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)

Prediction of future suffering could improve palliative care. To identify the factors contributing to physical symptoms, a prospective study was performed on two series of hospice inpatients with cancer (n = 150 and n = 200, respectively). Physical symptoms, patients' characteristics, and tumor locations were recorded using a structured protocol on admission and throughout the clinical course. Common symptoms on admission and during the patient's course were pain (65%, 88%), general malaise (58%, 77%), anorexia (57%, 94%), constipation (33%, 71%), dyspnea (33%, 66%), nausea/vomiting (29%, 48%), cough/sputum (29%, 48%), edema (27%, 65%), fever (26%, 70%), abdominal swelling (26%, 42%), and dry mouth (25%, 61%), respectively. The mean number of symptoms was 5.7 +/- 3.0 on admission and 9.6 +/- 3.1 during the course. Factors that contributed to the symptoms were young age (pain, abdominal swelling, dry mouth), performance status (anorexia, general malaise, edema, dyspnea), brain tumor (paralysis), neoplasms of lung/pleura (dyspnea, cough/sputum, death rattle), bone metastasis (pain, paralysis), gastric/pancreas cancer (abdominal swelling), peritoneal metastasis (general malaise, edema, nausea/vomiting, abdominal swelling, dry mouth), opioids (constipation, dry mouth, myoclonus), anticholinergics (dry mouth), and antidopaminergics (myoclonus). Opioid requirement was positively correlated with the presence of bone metastasis, and negatively correlated with age and brain involvement. Additional opioids were frequently used in the final 48 hours in cases with lung/pleura neoplasms. These data suggest that terminal symptoms in cancer patients are determined by local and/or general factors. Clinicians can predict the probability of future symptoms from patients' characteristics, general condition, tumor locations, and medications.
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PMID:Contributing factors to physical symptoms in terminally-ill cancer patients. 1058 57

After two days of malaise, headache, nausea, and vomiting, a 26-year-old man suddenly developed opsoclonus and stance and gait ataxia, without myoclonus. Having excluded a paraneoplastic etiology, we assumed that the disorder was probably related to a viral infection. Spontaneous resolution occurred in about two months. Opsoclonus became flutter dysmetria and then resolved. Saccadic eye movement recording disclosed the occurrence of hypermetria, increased velocity, and delayed latency, which also resolved. In this patient, the correspondence between clinical and ocular motor abnormality courses suggests a transient cerebellar dysfunction as the possible pathophysiologic mechanism for opsoclonus.
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PMID:Opsoclonus in a patient with cerebellar dysfunction. 1060 72

Tetrahydrobiopterin (BH4) deficiencies are a heterogeneous group of disorders caused by a defect in two of the three enzymes involved in its biosynthesis or in the two recycling enzymes. Except for the deficiency of dehydratase, an enzyme catalyzing a reaction in the recycling pathway, all other variants of BH4 deficiency are characterized by developmental delay, progressive neurological deterioration, hypokinesis, drooling, swallowing difficulty, truncal hypotonia, increased limb tone, myoclonus and brisk deep tendon reflexes. A deficiency of guanosine triphosphate cyclohydrolase I (GTPCH), the first enzyme in the biosynthetic pathway of BH4, is described in a 14-month-old male infant with hyperphenylalaninemia, developmental delay, hypertonia of the extremities, seizures, feeding difficulties, and vomiting. Urinary pteridine screening revealed very low levels of neopterin and biopterin which was highly suggestive of GTPCH deficiency. Low cerebrospinal fluid concentrations of 5-hydroxyindoleacetic acid (5HIAA) and homovanillic acid concentrations, together with no detectable neopterin and decreased concentrations of biopterin and folate, agreed with the diagnosis of GTPCH deficiency. Subsequently measured neopterin and biopterin synthesis in cytokine-stimulated skin fibroblasts confirmed GTPCH deficiency, albeit indirectly. The patient showed marked improvement on a low-protein low-phenylalanine diet with neurotransmitter precursor administration. The favorable outcome in this patient clearly shows that not only newborns with elevated phenylalanine levels but also older children with neurological signs and symptoms should be screened for a BH4 deficiency in order to have maximum benefit of the treatment.
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PMID:Guanosine triphosphate cyclohydrolase I deficiency: a rare cause of hyperphenylalaninemia. 1077 Jun 63

The occurrence of undesirable side effects due to opioids (delirium, confusion, myoclonus, nausea, emesis) is one of the major complications in the management of pain, especially in chronic cancer pain states. Methadone, as an alternative to morphine, has been proposed in the control of opioid-induced toxicity. Methadone is a synthetic opioid, with mu and delta receptor activity, associated with the capacity to inhibit N-methyl-D-aspartate receptors. Questions have arisen concerning its equianalgesic ratio since its rediscovery over the past few years and are certainly related to its receptor interactions. Aspects of its pharmacology, indications, and switching modalities are discussed here. Opioid rotation is a new tool in the management of cancer pain, deserving more attention.
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PMID:Opioid switch to oral methadone in cancer pain. 1088 15

The optimal management of opioid-related side effects is hampered by a lack of comparative studies of management strategies. The prevalence of such side effects is influenced by the extent of disease, the patient's age, the presence of coexistent renal and hepatic disease, pulmonary disease, and cognitive dysfunction, a prior opioid history, use of polypharmacy, dose of opioid drug being administered, and the route of administration. The most common opioid-related side effects are constipation, sedation, nausea, vomiting, and cognitive disturbance. Less frequent side effects include urinary retention, perceptual distortion, respiratory depression, and myoclonus. In an era emphasizing quality of life in cancer care, clinicians need to be aware of (1) factors that influence the prevalence of opioid-related side effects, (2) effective management strategies, and (3) how to recognize when symptoms are opioid related as opposed to caused by other etiologies, such as the patient's disease process or treatment approaches. The use of validated instruments and repeated assessment enhances such an evaluation and subsequent treatment. This article delineates the current optimal management of opioid-related nausea and vomiting, constipation, cognitive side effects, myoclonus, and respiratory depression.
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PMID:Current management of opioid-related side effects. 1127 83

This is the first case reported of vomiting-induced metabolic alkalosis associated with myoclonus. The report describes an unusual presentation of myoclonus secondary to acid-base disturbance caused by recreational drug-induced vomiting. The severe derangement of hyponatraemia, hypokalaemia, and alkalosis appears to have been reasonably well tolerated due to the gradual onset and relatively long history. The causes, mechanism, and management of metabolic alkalosis are discussed.
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PMID:Metabolic alkalosis and myoclonus. 1289 23

The explosive RDX (hexogen, cyclonite) is usually used for the production of C-4 explosive. The rare occurrence of accidental and intentional RDX intoxications has been reported during manufacturing process or in wartime. In this article, the authors report 5 cases of accidental oral RDX poisoning. On admission, observed signs and symptoms included repetitive generalized tonic-clonic convulsions, postictal coma, lethargy, confusion, hyperreflexia, postictal amnesia, nausea, vomiting, abdominal tenderness, sinusal tachycardia, dysrhythmia with frequent ventricular premature beats, generalized muscle spasms, and myoclonus. Leukocytosis, mild anemia, methemoglobinemia, elevated levels of blood glucose, serum aspartate transaminase, alanine transaminase, lactic dehydrogenase, creatine phosphokinase, amilase, hypokalemia, metabolic acidosis, proteinuria, glucosuria, and myoglobinuria were also noted. Plasma RDX concentrations were 268 to 969 ng/mL at 3 hours of ingestion. For management, supportive and symptomatic measures were taken. Whole-bowel irrigation might have been an effective therapeutic procedure due to probable slow gastrointestinal absorption of RDX. Three patients who developed severe metabolic acidosis underwent urgent hemodialysis. All patients were discharged 7 to 21 days after admission without any sequelae. Plasma RDX levels were strongly correlated with the clinical and laboratory manifestations. The available toxicological data on this rare accidental poisoning are reviewed in light of the literature.
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PMID:Accidental oral poisoning caused by RDX (cyclonite): a report of 5 cases. 1518 66

Subacute sclerosing panencephalitis can show variations in clinical course, and some ophthalmologic abnormalities can be seen as cortical blindness and optic atrophy. A 4-year-old girl was referred to our hospital with a complaint of diplopia, vomiting, and ataxia. On physical examination, she was found to have stage IV papilledema with retinal hemorrhage. She was diagnosed as having idiopathic intracranial high pressure until magnetic resonance imaging demonstrated T2-weighted hyperintense lesions. After observation of head drop attacks and detection of elevated antimeasles antibodies in cerebrospinal fluid, the diagnosis of subacute sclerosing panencephalitis was established, and isoprinosine and carbamazepine were started for treatment. However, because carbamazepine failed to control the head drop attacks, topiramate was also included, and the attacks were kept under control with topiramate. The case presented in this article is a good example of subacute sclerosing panencephalitis in which, at early stages, some of the signs and symptoms can lead to an erroneous diagnosis. In addition, we have demonstrated that topiramate might be a good choice for treatment for the persistent myoclonus seen in this type of patient.
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PMID:Unusual manifestation of subacute sclerosing panencephalitis: case with intracranial high-pressure symptoms. 1552 63

Fourteen patients, aged from 5 to 14 years, with syndrome of electrical status epilepticus during slow sleep (ESESS) have been studied. The absence of epileptic attacks was observed in 21.5% of patients and diagnosis was established by a combination of continuous diffuse epileptiform activity with marked cognitive disturbances. In 78.5% patients, epileptic attacks presented as follows: pharyngeal and oral, hemicephalgia (100% patients with attacks), hemiclonic (18%), atypical absences (27%), negative myoclonus (18%), automotor (18%), focal adverse with vomiting (18%), secondary generalized (36%). Drugs of choice were valproate (depakine) and topamax in patients with attacks; suxilep and frisium in the absence of attacks and in case of continuous diffuse epileptiform activity on the sleep EEG. Two variants have been singled out by the character of ESESS syndrome. The first one, a "symptom variant", was featured by mostly hemiclonic, secondary generalized and automotor epileptic attacks, presence of continuous regional or lateral, less frequent diffuse epileptiform activity, detected by the local structural lesions in MRI, marked cognitive disturbances persisting after stopping of the attacks. The second ("idiopathic") variant is characterized by normal development of children before attack manifestation, appearance of mostly "rolandic" attacks, atypical absences and negative myoclonus, presence of exclusively continuous diffuse epileptiform activity in the phase of slow sleep, standard MRI results (moderate cortical subatrophy in single cases), cessation or substantial decrease of cognitive disturbances after attack stopping. It is emphasized that prognosis of ESESS syndrome should be considered separately with regard to attacks and cognitive disturbances. A prognosis for attacks is always favorable. Cognitive disturbances despite the therapy can persist for a long time.
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PMID:[Epilepsy with electrical status epilepticus during slow sleep: diagnostic criteria and approaches to therapy]. 1673 53

Tiagabine is an anticonvulsant acting by selective inhibition of neuronal and glial gamma-aminobutyric acid uptake, resulting in increased gamma-aminobutyric acid-mediated inhibition in the brain. Few reports in the literature describe the clinical course of severe tiagabine intoxication. A 44-year-old woman presented after deliberate self-poisoning with 100 tiagabine 15 mg tablets (1,500 mg; 25 mg/kg). Serum tiagabine level was 4,600 microg/L (1,725 mmol/L) at presentation, 20 times levels associated with therapeutic dosing. Intoxication was manifested by profuse vomiting, coma, myoclonus, generalized rigidity, bradycardia, hypertension, hypersalivation and generalized piloerection within 2 h of ingestion. The patient was intubated and management was supportive. Coma lasted until 10 h post-ingestion, but recovery was complicated by severe agitated delirium lasting 12 h. The patient recovered fully within 26 h of ingestion. Tiagabine deliberate self-poisoning was associated with the rapid onset of coma and an unusual toxidrome. Recovery, although complicated by agitated delirium, was complete within 26 h.
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PMID:Deliberate self-poisoning with tiagabine: an unusual toxidrome. 1878 11


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