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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have carried out an open clinical study in Somalia to evaluate the efficacy and safety of a simplified dosage schedule of metrifonate in the treatment of Schistosoma haematobium infection. The doses used were: I. 10 mg X kg-1 once daily for 3 days II. 5 mg X kg-1 thrice daily for one day III. 7.5 mg X kg-1 thrice daily for one day. We screened a total of 550 subjects in four villages for egg excretion in urine, and selected patients with more than 200 eggs per 10 ml of urine. In the initial phase of the study eight patients were assigned to each of the three dose schedules. In an extended study 38 additional patients were treated with regimen II which gave the best outcome in the initial study. Dosage Schedules I and III turned out to be toxic, and none of the patients was treated with all three doses. Adverse effects, such as abdominal colic, nausea, salivation, dizziness, and headache, were seen in almost all the patients in those two groups. Two patients from Group I reported that they fainted within 2 h after the second dose. None of the patients in Group II reported adverse effects. After 4-6 weeks follow-up, egg reduction was 96-100% for Groups I and II and the cure rate was around 60%. This study has shown that a shorter course of treatment with metrifonate might be equally effective and safer than the recommended dosage schedule with three doses of 7.5-10 mg X kg-1 fortnightly.
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PMID:A simplified dosage schedule of metrifonate in the treatment of Schistosoma haematobium infection in Somalia. 311 73

Experimental and clinical experience with compounds containing antimony have shown that the trivalent compounds are generally more toxic than the pentavalent ones. APT can cause severe pain and tissue necrosis and is therefore not given by intramuscular or subcutaneous injection. APT has the actions and uses of AST, but it is less soluble and more irritating than the sodium salt which is therefore more suitable for intravenous use. Trivalent antimony compounds are toxic when used topically. Adverse effects are similar for all trivalent compounds, and include nausea, vomiting, weakness and myalgia, abdominal colic, diarrhoea, and skin rashes, including pustular eruptions. Hypersensitivity reactions also occur. Respiratory symptoms include cough, dyspnoea, and chronic lung changes. Cardiotoxicity is the most important and may produce arrhythmias, myocardial depression and damage, Stokes-Adams attacks, heart failure, and cardiac arrest. Hepatic damage and necrosis, as well as blood dyscrasias, may occur. Toxic effects on the kidney may follow chronic use. Continuous treatment with small doses of antimony may give rise to symptoms of subacute poisoning, similar to those of chronic arsenic poisoning, due to accumulation of antimony in the body, especially if trivalent compounds are used, because of their long biological half-lives. Reproductive disorders and chromosome damage have been reported; antimony compounds are, therefore, potentially toxic to reproduction and have mutagenic, and oncogenic potential. Antimony compounds should, therefore, not be used during pregnancy or in the presence of hepatic, renal, or heart disease. Pentavalent antimony preparations especially the organic compounds, together with non-metallic synthetic preparations, such as the diamidines, have now replaced APT for use in leishmaniasis. Because of the toxicity of antimony compounds, investigations have been undertaken to reduce their adverse effects by combining them with chelating agents. These preparations appear to have reduced the toxic effects of antimony without affecting the efficacy of the preparations. Liposome-encapsulated antimony products have, more recently, been shown to be much less toxic because of the reduced dose of the antimony compound required for effective therapy. The historical uses of antimony were based on the belief that the topical and systemic adverse effects, for example, skin eruptions and diarrhoea and vomiting, were signs that the condition being treated was responding by being brought to the surface to relieve congestion at the diseased area. There is no evidence in topical use, but there is evidence that such use can cause severe reactions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Toxicity of antimony and its compounds. 330 36

Buprenorphine, a new analgesic, was administered at a dose of 0.2 mg by intramuscular injection to 21 patients with acute ureteral colic. The patients consisted of 14 males and 7 females with a mean age of 42. In all cases, the diagnosis was confirmed based on intravenous urography performed after the treatment. In 19 of the 21 patients, colicky pain was reduced at least within one hour after the administration of buprenorphine. No significant changes in the pulse or blood pressure were observed. In 6 patients, mild dizziness or nausea was observed, and none of the patients required withdrawal of the treatment. Clinical use of buprenorphine was considered to the effective and safe in patients with ureteral colic.
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PMID:[Clinical effect of buprenorphine in ureteral colic]. 373 70

Non-steroidal, anti-inflammatory agents (NSAIDs), wellknown inhibitors of prostaglandins, have been used in the treatment of biliary and ureteral pain since the end of the 1970s. The efficacy and tolerance of a new injectable formulation of naproxen sodium in ureteral and biliary pain was investigated in 77 out-patients, observed in an emergency ward, and affected by acute lithiasic symptomatology. Forty-four patients received one 275 mg vial of naproxen sodium intramuscularly, while 33 patients were given one vial at the same dosage intravenously. In 56% of the cases complete relief of pain was achieved within 30 minutes of injection, while in 86% pain was completely relieved or greatly decreased within one hour. Side-effects (nausea, vomiting) occurred in three patients, but were linked to a simultaneous aggravation of the ureteral colic.
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PMID:Treatment of acute pain of ureteral and biliary colic with naproxen sodium administered by the parenteral route. 380 21

In the search for a superior alternative to conventional bowel preparation which often gives unsatisfactory results in children, we have introduced whole-gut irrigation for pediatric use. After a pilot study on 15 children during which adjustments on the technique were made, we settled on an intensive regimen with some notable modifications from conventional adult practice: the use of warm Hartmann's solution, a relatively large fluid load (mean volume 5.3 l/kg body weight, range 3.0 - 12.0 l/kg) and a rapid infusion rate (1.5 ml/kg/min). We then evaluated its safety, effectiveness, and acceptability prospectively on 45 patients undergoing colonoscopy or colorectal surgery, age ranging from 4 months to 11 years, with a mean of 3.9 years. Subjective complaints were mild and included nausea/vomiting, 12 cases (26.7 percent); abdominal colic, two (4.4 percent); and distending discomfort, three (6.7 percent). There was a mean weight gain of 4.0 percent but no gross electrolyte disturbances. Results of bowel preparation were satisfactory in 33 (73.3 percent), adequate in ten (22.2 percent) and poor in two (4.4 percent). Compared with our previous method, in which inadequate preparation occurred in 4/20 patients, (20 percent) by conventional measures, whole-gut irrigation represents a statistically significant improvement (P less than 0.05). In addition, whole-gut irrigation shortened hospital stay and obviated the traditional need of two to three days' dietary restrictions.
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PMID:Whole-gut irrigation in infants and young children. 394 16

The effect of glucagon administered as a bolus (1 mg) followed by a continuous infusion (2 mg/h) for 8 h and a placebo was compared in 37 adults with urographically demonstrated ureteral calculi less than 6 mm. The bolus injection was given 20 min after start of intravenous urography, and the infusion was initiated immediately afterwards. No effect on pain relief or passage of calculi was found. Nausea and/or vomiting were recorded significantly more frequently in patients who had glucagon than in patients who had the placebo. It is concluded that glucagon is of no value in acute ureteral colic.
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PMID:Glucagon in acute ureteral colic. A randomized trial. 394 97

Unexpected differences in clinical and biochemical findings in two brothers occupationally exposed to the same source of lead for dissimilar lengths of time are presented. Only the brother with the shorter period of lead exposure was anemic and afflicted by nausea, vomiting, abdominal colic and arthralgia. His urinary PBG output yielded the high orders of magnitude found in acute intermittent porphyria in relapse. Prior to administration of a single dose of EDTA (1 g of the calcium disodium salt given intravenously in 325 mL 0.15 mol/L NaCl), his blood lead levels averaged 3.6 mumol/L. The amount of chelatable lead retrieved from his urine, 31 mumol/day, was more than twice that found in his asymptomatic counterpart who was exposed to lead for 13 months and whose pre-EDTA blood lead levels averaged 4.0 mumol/L. Not only the activity of delta-aminolaevulinic acid dehydratase, but also that of uroporphyrinogen I synthetase, was markedly inhibited by lead in red cells of both brothers. These activities were restored to normal levels in vitro by addition to the assay system of zinc and dithiothreitol. This ruled out a coexisting genetic deficiency of either enzyme. The anemia of the symptomatic brother with the shorter period of lead exposure was alleviated by folic acid, 15 mg/day. The differences in findings between the two brothers point to differential susceptibility to lead and illustrate the extent to which symptomatic lead poisoning may mimic biochemical and clinical features of the acute porphyrias.
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PMID:Occupational lead exposure: studies in two brothers showing differential susceptibility to lead. 401 20

The side effects of nausea and diarrhea have frequently been observed following the administration of prostaglandin E2 or F2alpha for the induction of labor or abortion. The oral administration of prostaglandin E1 to volunteers has elicited similar reactions. Reports that aspirin might relieve some types of nausea or diarrhea led to the testing of aspirin against the diarrhea induced by the radiation therapy of cancer of the uterine cervix. The treatment of cervical cancer by a combination of external radiation and radium often produces diarrhea, probably because loops of bowel in the path of X-rays are damaged. 15 women between the ages of 47 and 65 who had been irradiated for cancer of the cervix and who had developed diarrhea that failed to respond to conventional therapy participated in a preliminary trial. When conventional therapy failed, it was abandoned and each patient was given 900 mg of soluble aspirin B.P. ("Slfrin") by mouth, 4 times daily. In 4 patients the diarrhea cleared up completely within 24 hours of taking the aspirin. The diarrhea was improved in 8 patients, although in 2 it relapsed 48 hours after improvement was 1st observed. Colicky pain which accompanied diarrhea in 3 patients disappeared during aspirin therapy. 1 patient who had severe nausea experienced marked relief. The findings indicate that aspirin may be of value in the treatment of diarrhea induced by radiation. Since prostaglandin synthesis can be provoked by many different forms of stimulation, and because aspirin at low concentrations inhibits this synthesis, it is suggested that prostaglandins are involved in radiation induced diarrhea. A carefully controlled trial of aspirin in the treatment of radiation induced diarrhea is now being conducted.
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PMID:Aspirin in radiation-induced diarrhoea. 412 59

Approximately 60 persons attended a Christmas dinner, at a Darwin hotel, where oysters were served au natural as part of the menu. Twenty-five of the 28 persons who ate oysters developed symptoms of food poisoning--an attack rate of 89%. Of the 60 persons attending the dinner 44 were investigated. The incubation period and duration of illness were about 36 hours. Diarrhoea occurred in 100% of patients, with colic and nausea in 88% and 80% respectively. Half the patients complained of vomiting and headache. The storage temperature at which the oysters were kept was satisfactory and no bacterial pathogens were grown from the oyster and stool specimens. Electron microscopy revealed two distinct parvovirus-like particles in stool specimens, one of which was identified as Norwalk virus. Serological studies by immune electron microscopy showed the development of antibodies to the Norwalk-like particle by seven out of 10 patients. Confirmatory studies by radioimmunoassay showed a significant rise in antibody titre to Norwalk virus in seven patients.
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PMID:The Darwin outbreak of oyster-associated viral gastroenteritis. 676 72

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95


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