Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Fainting syncopal events are caused by a transient functional neuronal paralysis. Reflex syncope happens for brainstem involving mediated by peripherical afferents. Sometimes gastroesophageal reflux (GER) has been implicated in the development of obstructive apnea. Gastroesophageal reflux, despite the absence of a clinical history of vomiting and regurgitation, is observed in a significant proportion of infants presenting with ALTE (Apparent Life Threatening Event): an episode characterized by some combination of apnea, color change, marked change in muscle tone, choking or gagging. Though a cause-and-effect relationship between GER and the development of ALTE remains to be established a possible direct relationship between oesophageal acidification and the onset of alterations in cardiopulmonary function and impairment of consciousness can be hypothesized. We refer the case of two female infants that developed recurrent ALTE(s) characterized by paleness, change in muscle tone and loss of consciousness. The infants resulted affected respectively by a mild and severe gastroesophageal reflux (score: 40, > 50); in one case an episode of GER was recorded by the intraoesophageal pH-monitoring during a syncopal episode. The treatment with antiacid drugs was effectual and the infants did not present ALTE(s). The cases presented are in favour of a routine search of gastroesophageal reflux in infants presenting with one or recurrent ALTE(s). The identification of these infants will permitt to develop a correct strategy of treatment.
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PMID:[Syncopal fainting episodes and gastroesophageal reflux]. 866 87

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

Three members of a Taiwanese kindred developed severe, systemic, early onset (< age 25 years), biopsy-proven amyloidosis. Clinical features included upper and lower extremity sensorimotor neuropathy, abdominal pain, vomiting, corneal ulcerations, cardiomyopathy, and syncope. Immunohistochemical analysis indicated that the deposits consisted of transthyretin. Molecular genetic studies revealed a heterozygous codon 55 point mutation, resulting in a proline for leucine-substitution, a mutation previously associated with aggressive familial amyloidosis in a US kindred of Dutch and German descent. The clinical courses and echocardiographic findings are typical for many types of amyloidosis; the pathologic data and genetic studies were necessary to establish a precise diagnosis.
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PMID:Familial amyloidosis in one Chinese family: clinical, immunological, and molecular genetic analysis. 915 4

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

Eptastigmine is a new acetylcholinesterase (AChE) inhibitor currently under development for the symptomatic treatment of Alzheimer disease. This study was conducted to establish the maximum tolerated dose and the pharmacodynamics of eptastigmine in nine healthy elderly volunteers. Subjects received single oral doses of 8 mg, 20 mg, 32 mg, and 40 mg eptastigmine and placebo according to a double-blind, randomized, rising-dose, five-way crossover design. Adverse events, blood pressure, heart rate, body temperature, forced expiratory volume, salivary flow, and pupilar activity were closely monitored during treatment. Pharmacodynamic activity of eptastigmine was evaluated with an assay of AChE activity in red blood cells. Eptastigmine doses of 8 mg, 20 mg, and 32 mg were well tolerated. Two of four subjects receiving the 40-mg dose developed profound AChE inhibition (58-59%) and reported severe adverse events (nausea, vomiting, syncope, and bradycardia), precluding further administration in the remaining subjects. Eptastigmine administration produced a weak effect on supine heart rate, body temperature, and pupil diameter. There were no effects on blood pressure, forced expiratory volume, salivary flow, and near point of focus. Acetylcholinesterase activity was inhibited in a dose-related fashion according to a sigmoidal (logistic) function. The mean (+/- SEM) maximum inhibition of AChE activity (Imax) was 14.5+/-3.3%, 20.4+/-2.3%, 28.7+/-2.9%, 45.2+/-1.3% and 53.6+/-2.9% after placebo, 8 mg, 20 mg, 32 mg, and 40 mg of eptastigmine, respectively. The theoretical maximum response (Emax) was 72.9%, and the dose that produced half of the maximum response (ED50) was 29.5 mg. At 24 hours, residual AChE inhibition ranged from 9% to 15%, with a half-life of recovery of the enzyme of approximately 10 hours. The maximum tolerated dose of eptastigmine after single-dose oral administration in healthy elderly subjects is 32 mg. Single oral doses of eptastigmine produce sustained, dose-related inhibition of AChE activity. Adverse events are related to the degree of AChE inhibition.
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PMID:Maximum tolerated dose and pharmacodynamics of eptastigmine in elderly healthy volunteers. 970 45

We report a case of Lhermitte-Duclos disease (dysplastic gangliocytoma of the cerebellum), an uncommon disorder of uncertain pathogenesis characterized by disarrangement of the normal cerebellar laminar cytoarchitecture. A 40-year-old man was admitted because of vomiting and syncope of a few days' duration, and a 2-month history of intermittent headaches and unsteady gait. A computed tomographic scan of the patient's head showed obstructive hydrocephalus due to displacement of the fourth ventricle by a large, nonenhancing cerebellar mass. The magnetic resonance images of the brain also revealed a space-occupying lesion within the right cerebellum with unusual septation. After surgery, the histologic examination confirmed the diagnosis of Lhermitte-Duclos disease. This is the first report of Lhermitte-Duclos disease in Taiwan.
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PMID:Lhermitte-Duclos disease: first report in Taiwan. 979 36

Paroxysmal supraventricular tachycardia (SVT) may have numerous electro-physiologic mechanisms. The most common type of SVT is AV-nodal reentry tachycardia (60%) followed by the bypass tract-mediated SVT (preexcitation. 30%) and a smaller group (10%) comprising paroxysmal atrial flutter or fibrillation and atrial ectopic tachycardia. In persons with otherwise normal hearts symptoms are usually mild and include palpitations or an uneasy feeling in the chest. But some describe precordial pain. Weakness, dizziness, nausea, vomiting, and even syncope. Whenever possible a 12-lead-ECG during an episode of SVT should be obtained. If not possible the use of several Holter-ECG or of an event-recorder may be helpful. Conversion of a SVT can be accomplished by vagal maneuvers or intravenous adenosine (6-18 mg bolus injection). Further diagnostic procedures should prove or rule out a significant structural heart disease. Therapeutic options (expectative, pharmacological prophylaxis, invasive electrophysiologic testing and catheter-mediated modification or ablation) are chosen according to the objective threat (e.g. ventricular fibrillation due to 1:1 conducted atrial fibrillation in a preexcitation syndrome) and the subjective complaints. Definitive healing of the AV-nodal reentry tachycardia and the bypass tract-mediated SVT can be achieved by use of catheter-mediated modification or ablation in 95 to nearly 100%.
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PMID:[Modern therapy of paroxysmal supraventricular tachycardia]. 1009 47

A 16-year-old female presented with weakness that began about 2 weeks earlier and has become progressively worse. It was accompanied by occasional dizziness and two brief episodes of syncope. Her history was remarkable for self-induced vomiting in order to lose weight. Her obvious diagnosis was bulimia nervosa, but it was further complicated by abnormal unexplained weakness. Upon careful questioning, she admitted using ipecac to induce vomiting for the past several weeks. She was placed on a strict eating disorder protocol combined with careful cardiac monitoring and her weakness eventually resolved.
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PMID:Generalized Weakness. 1035 83

This review will focus on the mechanisms of emesis initiated or inhibited from receptors located in the periphery or activated by a peripherally released humoral factor. Excitatory and inhibitory receptors have been found in the thorax. Nausea and vomiting sometimes occur after coronary artery occlusion or with vasovagal syncope, and the receptors of this emetic response are probably tension receptors of the left ventricle. The thorax is also source of antiemetic receptors. Vagal section above the level of the heart causes an intractable vomiting syndrome and central cervical vagal stimulation inhibits vomiting. In addition, respiratory maneuvers that decrease activation of pulmonary afferents enhance the sensitivity to motion sickness. Therefore, pulmonary vagal afferent fibers may tonically inhibit retching and vomiting. Abdominal stimulation by irritants or toxins can activate nausea and vomiting through mechano- or chemoreceptors. Mechanoreceptors have been found in the stomach, jejunum and ileum, but the location of these receptors in the gut wall or the type of mechanical stimuli most effective in exciting these receptors is unknown. The chemoreceptors have a similar distribution and are probably located in the mucosa and respond to a variety of noxious agents, eg, CuSO4. CuSO4-induced vomiting is mediated by peripheral 5-HT4 receptors. Two clinically relevant toxic stimuli, x-irradiation and chemotherapeutic agents, have been found to activate vomiting through 5-HT3 receptors in the digestive tract. Regardless of the stimulus, the afferent neural pathways mediating emesis from the abdomen may be the same. The noxious stimulus may cause release of serotonin from enterochromaffin cells of the digestive tract, which activates visceral afferents. The vagus nerves mediate responses from the stomach and proximal small intestine and the splanchnic nerves and spinal cord mediate responses from the entire small intestine. Emesis-related afferents from the periphery terminate primarily in the nucleus tractus solitarius and area postrema. The area postrema contains the chemoreceptive trigger zone that can be activated by endogenous agents released into the circulation from the periphery. The role of peripheral receptors or peripherally released agents in the etiology of cyclic vomiting is unknown, but multiple pathways have been identified that can form a brain-gut interaction to provide a possible mechanism of cyclic vomiting.
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PMID:Noxious stimulation of emesis. 1049 41


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