimotor function of the proximal stomach. A gastric barostat study combined with a 30-min acid (HCl 0.15 mol L(-1)) or saline infusion in the distal oesophagus was performed in 18 healthy volunteers. Gastric and cutaneous sensitivity was assessed before and up to 2 h after the start of infusion. Directly after acid infusion, but not after saline, the threshold for discomfort decreased (-6.4 +/- 1.7 vs 0.4 +/- 0.4 mmHg; P = 0.028) and distension-induced symptoms increased significantly compared with the baseline (122 +/- 49% vs -3 +/- 9%). Cutaneous sensitivity remained unaffected by acid infusion. In contrast, when the infused liquid was aspirated 3 cm more distally, at the level of the lower oesophageal sphincter, the effect of acid infusion on gastric sensitivity was abolished and the increase in distension-induced symptoms was reduced (61 +/- 24%). Distal oesophageal acid infusion induces visceral hypersensitivity without affecting somatic sensitivity arguing against a similar mechanism of central sensitization as observed in non-cardiac chest pain. As reduction of the acid load to the stomach prevented this effect, our findings indicate that either gastric and/or duodenal acidification is involved. It should be emphasized though that aspiration from distal oesophagus may have attenuated the effect by reducing the acid-exposed area or by reducing the contact time.
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PMID:Gastric hypersensitivity induced by oesophageal acid infusion in healthy volunteers. 1871 12