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)

A 36-year-old woman had for two months experienced progressively more marked diffuse abdominal pain, at times colicky, as well as nausea, vomiting and severe constipation. In addition, paraesthesias and motor weakness developed in the thighs. This was accompanied by a normochromic, normocytic anaemia with a haemoglobin concentration of 9.6 g/l. A short time later her mother and daughter also fell ill with similar symptoms. After symptomatic treatment had failed, secondary coproporphyria due to lead poisoning was found. The poisoning had resulted from criminal contamination of food, especially of cocoa powder, with lead acetate. Raised lead concentrations in serum were found in two other members of the family. In all the patients treatment was undertaken with sodium calcium edetate (20 mg/kg body-weight) in several three-day cycles, achieving a gradual fall in serum lead concentration. When the level had fallen to below 4 mumol/l the symptoms disappeared. Below 3 mumol/l porphyria was no longer demonstrable and the anaemia regressed. It is pointed out that, as lead poisoning may be fatal, it should be considered in the differential diagnosis of acute abdominal colic of unclear cause.
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PMID:[Acute lead poisoning]. 189 43

Recently, three young individuals died unexpectedly outside hospital. Their past medical histories revealed complaints of weakness, anorexia and nausea, none of which had led to adequate medical examination. The present paper calls for vigilance when patients present with non-specific manifestations such as anorexia and weakness. Autopsies confirmed that the deaths were caused by adrenalitis, a diagnosis unsuspected at the time of death. The value of different post-mortem laboratory findings is discussed.
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PMID:Rapidly fatal Addison's disease: three case reports. 194 Jul 84

Digitalis intoxication is among the most common serious adverse drug reactions in clinical medicine. While the recent development of a radioimmunoassay to accurately measure serum concentrations of digoxin has been of assistance, digitalis intoxication remains a difficult diagnosis to make with certainty. The difficulty in diagnosing digitalis intoxication arises from the nonspecificity of its associated signs and symptoms. The most common symptoms include fatigue, weakness, nausea, and anorexia. These symptoms can occur with many illnesses other than digitalis intoxication. Similarly, the electrocardiographic disturbances caused by cardiac glycosides may be nondiagnostic. The arrhythmias commonly associated with digitalis toxicity are often nonspecific and can be a reflection of the patient's underlying heart disease. The measurement of serum digoxin levels is useful, but studies have demonstrated overlap of the levels between groups with and without toxicity. Due to the modulation of the cardiac effects of digitalis glycosides by such clinical variables as underlying myocardial or renal disease, electrolyte and acid-base imbalances, and other factors, the correlation of toxicity with particular serum digoxin concentrations may vary. Because of the inherent difficulties in confirming the diagnosis of digitalis intoxication in some cases, digoxin-specific Fab antibodies may play a role as a diagnostic tool. Certainly, digoxin-specific Fab antibodies play a significant part in the treatment of digitalis intoxication. Fab antibodies have been successfully used to reverse the effects of digoxin, digitoxin, and oleander poisoning. These antibodies are useful in the treatment of acute and chronic digitalis intoxication in all age groups, including geriatric and pediatric populations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recognition and management of digitalis intoxication: implications for emergency medicine. 199 19

In this report we present aspects of the epidemiology of headache (i.e., pain in the head, face, ear, or neck) among children with brain tumors. The data are derived from the 3,291 subjects in the Childhood Brain Tumor Consortium databank. Overall, 62% of the children with brain tumors experienced chronic or frequent headaches prior to their first hospitalization: 58% of children with supratentorial tumors and 70% of children with infratentorial tumors. The relative frequency of headache increased through age 7 and then leveled off regardless of tumor location. For children under age 5, headache rarely had a duration of more than 1 year prior to hospitalization. Among children over age 4, headache duration of at least one year was significantly greater for supratentorial than for infratentorial tumors. Children with a brain tumor and headache had a different distribution of symptoms and neurologic signs than those without headache. Tumor location and headache status were interactively associated with the presence of other symptoms and neurologic signs. Children with headache had a greater number of other symptoms and neurologic signs. Regardless of tumor location among children with headache, nausea or vomiting, papilledema, and hypoactive tendon reflexes were more frequent, while upper extremity weakness, optic atrophy, and irritability were less frequent. Diplopia, coma, stiff neck, anesthesia or hypesthesia, pupillary abnormalities, and abnormalities of personality, academic performance, or speech were associated with headache in children with supratentorial tumors. No specific symptoms or neurologic signs were associated with headache in children with infratentorial tumors. Supratentorial craniopharyngioma, ependymoma, and protoplasmic astrocytoma were associated with significantly high rates of headache as was infratentorial pilocytic astrocytoma.
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PMID:The epidemiology of headache among children with brain tumor. Headache in children with brain tumors. The Childhood Brain Tumor Consortium. 202 72

The effects of intrathecal baclofen infusion were studied in 9 spinal cord injury patients whose spasticity had been refractory to oral medications. In a two stage, placebo controlled trial, baclofen was administered into the lumbar intrathecal space and subsequent clinical and neurophysiologic changes were assessed. In stage 1, 9 patients underwent a 5 day percutaneous infusion of baclofen and placebo via an external pump. Ashworth and reflex scores were assessed at time of enrollment, after infusion of that amount of baclofen which provided optimal spasticity control and after intrathecal infusion of placebo. The mean Ashworth grade decreased from 3.78 +/- 1.34 to 1.16 +/- 0.48 (p less than 0.001) while mean reflex score decreased from 3.57 +/- 1.05 to 0.64 +/- 0.87 (p less than 0.001). These values differed significantly from those associated with placebo therapy (Ashworth grade--2.54 +/- 1.04, p less than 0.001; reflex score--2.56 +/- 1.04, p less than 0.01). Objective improvements in functional abilities and independence were noted in 8 patients, while somatosensory and brainstem auditory evoked potentials were unchanged in all patients. Urodynamic evaluation revealed increased bladder capacity in 3 patients, while in 4 no change was observed. In Stage 2, permanent programmable infusion pumps were implanted in 7 patients who demonstrated a good response during Stage 1. In this group, mean Ashworth score decreased from 3.79 +/- 0.69 to 2 +/- 0.96 (p less than 0.001) and mean reflex score decreased from 3.85 +/- 0.62 to 2.18 +/- 0.43 (p less than 0.001). Baclofen dosage increased from 182 +/- 135 to 528 +/- 266 mcg/day over the 3-22 month follow-up period. Most of the dosage increase occurred within the initial 12 months following infusion pump implantation and tended to plateau thereafter. Minor complications such as catheter dislodgement/kinking and nausea occurred infrequently while no device related infections were observed. There was no clinical evidence of any significant baclofen neurotoxicity either in Stage 1 or 2. The only ambulatory patient developed marked lower extremity weakness during Stage 1 intrathecal baclofen infusion and was temporarily unable to walk. We conclude that continuous administration of intrathecal baclofen is an effective and safe modality for spasticity control in patients who are refractory to oral medications.
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PMID:Continuous infusion of intrathecal baclofen: long-term effects on spasticity in spinal cord injury. 202 70

Approximately one in four cancer patients during the course of repeated treatments begins to experience nausea in anticipation of chemotherapy treatments. The following characteristics have been associated with the development of this anticipatory nausea: (1) patient age; (2) the experience of nausea/vomiting after first treatment; (3) the severity of nausea after chemotherapy treatment; (4) the severity of vomiting after chemotherapy treatment; (5) feeling warm or hot all over after treatment; (6) a susceptibility to motion sickness; (7) sweating following treatment; (8) feeling of generalized weakness following treatment. The purpose of this study was to replicate and extend previous research linking these characteristics to anticipatory nausea (AN), with special attention to the potential contribution made by interactions of the characteristics. Logistic analyses demonstrated significant contributions to anticipatory nausea aetiology from the learning-based characteristics of nausea and vomiting presence and their severity; individual difference measures of age and susceptibility to motion sickness were also found to contribute significantly to AN development. Results support a learning theory-based model of anticipatory side-effect development as well as the potential contribution of individual difference measures of AN susceptibility.
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PMID:Anticipatory nausea development in cancer patients: replication and extension of a learning model. 202 5

An algorithm based on learning theory and previous research for predicting which cancer patients would develop nausea in anticipation of chemotherapy treatments was tested. Patients with four or more of the following eight characteristics after their first treatment were predicted to develop anticipatory nausea (AN) by their fourth chemotherapy treatment: experienced nausea and/or vomiting after first treatment; nausea after treatment described as "moderate, severe, or intolerable;" vomiting after treatment described as "moderate, severe, or intolerable;" less than 50 yr of age; a susceptibilty to motion sickness; feeling warm or hot all over after treatment; sweating following treatment; feelings of generalized weakness following treatment. The characteristics significantly predicted subsequent anticipatory nausea development (p less than .01) by their fourth treatment in 355 consecutive cancer patients. Results were independent of the type of cancer being treated. The accuracy of the prediction was less specific than prior research, 34% of patients predicted to develop AN did so, compared to 16% of the total sample. Results are consistent with a learned etiology for the development of anticipatory side effects and support the importance of predictive methodologies in investigating mechanisms of anticipatory nausea development.
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PMID:Predicting development of anticipatory nausea in cancer patients: prospective examination of eight clinical characteristics. 203 Feb 96

In 1988-1989 two outbreaks of trichinosis were recorded. The first case was group disease developed in 3 members of the family. The source of infection was rissoles rolled in cabbage leaves [correction of goloubets] stuffed with minced pork. The second outbreak affected 13 persons who had eaten home-made pork sausage and fat. All the patients displayed fever, weakness, muscular pain, subcutaneous fat edema, predominantly of the face. The patients suffered from dry mouth, thirst, deteriorated appetite, exanthema, eosinophilia, more occasionally, nausea, vomiting, abdominal pain and diarrhea. Trichinosis was confirmed serologically. Vermox therapy (300 mg per day) was performed for 7 to 12 days. The disease was severe, moderate and mild in 5, 7 and 4 patients, respectively. A brief abstract from a case record of a patient with severe trichinosis complicated by allergic myocarditis is presented. The severity of the disease was associated with the infecting dose and the time at which etiotropic therapy was started. Vermox had a good therapeutic effect and caused no adverse events.
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PMID:[The clinical characteristics of 2 outbreaks of trichinelliasis]. 214 73

A 17-year-old boy who had mitochondrial encephalomyopathy with focal deficiency of cytochrome c oxidase (CCO) activity is described. He experienced 3 episodes of muscle weakness, fatigability, nausea, vomiting and concomitant increase of serum creatine kinase activity, at the age of 13, 15 and 17 years. During interval there was no muscle weakness and the serum creatine kinase activity was within normal range. Increased levels of lactic acid and pyruvic acid were observed in the blood and cerebrospinal fluid. After an aerobic exercise test, lactic acid and pyruvic acid in the blood increased to an abnormally high level, and the arterial blood became acidic (pH 7.297). On EEG, occasional intermittent irregular theta activities were observed in the anterior region, but there were no abnormalities on CT and MRI in the central nervous system. In the biopsied muscle, ragged-red fibers comprised 20% on modified Gomori-trichrome staining and a number of fibers with no CCO activity were scattered throughout. The CCO activity in the mitochondria isolated from the biopsied muscle was reduced to 49.2 nmol/min/mg protein (normal range 144.7-355.8), while other mitochondrial enzyme activities in the electron transport system were normal. From these data, the patient was considered to have a unique form of mitochondrial encephalomyopathy. By the administration of a large amount of coenzyme Q10, episodes of muscle weakness and nausea, and an increase of lactic acid and pyruvic acid in the blood after aerobic exercise test were no longer observed.
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PMID:[Mitochondrial encephalomyopathy (focal cytochrome c oxidase deficiency) with transient episodes of muscle weakness and elevation of serum creatine kinase activity]. 216 88

Hypercalcemia is a potentially lethal endocrine disorder occurring in 10% to 20% of cancer patients at some time during the course of their disease. Clinical manifestations vary in severity, depending on the degree and duration of hypercalcemia, rapidity of onset, patient's age, performance status, sites of metastases, previous antineoplastic therapy, and the presence of hepatic or renal dysfunction. The clinical features of hypercalcemia are protean and affect multiple organ systems, resulting most prominently in neurologic, gastrointestinal, renal, cardiovascular, and musculoskeletal morbidity. Recognition of the disorder requires a high index of suspicion because many of its symptoms, such as nausea, anorexia, weakness, fatigue, lethargy, and confusion, are non-specific and, in the patient with a malignancy, can result from other complications of the primary disorder. If identified appropriately as being related to hypercalcemia, such symptomatology is potentially reversible with treatment. Whereas in the ambulatory general medical population the most common cause of hypercalcemia is primary hyperparathyroidism, in cancer patients and hospitalized patients in general, the most common cause is malignancy. Hypercalcemia in cancer patients is, in most cases, due to advanced metastasized disease. Diagnostic tests are useful in the differential diagnosis of hypercalcemia, and such tests, together with an accurate history and careful clinical observation, permit the best therapeutic approach to an individual patient.
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PMID:Clinical manifestations of cancer-related hypercalcemia. 218 49


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