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

Forty-one dogs with a variety of histopathologically diagnosed, measurable tumors were treated with cisplatin (cis-diamminedichloroplatinum, Platinol, Bristol Laboratories, Syracuse, NY 13221-4755) as a single agent at a dosage of 60 mg/m2 given intravenously at 3-week intervals. In an attempt to avoid renal toxicity of cisplatin, saline diuresis was induced and maintained for 4 hours before and 2 hours following cisplatin administration. The dogs received one to ten doses of cisplatin. To determine response to therapy and to monitor toxicity of the drug, the dogs were evaluated with physical examinations including tumor measurements, radiography, complete blood counts, platelet counts, urinalyses, serum urea nitrogen concentrations, and serum creatinine concentrations. An overall response rate of 19% was observed. Complete remission occurred in one of 11 dogs with squamous cell carcinomas and one of one dog with a mediastinal undifferentiated carcinoma. Partial remissions were documented in one of 11 dogs with squamous cell carcinomas, two of three dogs with metastatic osteosarcomas, one of three dogs with nasal adenocarcinomas, and one of one dog with a thyroid adenocarcinoma. Toxic side effects were primarily gastrointestinal in nature, with vomiting occurring 1-6 hours after cisplatin administration in 27 of 41 dogs. Severe anorexia occurred in three dogs, and hemorrhagic diarrhea was observed in one dog. One dog developed grand mal seizures and died 3 hours following therapy. Granulocytopenia was documented in six dogs, and thrombocytopenia was observed in four dogs. One dog showed an increase in serum urea nitrogen and creatinine concentrations, but this patient had known pre-existing renal disease.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cisplatin therapy in 41 dogs with malignant tumors. 322 54

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
 ...
PMID:Phenytoin-induced hypersensitivity reactions. 367 71

A sequential sample of 101 patients hospitalized for ethanol withdrawal and requiring sedation for evolving withdrawal syndromes was assigned randomly according to a double-blind protocol to treatment with either alprazolam or chlordiazepoxide administered orally. The data from one patient were unevaluable due to acute bleeding, leaving a sample of 100 (50 in each condition). At discharge, three independent ratings of diaphoresis, tremor, hallucinations, nausea/vomiting, and overall severity of withdrawal were obtained, and the occurrence of delirium tremens and grand mal seizures was noted. Patients also completed the Beck Depression Inventory, and their disposition following discharge was recorded. There were no statistically significant differences between the two treatment groups on any of the dependent variables studied. It was concluded that the choice between alprazolam and chlordiazepoxide for managing ethanol withdrawal should be based on criteria other than efficacy of control. Potential antidepressant effects and drug kinetics were suggested as the basis for rational decision-making.
 ...
PMID:Double-blind trial of alprazolam and chlordiazepoxide in the management of the acute ethanol withdrawal syndrome. 388 64

The diagnosis, evaluation and assessment, supportive care, and pharmacologic treatment of acute alcohol withdrawal are reviewed. Patients in alcohol withdrawal have decreased or stopped their heavy, prolonged ingestion of alcohol and have subsequently begun to have at least two of the following symptoms: autonomic hyperactivity, tremor, nausea or vomiting, hallucinations, psychomotor agitation, anxiety, and grand mal seizures. Evaluation of the patient at risk for alcohol withdrawal should include a complete history and physical examination; laboratory tests are often indicated. The patient's progress should be assessed before, during, and after therapy, preferably with a validated instrument. After the initial evaluation and assessment but before the administration of dextrose-containing solutions, a 100-mg dose of thiamine hydrochloride should be given by i.m. or i.v. injection. Routine supplementation with calcium, magnesium, and phosphate is questionable. The need for fluid and electrolyte administration varies depending on losses. Most patients in alcohol withdrawal can be managed with supportive care alone, but for more severe or complicated withdrawal, pharmacologic therapy may be necessary. Benzodiazepines, especially diazepam and chlordiazepoxide, are the drugs of choice. Barbiturates, beta-blockers, and antipsychotics are generally not recommended as first-line therapy. Several drugs in other classes, including carbamazepine and clonidine, have been shown to be about as effective as benzodiazepines in a few studies, but the studies were small, the patients were usually in mild withdrawal, and validated instruments for assessing withdrawal were often not used. Some agents, such as beta-blockers, may play a role as adjuncts to, not replacements for, benzodiazepine therapy. For patients in alcohol withdrawal who do not respond to supportive care, benzodiazepines are the treatment of choice.
 ...
PMID:Management of alcohol withdrawal. 762 38

A 32-year-old woman with migraine for several years again had a migraine attack with headache, nausea, vomiting and eye-muscle disorder, 14 days after an uncomplicated delivery. Within 24 hours a left-dominant hemiparesis developed, followed 12 hours later by tonic-clonic seizure and deep unconsciousness (Glasgow score: 3); the patient could not be aroused. Cranial computed tomography revealed extensive infarction of the brainstem and cerebellum. Angiography demonstrated occlusion of the basilar artery but not other abnormalities of other vessels. There was no evidence for vascular anomalies and the clotting tests were normal. Transoesophageal echocardiography demonstrated an atrial septal aneurysm. But any interatrial shunt (e.g. through a patent foramen ovale) was excluded by colour Doppler sonography, making it highly unlikely that a paradoxical embolus was the cause of the infarction. The brainstem infarction resulting from the basilar artery occlusion did not respond to treatment and the patient died 10 days after the initial seizure.
 ...
PMID:[Atrial septum aneurysm as the cause of a thromboembolic infarction of the brain stem and cerebellum?]. 835 49

Exercise-induced hyponatremia is commonly believed to be associated only with extraordinary physical efforts, or particularly strenuous exercise. Hyponatremia complicating moderate exercise has not been described previously. The authors describe the characteristics of seven patients with life-threatening hyponatremia associated with mild to moderate exercise. All patients suffered from nausea, vomiting, agitation, and confusion, appearing during or after moderate physical activity. Grand mal convulsions occurred in five of the patients. In laboratory results, hyponatremia was as low as 115 mEq/L, with a relatively high sodium concentration in the urine. High serum creatine kinase activity levels were found in most of the patients. All patients were discharged in good condition, without neurologic sequela. The authors conclude that hyponatremia is a possible complication of moderate exercise, and not only of endurance sports, and that exercise-induced hyponatremia can produce severe neurologic manifestations. The mechanism of the hyponatremia is unclear, but may be due to a hemodynamically inappropriate stimulus for antidiuretic hormone secretion.
 ...
PMID:Case series: hyponatremia associated with moderate exercise. 861 81

We present the case of a 71-year-old female suffering from bipolar affective disorder type 2 and an old lacunar brain infarct who, under the combined treatment of fluoxetine for depression and low dose trazodone for the accompanying insomnia, developed a toxic delirium. The subject presented with mental state changes (confusion and agitation), hyperreflexia, diaphoresis, nausea, vomiting, fever, and a general tonic-clonic seizure which developed soon after an increase in the trazodone dose. One year prior to the above episode, she was hospitalized for a transient episode of agitated confusion while being treated with fluvoxamine for depression, alprazolam and brotazolam for the accompanying anxiety and insomnia. Both episodes subsided spontaneously when treatment was discontinued. This case reports the possible existence of increased vulnerability to hyperserotonergic states in elderly patients suffering from concomitant psychiatric and neurological disorders.
 ...
PMID:Recurrent toxic delirium in a patient treated with SSRIs: is old age a risk factor? 923 73

Since isoniazid is increasingly being used to control the spread of tuberculosis, physicians must be aware of its potentially fatal effects. The ingestion of toxic amounts of isoniazid causes recurrent seizures, profound metabolic acidosis, coma and even death. In adults, toxicity can occur with the acute ingestion of as little as 1.5 g of isoniazid. Doses larger than 30 mg per kg often produce seizures. When ingested in amounts of 80 to 150 mg per kg or more, isoniazid can be rapidly fatal. The first signs and symptoms of isoniazid toxicity usually appear 30 minutes to two hours after ingestion and include nausea, vomiting, slurred speech, dizziness, tachycardia and urinary retention, followed by stupor, coma and recurrent grand mal seizures. The seizures produced by isoniazid toxicity are often refractory to anticonvulsant therapy. Given in gram-per-gram amounts of the isoniazid ingested, pyridoxine (vitamin B6) usually eliminates seizure activity and helps to correct the patient's metabolic acidosis. Isoniazid toxicity should be suspected in any patient who presents with refractory seizures and metabolic acidosis.
 ...
PMID:Isoniazid overdose: recognition and management. 949 Sep 97

The purpose of this study was to determine the maximally tolerated dose of doxorubicin administered during two cycles of intensive chemotherapy with cyclophosphamide and doxorubicin without stem cell support in patients with advanced cancer and to assess the cumulative cardiac toxicity of the regimen by noninvasive radionuclide imaging and by pre-and postchemotherapy endomyocardial biopsies. Thirty-eight patients (thirty-six with high risk or metastatic breast cancer) were treated in a dose-escalation trial using a fixed dose of i.v. cyclophosphamide (4.2 g/m2) administered over 2 h on day 5 and escalating doses of doxorubicin (50-175 mg/m2) given as a 96-h continuous i.v. infusion on days 1-4, using Filgrastim (granulocyte colony-stimulating factor) for hematological support beginning on day 6. All patients underwent pretreatment, and 28 patients underwent postchemotherapy endomyocardial biopsies. Twenty-nine of 38 patients received two cycles of treatment (median number of days between cycles, 44; range, 34-62). Twenty-one patients had received doxorubicin previously at cumulative dose levels </=150 mg/m2; all patients had pretreatment endomyocardial biopsy scores less than 1. One patient treated at the highest dose level of doxorubicin (175 mg/m2) developed symptoms of mild congestive heart failure following two cycles of chemotherapy. Pre- and posttreatment radionuclide ejection fractions were 65 and 45%, respectively; this patient had a posttreatment endomyocardial biopsy score of 1 (damage to <5% of myocytes). One additional patient at this dose level had an asymptomatic biopsy score of 1, with a decrease in ejection fraction from 62 to 43%; this recovered to 58% 5 months after completion of chemotherapy. Six additional patients treated at lower dose levels had abnormal posttreatment endomyocardial biopsies without abnormal posttreatment ejection fractions. Nine patients received only one cycle of chemotherapy: five patients due to decreased cardiac ejection fraction following cycle 1 (two of these patients had normal endomyocardial biopsies, and two patients had biopsy scores of 1); one patient secondary to tumor progression following cycle one; one patient due to persistently detectable Clostridium difficile toxin in the stool; one patient refused cycle two; and one patient died following cycle one of complications related to sepsis. A single patient experienced a grand mal seizure associated with orthostatic hypotension, which was considered the dose-limiting toxicity. The median duration (over two cycles) of granulocytopenia (absolute granulocyte count <500/microliter) at the maximally tolerated dose level of 150 mg/m2 was 8.5 days (range, 5-13 days), and the median duration of thrombocytopenia (platelets <20,000/microliter) was 2.5 days (range, 0-9 days). The median duration of hospitalization including chemotherapy administration was 23 days (range, 19-36 days). Other toxicities included stomatitis, fever, diarrhea, and emesis. One patient developed acute leukemia 54 months posttreatment. We conclude that two courses of high-dose cyclophosphamide and doxorubicin using granulocyte colony-stimulating factor are feasible and safe with tolerable myocardial toxicity as evidenced by serial endomyocardial biopsies. The dose-limiting toxicity encountered was a grand mal seizure. The recommended Phase II dose is doxorubicin 150 mg/m2 administered as a 96-h infusion on days 1-4, with cyclophosphamide 4. 2 g/m2 on day 5 and G-CSF 5 microgram/kg/day started on day 6 and administered until the total WBC is above 10,000/microliter for three consecutive days.
 ...
PMID:High-dose infusional doxorubicin and cyclophosphamide: a feasibility study of tandem high-dose chemotherapy cycles without stem cell support. 981 32

We compared clinical presentation and course of exercise-associated hyponatremia with heat exhaustion among summertime hikers in Grand Canyon National Park. Cases were selected from among hikers who requested medical help from the National Park Service Emergency Medical Service (EMS) or who presented to the medical clinic on the rim of the canyon with complaints related to exercise in the heat. Of 44 patients who had serum samples analyzed, 7 had hyponatremia with clinically significant symptoms and serum sodium levels <130 mmol/L: 3 had grand mal seizures, 2 had other major central nervous system disorders, and 2 had minor neurological symptoms. Seizures and change of mental status distinguished hyponatremia, (P = 0.0002). Indirect evidence suggests that hyponatremic patients were hyperhydrated. Other common symptoms included nausea, vomiting, headache, and dizziness, but these symptoms did not predict the level of serum sodium. When exercise in the heat is prolonged, hyponatremia is suggested either by altered mental status or by seizures without hyperpyrexia or hypoglycemia. No mortality or long-term morbidity occurred in any of these cases of hyponatremia.
 ...
PMID:Exertional heat illness and hyponatremia in hikers. 1053 May 29


<< Previous 1 2 3 4 5 6 Next >>