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)

The Isoparaffins covered in this manuscript are branched aliphatic hydrocarbons with a carbon skeleton length ranging from approximately C10 to C15. They are used in the manufacture of liquid imaging toners, paint formulations, charcoal lighter fluid, furniture polishes and floor clearners. Potential exposure exists in the petroleum, printing and paint industries. Isoparaffins have a very low order of acute toxicity, being practically non-toxic by oral, dermal and inhalation routes. However, aspiration of liquid isoparaffins into the lungs during oral ingestion could result in severe pulmonary injury. Dermally, isoparaffins have produced slight to moderate irritation in animals and humans under occluded patch conditions where evaporation cannot freely occur. However, they are not irritating in non-occluded tests, which are a more realistic simulation of human exposure. They have not been found to be sensitizers in guinea pig or human patch testing. However, occasional rare idiosyncratic sensitization reactions in humans have been reported. Instillation of isoparaffins into rabbit eyes produces only slight irritation. Several studies have evaluated sensory irritation in laboratory animals or odor or sensory response in humans. When evaluated by a standard procedure to assess upper airway irritation, isoparaffins did not produce sensory irritation in mice exposed to up to 400 ppm isoparaffin in air. Human volunteers were exposed for six hours to 100 ppm isoparaffin. The subjects were given a self-administered questionnaire to evaluate symptoms, which included dryness of the mucous membranes, loss of appetite, nausea, vomiting, diarrhea, fatigue, headache, dizziness, feeling of inebriation, visual disturbances, tremor, muscular weakness, impairment of coordination or paresthesia. No symptoms associated with solvent exposure were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxicology update isoparaffinic hydrocarbons: a summary of physical properties, toxicity studies and human exposure data. 219 78

The toxic effects and tissue uptake of both cisplatin and oxaliplatin--[(1R, 2R)-1,2-cyclohexanediamine-N,N'] [oxalato(2-)-O,O']platinum--were previously shown to vary similarly according to dosing time in mice. A 4-hour infusion of cisplatin resulted in fewer side effects and allowed administration of higher doses at 16 hours than at 4 hours in patients with cancer. We hypothesized that the continuous venous infusion of oxaliplatin for 5 days would be less toxic and would deliver a higher dose to the patient if the drug were infused at a circadian rhythm-modulated rate (peak at 16 hr; schedule B) rather than at a constant rate (schedule A). We tested this hypothesis in a randomized phase I trial. We escalated the dose of oxaliplatin to the patient by 25 mg/m2 per course. Courses were repeated every 3 weeks. An external, multichannel, programmable-in-time pump was used for the infusions. Toxicity was assessable for 94 courses in 23 patients (12 patients with breast carcinoma, nine with hepatocellular carcinoma, and two with cholangiocarcinoma). The incidence of neutropenia of World Health Organization grades II-IV and the incidence of distal paresthesias were 10 or more times higher (P less than .05) with schedule A than with schedule B. In addition, vomiting was 55% higher (P = .15) with schedule A than with schedule B. Furthermore, with schedule B, the mean dose of oxaliplatin (P less than .001) and its maximum tolerated dose (P = .06) could be increased by 15% over those doses with schedule A. An objective response was achieved in two of the 12 patients with previously treated breast cancer. We recommend that the dose of oxaliplatin for phase II trials be 175 mg/m2, delivered according to the circadian rhythm-modulated rate.
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PMID:Phase I trial of 5-day continuous venous infusion of oxaliplatin at circadian rhythm-modulated rate compared with constant rate. 234 69

Electrocardiographic (ECG) monitoring was performed on 291 donors during apheresis. Twenty-one donors (7.2%) had clinical symptoms such as discomfort, nausea, chill, numbness, and paresthesia, and 13 of this group exhibited ECG abnormalities, such as tachycardia, bradycardia, and other abnormal wave patterns. The donors with tachycardia and slight bradycardia had no symptoms. Ten donors had moderate to severe bradycardia with pulse rates less than 50 beats per minute; four of them had severe bradycardia (less than 45 beats per minute), and three of the four exhibited severe hypotension, vomiting, fainting, or convulsion. Other abnormal ECG changes, such as supraventricular and ventricular premature contractions, right bundle branch block, ST segment elevation or ST segment depression, and tall, flattened, or inverted T waves were observed in 29 donors (10%). These changes were not associated with symptoms. Only three of these donors complained of discomfort or chest heaviness. The abnormal waves appeared more often in granulocytapheresis donors than in plateletapheresis donors.
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PMID:Abnormal electrocardiographic findings in apheresis donors. 245 70

Cases of ciguatera fish poisoning no longer are confined to endemic areas. This makes awareness of this entity important. The diagnosis usually is made by the presence of gastrointestinal symptoms, nausea, vomiting, and diarrhea, and of neurological symptoms such as paresthesias, paresis, and pruritus. The detection of ciguatoxin in the ingested fish by any of the available bioassays, will confirm the diagnosis. The treatment of this food poisoning is supportive, although intravenous mannitol is reported to be safe and effective. The prognosis is good and complete recovery is to be expected. However, relapses can occur, especially on re-exposure to the toxin.
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PMID:Ciguatera fish poisoning. 250 19

Control of cisplatin-induced nephrotoxicity and nausea/vomiting has enabled the development of very high-dose cisplatin regimens (monthly total dose, 200 mg/m2). Neurotoxicity is now recognized to be the dose-limiting toxicity of these regimens. However, during a pilot study involving 5 mg/m2 vinblastine and 100 mg/m2 cisplatin given every 28 days on days 1 and 8 for the treatment of advanced non-small-cell lung cancer, we noted a high incidence of progressive peripheral neuropathy, which continued for several months after the discontinuation of cisplatin chemotherapy. Of the six patients treated, four received at least three cycles of therapy (median total cisplatin dose, 685 mg/m2; range, 500-725 mg/m2). All four patients developed a progressive peripheral neuropathy, with a worsening of toxicity by 1-3 grades over the 2-3 months after cisplatin discontinuation. One patient progressed from grade I (mild paresthesia) to grade IV (inability to ambulate) over a period of 3 months after the discontinuation of therapy. Stricter rules for early dose de-escalation and discontinuation may be required for very high-dose cisplatin regimens. Delayed progressive neuropathy should be recognized as a possible late complication of this form of therapy.
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PMID:Progressive paresthesias after cessation of therapy with very high-dose cisplatin. 255 19

Twenty-six patients with metastatic breast cancer who had previously responded to one or more endocrine therapies participated in a clinical trial of the combination of trilostane and hydrocortisone for subsequent disease progression. Of these, one patient achieved complete remission (4%), and five had partial response (19%). The median time to progression from initiation of therapy for responding patients was six months (range: 4 - 32 + months). Major toxicities included nausea/vomiting (16 patients), facial flushing (14), abdominal cramping (11), and oral paresthesia (10). Therapy was discontinued in four patients (15%) because of drug intolerance. Fourteen patients who failed trilostane were treated with aminoglutethimide and hydrocortisone. Six patients showed objective response (PR + MR). These data show that trilostane and hydrocortisone in combination can produce an objective response in a significant fraction of patients and that the combination has a different spectrum of toxicity from aminoglutethimide/hydrocortisone. A small number of patients crossed over to aminoglutethimide showed a few objective responses, suggesting a partial lack of cross-resistance between the two antiadrenal drugs.
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PMID:Trilostane with hydrocortisone in treatment of metastatic breast cancer. 265 3

It is generally agreed that bicarbonate dialysate is preferable to acetate dialysate, but the major limiting factors of high cost and technical difficulty in maintaining its stability for prolonged periods preclude its widespread use. The procedure developed by the authors stabilizes bicarbonate dialysate for up to 4 days, rendering bicarbonate dialysate feasible for routine out-patient use. HCO3 dialysate is produced in our dialysis unit after an initial investment of $10,000.00, at a cost per 4-h treatment of $1.22 at a dialysate flow of 500 cc/min. One hundred fifty-one chronic dialysis patients participated in an 18-week study to evaluate clinical symptomatology when bicarbonate was substituted for acetate as the dialysis base buffer. Evaluation of each dialysis treatment (total of 8,183 treatments) consisted of both subjective and objective criteria (vomiting, angina, cramps, hypotension, and frequency of use of mannitol, hypertonic saline, and nitroglycerine). The patients were unaware of the change in dialysate solutions. There was a significant reduction (p less than 0.001) in the incidence of vomiting, cramps, hypotension, nausea, flushing, and the use of mannitol and hypertonic saline during bicarbonate dialysate treatment compared with acetate dialysate. Shortness of breath, angina, mental confusion, and paresthesias were not statistically changed. Although the method of HCO3 dialysate production is associated with occasional higher bacterial count than currently recommended by AAMI standards, no adverse reactions were observed in patients treated with standard efficiency dialyzers. It is concluded that the process for incenter HCO3 production is safe, economical, and better tolerated than acetate dialysate.
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PMID:An economical new process for incenter bicarbonate dialysate production: comparison with acetate in a large dialysis population. 280 52

The authors review the literature discribing non-dyskinetic antipsychotic withdrawal phenomena. Withdrawal of these agents can cause nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgia, paresthesia, anxiety, agitation, restlessness, and insomnia. Psychotic relapse is often presaged by increased anxiety, agitation, restlessness and insomnia, but the temporal relationship of these prodromal symptoms to reduction in the dosage or discontinuation of neuroleptics distinguishes them from the effects of abrupt withdrawal.
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PMID:Antipsychotic withdrawal symptoms: phenomenology and pathophysiology. 289 77

The literature describing nondyskinetic antipsychotic withdrawal symptoms is reviewed. The withdrawal of antipsychotic agents can result in nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgias, paresthesias, anxiety, agitation, restlessness, and insomnia. Psychotic relapse is often presaged by increased anxiety, agitation, restlessness, and insomnia. However, the temporal relationship of these prodromal symptoms to reduction in the dosage or discontinuation of neuroleptics distinguishes them from the effects of abrupt withdrawal.
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PMID:Antipsychotic withdrawal phenomena in the medical-surgical setting. 290 18

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87


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