Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 26-year-old male has a tooth extracted at a dental surgery, and was given 40 mg Froben, as an anti-inflammatory analgesic agent, and ingested one tablet without water. After 2 days, anterior chest pain occurred. Esophagography and endoscopy were performed and multiple esophageal ulcers were confirmed. Esophagography revealed an esophageal stenosis which was considered to be caused by the extramural compression on the oral side of the ulcers. In the chest roentogenography and CT scanning, the right aortic arch was observed. This case was diagnosed as having drug-induced esophageal ulcer developed at the esophageal constriction due to the vascular ring.
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PMID:[A case of drug-induced esophageal ulcer developed at the esophageal constriction due to the right aortic arch]. 150 9

It has been shown that food ingestion can provoke esophageal motor abnormalities in patients with otherwise normal manometry. Such motor abnormalities are usually nonspecific in character. We now report water swallow and food ingestion data on 12 patients with a history of dysphagia and/or chest pain who satisfied strict manometric diagnostic requirements for diffuse esophageal spasm. Three of these patients had normal water swallow manometry, yet, during food ingestion, showed manometric evidence of diffuse esophageal spasm. In the other nine patients, the occurrence of nonperistaltic contractions was greater, and there was a greater incidence of nonperistaltic contractions of 100 mm Hg or more after ingestion of food. We conclude that food ingestion increases the diagnostic yield of manometric testing for diffuse esophageal spasm and, not infrequently, magnifies an abnormality seen during standard water-swallow testing.
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PMID:Manometry during food ingestion aids in the diagnosis of diffuse esophageal spasm. 159 42

Pneumopericardium is defined as the presence of air in the pericardial cavity. It is a rare condition in adults, usually due to trauma; it is commoner in the more exposed neonate and usually iatrogenic. The clinical presentation of chest pain and shortness of breath is associated with the pathognomonic auscultatory sign described by Bricheteau: a water-mill bruit. The diagnosis is confirmed by chest X-ray which shows the air-gap sign surrounding the cardiac silhouette. The principal differential diagnosis is a pneumomediastinum. The prognosis of pneumopericardium depends on the cause and complications of which tamponade and infection are the most serious and potentially life-threatening. The treatment of pneumopericardium is bed rest and surveillance when uncomplicated: evacuation of the air becomes necessary when complications set in.
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PMID:[Spontaneous pneumopericardium. Review of the literature apropos of 2 cases in the young adult]. 201 79

Positron emission tomography (PET) was performed in two patients who exhibited transient ST-T elevation during their attack. The myocardial blood flow (MBF) and tissue fraction were quantitatively measured using dynamic PET and O-15 water. Myocardial exogenous glucose utilization was also determined by PET and F-18 fluoro-deoxyglucose (FDG). The FDG uptake index (FUI), obtained by dividing the total FDG count in the region of interest by the total amount of FDG, was used. These values were free from the partial volume effect because of the correction of the tissue fraction. Case 1: A 61-year-old woman was admitted to our hospital because of ST-T elevation on her ECG during her abdominal surgery. Her myocardiogenic enzymes were elevated. The emergency coronary angiogram showed no pathological coronary artery stenosis or occlusion, but the levogram showed abnormal wall motion. About one month later, the repeat coronary angiogram showed restoration to normal wall motion. In a PET study, myocardial blood flow and FUI were increased above the normal range. Case 2: A 65-year-old man was admitted to our hospital because of ST-T elevation on his ECG during chest oppression. In a PET study one month after the last chest pain, myocardial blood flow was normal, but there was a high uptake of FDG in the transient ischemic area. The coronary angiogram revealed no pathological lesions. It was suggested that the high uptake of FDG is related to a previous ischemic event; not to a present ischemic state. It is thought that these two cases exemplify so-called "myocardial stunning".
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PMID:[PET evaluations of ischemic heart disease showing transient ST-T elevation: report of two cases]. 209 58

Surveys of athletes, primarily runners, have shown that digestive disorders are common, associated both with training and racing. Women, in particular, seem to suffer most commonly. Nearly half have loose stools and nausea and vomiting occur frequently after hard runs. Diarrhoea, incontinence and rectal bleeding occur with surprising frequency. Runners may use medications prophylactically to minimise some of these symptoms. Upper digestive symptoms seem to occur more commonly in multisport events such as triathlons or enduro. The published literature is difficult to analyse and the basic intestinal physiology not well studied. Most gastroenterologists are accustomed to evaluating the fasting patient at rest and exercise physiologists are seldom experienced with digestive techniques. Digestive symptoms occurring with exercise referable to the oesophagus include chest pain, gastro-oesophageal reflux symptoms, or symptoms related to alterations in motility. While little is known of the oesophageal physiology during exercise, it is believed that only minimal changes occur in most subjects. Gastro-oesophageal reflux occurs more frequently with exercise than at rest and may produce symptoms of chest pain suggestive of ischaemic disease. Acid exposure may be reduced by pretreatment with histamine H2-receptor antagonists. Oesophageal symptoms, though common, are rarely disabling to the athlete, and the clinical importance lies in confusion with ischaemic disease. Cases of acute gastric stasis following running have been reported and gastric physiology during exercise, particularly bicycling, has been more actively investigated. Gastric emptying during exercise is subject to a number of factors including calorie count, meal osmolality, meal temperature and exercise conditions. However, it is generally accepted that light exercise accelerates liquid emptying, vigorous exercise delays solid emptying and has little effect upon liquid emptying until near exhaustion. Gastric acid secretion probably changes little with exercise although some have postulated that ulcer patients may increase secretion with exercise. Some exercise-associated digestive symptoms, such as diarrhoea and abdominal pain, have been attributed to changes in intestine function. Small bowel transit is delayed by exercise when measured by breath hydrogen oral caecal transit times and motility may be reduced as well. Intestinal absorption during exercise has not been well evaluated but probably changes little in ordinary circumstances. Passive absorption of water, electrolytes and xylose are not affected by submaximal effort. Colonic transit and function is even more difficult to evaluate and published results have been conflicting. However, it is likely that many of the lower digestive complaints of runners such as diarrhoea and lower abdominal cramps are due to direct effects of exercise upon the colon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of exercise on the gastrointestinal tract. 218 30

The symptoms and presentations of gastroesophageal reflux disease are rather numerous. These include the typical symptoms, such as heartburn, regurgitation, water brash, or dysphagia. However, reflux may also be responsible for such symptoms as hoarseness, pulmonary aspiration, or asthma. It may also be an important cause of noncardiac chest pain. Thus, gastroesophageal reflux disease may be considered a disease with more than just "esophageal" symptoms.
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PMID:The spectrum of the symptoms and presentations of gastroesophageal reflux disease. 222 66

A case of pulmonary embolism associated with diabetes insipidus is reported in an 18-year-old male. The patient, who had been treated with DDAVP for diabetes insipidus and hydrocortisone for hypocorticism for two years after first operation for the removal of craniopharyngioma, was admitted with recurrence of that tumor. Diabetes insipidus immediately after second operation was controlled with intermittent drip infusion of a small amount of aqueous pitressin under monitorings of body weight hourly using a patient weighing system to keep the weight changes within +/- one kilogram. Serum and urine electrolytes levels, osmolarity, and free water clearance were also monitored every three hours to maintain water-electrolytes balances appropriately. Postoperative course had been uneventful except that CSF rhinorrhea occurred 7 days after operation. The patient was, then, kept in bed with horizontal plane to avoid further leakage of CSF. Two days later, he developed chest pain suddenly with tachypnea, tachycardia, and general cyanosis. The arterial-BGA showed PaO2 of 53.5mmHg and PaCO2 of 35.3mmHg in room air. The definite diagnosis of pulmonary embolism was made by technetium microaggregate lung perfusion scans and by pulmonary angiograms. The patient was treated with heparin, 15000IU/day, and urokinase, 720000IU/day. The symptoms due to pulmonary embolism had improved gradually within a couple of weeks. Recent articles have shown an unexpected high incidence of deep vein thrombosis and pulmonary embolism in neurosurgical patients associated with the elevation of blood coagulability. Brain tumors, especially suprasellar mass with hypothalamic dysfunction have been suggested to cause thromboembolic disorders frequently. The clinical course was described and factors causing pulmonary embolism on this patient was discussed.
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PMID:[A case of pulmonary embolism with diabetes insipidus developed after removal of craniopharyngioma]. 233 47

Angiographically normal coronary arteries are found in a substantial number of patients evaluated for angina pectoris. One third to one half of such patients demonstrate abnormalities of myocardial perfusion or metabolism when evaluated with invasive techniques. This study was designed to determine whether angina in such patients is attributable to abnormalities of perfusion at rest, maximal perfusion or vasodilator reserve and whether any identified abnormalities were global or regional in nature. Positron emission tomography was performed with oxygen-15-labeled water (H2(15)O) and oxygen-15-labeled carbon monoxide (C15O) before and after intravenous dipyridamole to assess regional myocardial perfusion and perfusion reserve in absolute terms in 16 normal subjects and 17 patients with chest pain and angiographically normal coronary arteries. Eight of the 17 patients had a myocardial perfusion reserve less than 2.5 (the lower limit of normal in studies with positron emission tomography, as well as with other techniques) and 9 of 17 patients had a normal response. In the patients with an impaired perfusion reserve, perfusion at rest was significantly higher than that measured in normal subjects (1.61 +/- 0.38 versus 1.25 +/- 0.28 ml/g per min, p less than 0.02) and maximal flow and perfusion reserve were significantly reduced (2.26 +/- 0.92 versus 4.62 +/- 1.58 ml/g per min and 1.4 +/- 0.5 versus 3.8 +/- 1.1, respectively; p less than 0.001 for both comparisons). Abnormalities of perfusion and perfusion reserve were spatially homogeneous without detectable regional disparities. Thus, nearly half of patients with chest pain and normal coronary arteries have abnormalities of myocardial perfusion that are detectable noninvasively with positron emission tomography and H2(15)O.
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PMID:Increased myocardial perfusion at rest and diminished perfusion reserve in patients with angina and angiographically normal coronary arteries. 238 32

Data from 100 consecutive patients with chest pain or dysphagia, or both, who underwent esophageal testing with standard water swallows and upright food ingestion were retrospectively evaluated. In addition to having manometric patterns monitored, patients were asked to relate symptoms during testing. Of 77 patients with a history of dysphagia, significantly more had abnormal manometry during the test meal than with water swallows (79 vs. 43%, p less than 0.005). Additionally, dysphagia, although reported in only 8% of these patients during standard testing, occurred in 47% during the test meal (p less than 0.001). Of 60 patients with chest pain, symptoms were rarely reported (5%) with water or with food ingestion. We conclude that manometry with food ingestion should be used as a provocative test in anatomically normal patients with dysphagia.
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PMID:Water swallows versus food ingestion as manometric tests for esophageal dysfunction. 291 60

The effects upon esophageal motility of water at room temperature and 0 degrees C, taken as repeated small boluses and as 200-ml volumes swallowed as rapidly as possible, were compared before and after pretreatment with isosorbide denitrate 5 mg sublingually, in nine young healthy subjects and two patients with esophageal spasm. Iced water caused reduced strength, increased duration, and reduced velocity of distal esophageal contractions. It also reduced the force of lower esophageal sphincteric contraction, an effect that was more transient than that seen in the esophageal body, but it did not alter the magnitude of sphincteric relaxation. Esophageal responses in normal subjects with water at the two temperatures were not affected by isosorbide denitrate. The responses to iced water in the two patients with esophageal spasm were qualitatively similar to those in normal subjects. These findings indicate that cooling brings about a transient state of relative paralysis in the distal esophagus and lower esophageal sphincter. Taken in conjunction with other observations, they are consistent with the notion that cold-induced chest pain, whether in normal subjects or in patients with esophageal motor disorders, is related to esophageal distension.
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PMID:Changes in distal esophageal function in response to cooling. 379 79


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