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)

Clinical data on the first 100 patients who underwent dipyridamole-thallium stress testing in our hospital were reviewed in order to re-evaluate safety guidelines and diagnostic utility in patients with coronary artery disease. Forty patients developed symptoms, including three major ones. One patient had significant bronchospasm, and two others developed significant hypotension with near syncope. The rest had nonspecific chest, shoulder, arm or throat pain, dyspnea, nausea, vomiting, and paresthesia. Most symptoms occurred within the first 10 minutes of dipyridamole infusion. Twenty-eight patients required treatment with intravenous (IV) aminophylline. Of the remaining 60 patients, 30 became hypotensive but remained asymptomatic. Fourteen of 20 patients who underwent coronary angiography had coronary disease. Thirteen were correctly identified by thallium imaging, and only one was identified by electrocardiogram (EKG). Six patients' angiographies showed no evidence of coronary disease. Five of these patients developed perfusion abnormalities during thallium scintigraphy. These results suggest that dipyridamole is a relatively safe drug for pharmacologic stress testing even though the incidence of side effects is relatively high. The high incidence of thallium perfusion abnormalities in patients without coronary disease probably reflects bias in patient selection for coronary angiography, resulting in a relatively small sample of catheterized patients. However, this requires further investigation.
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PMID:Dipyridamole-thallium stress testing: a local community hospital experience. 841 26

The nature of most syncopal episodes, previously unknown, was recently elucidated by new diagnostic techniques such as the use of the tilt test. The vasovagal syncope can be clinically diagnosed by means of the tilt test. The transitory loss of consciousness during prolonged orthostasis is typically associated with sudden hypotension and bradycardia, which are commonly preceded by relative tachycardia and by premonitory symptoms such as pallor, nausea, asthenia, yawns, hyperventilation, mydriasis, humming, lasting several minutes. The nature of the vasovagal reflex is now better understood: in subjects with vasovagal syncope, during prolonged orthostasis, it was observed a fall in the venous return, inducing an increased sympathetic drive to the heart (with positive inotropic and chronotropic effect) and a lower ventricular filling. The powerful contraction around an almost empty cardiac chamber induces the activation of ventricular mechanoreceptors, and through a reflex mechanism, a sudden increase in the vagal and a sudden reduction in the sympathetic drive. These autonomic changes are responsible for a sudden hypotension and bradycardia. The discussion is still open about the origin of the reduced venous return: it probably originates from a redistribution in the blood volume, due to a venous pooling in the lower limbs or from a reduced muscle tone, because many subjects with vasovagal syncope are slender and with less developed muscle apparatus. Others suggest that a reduction in the sympathetic drive to the vessels, responsible for a progressive hypotension in the minutes preceding syncopal episodes, is the origin of the reduced venous return. In this review a diagnostic pattern for the assessment of the vasovagal syncope is suggested. The medical history, clinical examination, electro- and echocardiogram, chest x-ray identify two main groups of patients (with or without cardiopathy) who will follow different diagnostic protocols. The therapy of vasovagal syncope, which is based on beta-blockers, scopolamine, dysopiramide and plasma expanders, is reviewed.
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PMID:[Vasovagal syncope]. 851 54

Endotoxemia occurs when intestinal ischemia allows bacterial lipopolysaccharide to translocate from colonic flora into the bloodstream, which triggers release of cytokines that can cause hypotension, rigors, fever, shock, and even death. Recently, blood endotoxin levels were shown to be higher in athletes needing medical attention (330 pg.ml-1) than in their competitors with similar performances (81 pg.ml-1). Though there were no data showing that these athletes had elevated core temperatures or severe illness, speculation followed that endotoxin may play a causal role in heat stroke. We examined the relationship between endotoxemia and mild post-exertional illness in 39 cyclists after a 100-mile ride. Thirteen cyclists had at least one of the following: orthostatic hypotension, rigors, nausea, vomiting, diarrhea, or syncope. Only 2/26 case-controls had any of these symptoms. Data were collected on vital signs, hemoglobin, sodium, creatine kinase, creatinine, and uric acid. Endotoxin titer was determined by chromogenic assay; tumor necrosis factor alpha (TNF-alpha) titer was determined by ELISA. One ill cyclist had an endotoxin level of 330 pg.ml-1, one control had an endotoxin level of 150 pg.ml-1, but endotoxin level was < or = 64 pg.ml-1 in all others. Comparison of pre- and post-ride data showed that controls increased creatine kinase activity (154 +/- 34 vs 561 +/- 191 IU.dl, P < 0.05), creatinine concentration (1.5 +/- 0.0 vs 1.6 +/- 0.0 mg.dl-1, P < 0.05), and uric acid concentration (5.4 +/- 0.3 vs 6.3 +/- 0.3 mg.dl-1, P < 0.05). Ill cyclists had lower serum sodium than post-ride controls (138 +/- 2 vs 142 +/- 0.6 mEq.l-1, P < 0.05), but there were no differences between groups in CK, creatinine, or uric acid. These findings suggest that endotoxemia may complicate, but does not cause mild post-exertional illness in cyclists.
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PMID:Exercise-associated collapse in cyclists is unrelated to endotoxemia. 853 21

Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine conditions for this dramatic syndrome are poorly understood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently developed vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40 mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -40 mmHg 11 subjects had vasodepressor reactions, with sudden hypotension, nausea, and dizziness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15 mmHg (delta = -0.06 +/- (SEM) 0.04 pmol min-1 100mL-1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (delta = 0.31 +/- 0.13 pmol min-1 100mL-1). Plasma levels of beta-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinhibition, and release of endogenous opioids can precede vasodepressor syncope.
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PMID:Neurohumoral antecedents of vasodepressor reactions. 855 62

We report a case of 44-year-old Japanese man who presented with exercise-induced anaphylaxis. He was admitted to our hospital with chief complaints of repeated episodes of urticaria and nausea induced by exercise. He had allergy to the radiologic contrast iodine material, but no history of atopic dermatitis. Physical and neurological examinations were unremarkable. Treadmill test induced urticaria and nausea in 10 minutes after starting the exercise and the test was discontinued. The systolic blood pressure finally fell down to 51mmHg about 17 minutes after ceasing the exercise, and it returned to normal value with hydrocortisone and noradrenalin injection. Treadmill test increased the serum histamine level, but did not increase serotonin nor IgE levels. Administration of antihistamines and avoidance of hard exercise has protected him from a new attack. We have to pay attention to exercise-induced anaphylaxis as one of the important causes of syncope.
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PMID:[A case report of exercise-induced anaphylaxis]. 890 89

Mastocytosis is a rare disease of mast-cell proliferation with involvement of the reticuloendothelial systems including skin, bone, gastrointestinal tract, liver, lungs, spleen, and lymph nodes. Systemic mastocytosis is characterized by a combination of symptoms that relate to the mast cells' release of vasoactive substances, such as histamine. These symptoms include urticaria pigmentosa, flushing, syncope with hypotension, headaches, nausea, vomiting, diarrhea, and occasional bronchospasm. The diagnosis of mastocytosis is typically based on the presence of the characteristic extraosseus manifestations. A well recognized roentgenographic feature seen in 70-75% of patients with mastocytosis is diffuse osteolysis and osteosclerosis, affecting primarily the axial skeleton and the ends of the long bones. Rarely, the bony involvement consists of generalized osteoporosis, which may lead to pathologic fracture, or solitary lesions (mastocytomas) which may cause symptoms of localized pain. Four patients with previously diagnosed systemic mastocytosis had unusual skeletal lesions. Clinical and laboratory evaluation of these patients eventually led to the correct diagnosis of systemic mastocytosis. We report these four cases to emphasize the need for thorough evaluation of unusual musculoskeletal findings in association with extraosseus symptoms that are characteristic of mastocytosis. Knowledge of a wide differential diagnosis of unusual skeletal lesions should include systemic mastosytosis.
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PMID:Mastocytosis presenting as a skeletal disorder. 912 84

It has been shown that the elderly, and certain other groups, may have atypical clinical presentations of acute MI. It is important for the clinician to educate patients about the common atypical symptoms that may be experienced with an MI, such as dyspnea, fatigue, nausea, vomiting, and syncope. The clinician must always rule out acute MI in any patient who presents with these symptoms, or who presents with falls, sudden weakness, or worsening CHF. In order to treat patients aggressively and with the greatest benefit (i.e. thrombolytics or other reperfusion therapy), we must teach our patients and ourselves to recognize "silent" MIs. This will decrease the morbidity and mortality rates of acute MI in the elderly.
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PMID:Atypical chest pain in the elderly. 917 31

Throughout the world people who have epilepsy and seizures are prohibited from donating blood. These restrictions are based on the assumption that they are prone to adverse donor reactions, specifically, syncope and convulsions. We describe a study evaluating whether that concern is warranted. During a two year period beginning in 1987, blood donors with a history of seizures were actively recruited by the American Red Cross in the state of Maryland, USA. According to accepted standards, adverse reactions were classified as "slight", for dizziness and nausea without loss of consciousness; "moderate", denoting syncope; and "severe", indicating convulsive syncope. We reviewed a total of 329,143 satisfactory blood donations, and 613 individuals reporting a history of seizures donated blood 723 times. Among donors with seizures, 186 (25.7%) were taking antiepileptic medication, and 61 (8.4%) had one or more seizures in the preceding year. Individuals with seizures had a low incidence of adverse reactions (3.34%). Although slightly higher than the entire population (2.24%), this difference was not statistically significant. In particular, the risk of syncope with or without convulsive activity was low for people with seizures (.21%) and not significantly increased as compared to other donors (.28%). Our study supports the view that individuals with seizures or epilepsy are not at greater risk for adverse reactions after blood donation. Major restrictions on individuals with epilepsy and seizures as blood donors are not warranted.
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PMID:Regulations prohibiting blood donation by individuals with seizures or epilepsy are not necessary. 921 25

It is well known that some patients with neurally mediated syncope have a feeling of aura before the onset of syncope. A case is reported in which cerebral dysfunction recorded by EEG was present before the onset of a vasovagal reaction. The vasovagal reaction, bradycardia and/or asystole, was preceded by abnormal EEG findings when the patient complained of feeling a headache, photophobia, and nausea. These findings suggest that cerebral hypoperfusion, such as with cerebral vasospasms, before the onset of bradycardia might be involved in the mechanism of neurally mediated syncope in patients with an aura.
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PMID:Possible involvement of cerebral hypoperfusion as trigger of neurally-mediated vasovagal syncope. 955 95

A retrospective observational study using database registry of consecutive patients admitted to 16 King County hospital Coronary Care Units (CCU) was conducted to assess gender differences in symptom presentation for acute myocardial infarction (AMI) and investigate how symptom presentation relates to prehospital delay time interval from acute symptom onset to emergency department (ED) presentation. Between January 1991 and February 1993, 4,497 patients were admitted to the CCUs with diagnosed AMI. Accredited record technicians abstracted age, gender, race, transport method, symptom presentation (chest pain, sweating, nausea, shortness of breath, epigastric pain, and fainting), delay time interval between acute symptom onset and presentation to hospital ED, and discharge diagnosis from the patients' medical records. After adjusting for age and history of diabetes, no gender differences remained for frequencies of chest pain, fainting, or epigastric pain. Women reported more nausea and shortness of breath but less sweating than men as symptoms of AMI. Chest pain, sweating, and fainting were associated with decreasing delay time intervals. Age, gender, histories of AMI and diabetes, and transport choice were also significantly related to delay time interval. These results show that gender differences occur in AMI symptom experience. However, how symptoms relate to the gender gap in delay time interval is not clear. These findings suggest that health care professionals need to tailor information about possible symptoms of AMI to the patient's gender, age, and medical history.
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PMID:Gender differences in reported symptoms for acute myocardial infarction: impact on prehospital delay time interval. 1045 54


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