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)

Green-tobacco sickness is an occupational illness of tobacco harvesters. Symptoms include nausea, vomiting, dizziness, and prostration. The disease is self-limited and of short duration, but recurs frequently in susceptible workers. The aetiology is not known, but nicotine has been suspected as a causative agent. Thirty-two workers on four North Carolina tobacco farms were studied during harvesting. None of these workers smoked or chewed tobacco. Urinary cotinine (the major metabolite of nicotine) levels were monitored over a 24-hour period to evaluate nicotine absorption. There was a tenfold rise in mean excretion of cotinine among workers who had greatest contact with the tobacco. Less cotinine was found in urine of workers who had less exposure. Levels of cotinine exceeded those found in novice smokers who smoked 3 cigarettes in succession. Absorption of nicotine from tobacco leaf is the likely cause of tobacco sickness.
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PMID:Nicotine absorption by workers harvesting green tobacco. 4 56

The sleep of eight volunteers (mean age 55) was recorded electrophysiologically while viloxazine 200 mg was taken daily for 3 weeks, preceded and followed by a week of matching blanks. The volunteers also made ratings of their feelings on visual analogue scales. Another 15 volunteers (mean age 34) took viloxazine 300 mg daily for 3 weeks, preceded and followed by 3 weeks of matching blanks, and they also made daily ratings of feelings. The drug diminished sleep duration and caused more frequent and longer transitions into wakefulness and drowsiness. Slow-wave sleep decreased and stage 2 increased. REM sleep was markedly reduced, especially initially, and there was a withdrawal rebound. Viloxazine impaired subjective concentration mood, and quality of sleep. Three volunteers, however, had striking mood elevation. The drug caused a small loss of weight, which correlated with gastrointestinal symptoms. Three older subjects experienced withdrawal vomiting and prostration. Viloxazine shares properties with imipramine and with amphetamines.
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PMID:Viloxazine, sleep, and subjective feelings. 20 85

Five patients who had injected intravenous (i.v.) phenmetrazine or methamphetamine developed marked prostration resembling septic shock, disseminated intravascular coagulation, rhabdomyolysis with myoglobinuria, and azotemia. Soon after injection, four noted chills, fever, sweats, nausea, and abdominal cramps. Within hours, they developed vomiting, myalgias, paresthesias, headache, and orthostasis. Cardiorespiratory arrest, accelerated bleeding, and noncardiac pulmonary edema were observed in one patient. From 4 to 11 litres of saline were required in the first 24 h to maintain blood pressure and urine output, suggesting that shock resulted from massive loss of intravascular volume into necrotic muscle. Recognition of this syndrome and treatment by aggressive volume replacement led to the recovery of all five patients.
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PMID:Rhabdomyolysis and shock after intravenous amphetamine administration. 84 98

Adverse effects occurred in four youths after intravenous injection of an aqueous cannabis-seed tea, which was prepared by boiling the seeds. The effects were immediate and included nausea, vomiting, abdominal pain, watery diarrhea, chills, fever, hypovolemic shock, hypotension, and non-oligemic transitory renal failure. Other manifestations included persistent hypoglycemia, tachycardia, gastrointestinal bleeding, conjunctival hemorrhage, injury, jaundice, splenomegaly, leucocytosis, myalgia, arthralgia, motor weakness, and prostration. Ischemia was noted on electrocardiogram (EKG). All manifestations appeared to reverse within weeks, but these effects had been potentially fatal.
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PMID:Adverse effects of intravenous cannabis tea. 87 75

We have used an antihuman tumor necrosis factor monoclonal antibody, CB006 (murine IgG1), to prevent the OKT3-induced acute clinical syndrome. This syndrome is due to the massive, although transient release in the circulation of various cytokines (TNF, interferon gamma, interleukin 2, interleukin 6) and represents one important side effect linked to in vivo use of OKT3. Fourteen kidney allograft recipients undergoing prophylactic OKT3 therapy were treated with CB006 in a single i.v. injection of either 0.4 mg/kg (group I, 7 patients) or 2 mg/kg (group II, 7 patients), 1 hr before the first OKT3 administration. Nineteen consecutive patients formed a historical control group. None of the CB006-pretreated patients showed any of the common, severe OKT3-associated symptoms (hypotension, respiratory distress, or neurotoxicity), which were observed in 10% of the historical controls. In addition, CB006-treated patients showed a lower frequency of pyrexia (> or = 39 degrees C) and gastrointestinal symptoms. None of the CB006-treated patients presented severe vomiting or diarrhea, defined as repeated episodes inducing significant fluid and electrolyte loss. Two out of the 7 patients in group I and group II had mild transitory diarrhea. Mild single vomiting episodes occurred in 2 group I patients and 3 group II patients. At variance in all controls, gastrointestinal symptoms were long lasting and associated with major prostration due to electrolyte and fluid loss. Importantly, CB006-treated patients who presented mild symptoms had detectable bioactive circulating TNF, showing incomplete inactivation of OKT3-induced TNF by CB006. CB006 was perfectly well tolerated, did not induce xenosensitization, and did not affect the biological or clinical effectiveness of OKT3.
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PMID:Evidence that antihuman tumor necrosis factor monoclonal antibody prevents OKT3-induced acute syndrome. 146 94

This study analyzed the capacity of an anti-human tumour necrosis factor (TNF) monoclonal antibody, CB006 (murine IgG1, Celltech), to prevent the OKT3-induced acute clinical syndrome. Fourteen renal allograft recipients undergoing prophylactic OKT3 therapy were included. CB006 was administered as a single i.v. injection, 0.4 mg/kg (Group I, 7 patients) and 2 mg/kg (Group II, 7 patients), one hour prior to the first OKT3 administration. Nineteen consecutive patients that were part of a randomized multicenter trial constituted the historical control group. In all patients CB006 was perfectly well tolerated and significantly decreased the frequency of the common OKT3-associated acute symptoms. None of the CB006 pretreated patients showed severe life threatening symptoms (hypotension, respiratory distress or neurotoxicity), observed in 10 per cent of historical controls. At variance with controls, in CB006 treated patients gastrointestinal symptoms (vomiting, diarrhea) and pyrexia (body temperature greater than or equal to 39 degrees C) appeared in low frequency, were mild and short lasting, never promoting major prostration of the patients due to electrolytes and fluid loss. Importantly, the presence in some patients of these mild symptoms, correlated with detectable bioactive TNF in the circulation thus reflecting incomplete blockade by CB006 of OKT3-induced TNF. CB006 pharmacokinetics data further stressed the need for adequate dosage adaptation. CB006 did not affect the biological or clinical effectiveness of OKT3. None of the patients showed evidence of anti-CB006 xeno-sensitization.
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PMID:[Acute clinical syndrome associated with OKT3 administration. Prevention by single injection of an anti-human TNF monoclonal antibody]. 183 13

N-(2,2-Diphenylethyl)adenosine (DPEA) has been identified as a potential antipsychotic agent acting via stimulation of adenosine receptors. The projected human therapeutic dose, based on animal studies, is 2-3 mg/kg. DPEA has been tested for potential toxicity in mice, rats, dogs and monkeys. Following single oral doses, median lethal dose values were approximately 10-fold greater in rats than in mice, although similar clinical signs including reduced activity, prostration, and necrosis of the tail were seen in both species. DPEA was well tolerated at daily doses up to 40 mg/kg in rats for 2 weeks. A no observed effect level (NOEL) was not identified in the dog or monkey studies. Reduced activity, dacryorrhea, ptosis, hypothermia, necrosis of the tail, and death occurred in rats given 120 and 160 mg/kg. Pathologic changes consisted of pancreatitis, gastric erosion/ulceration, lymphocyte depletion of the thymus, and pulmonary congestion and hemorrhage at 80 mg/kg or greater. In dogs, sporadic emesis was noted at 12.5 mg/kg and greater, and significant pathologic changes consisted of coronary arteritis associated with myocardial lesions and lymphocyte depletion at 25 and 50 mg/kg, pancreatic acinar necrosis at 50 mg/kg, and renal tubular degeneration at 12.5 mg/kg and greater. Emesis and depression were noted at 25 and 50 mg/kg in monkeys. Renal tubular dilatation and degeneration at 25 and 50 mg/kg were noted in the monkeys. These studies demonstrated that DPEA produced a range of adverse effects in common laboratory animal species.
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PMID:Preclinical toxicity studies of an adenosine agonist, N-(2,2-diphenylethyl) adenosine. 187 77

Acute and 1-month toxicity studies with SCH 31846, a nonsulfhydryl anti-hypertensive agent which acts by inhibiting angiotensin-converting enzyme, were initiated to evaluate its toxicity. The oral LD50s in mice and rats were approximately 1.8 and 2.5 g/kg, respectively, while the iv LD50 was approximately 450 mg/kg in mice and 150 mg/kg in rats. Signs of acute toxicity in rats and mice included salivation, hypoactivity, ataxia, prostration, and convulsions. In a 1-month dog study at oral doses of 25, 75, or 150 mg/kg, there was a dose-related increase in emesis between 1 and 2 hr after dosing. Absorption studies showed peak blood concentrations occurring in dogs between 0.3 and 1 hr after dosing. No other noteworthy antemortem changes were observed. In a 1-month rat study at oral doses of 30, 180, or 600 mg/kg, the hematocrit and hemoglobin values of the 600 mg/kg-dosed female rats were slightly but significantly (p less than 0.05) decreased and the blood urea nitrogen was slightly but significantly (p less than 0.05) increased in all SCH 31846-dosed male rats and the 600 mg/kg-dosed female rats. Absorption studies in male rats at doses of 30, 180, and 600 mg/kg indicate that SCH 31846 is well absorbed in rats. The 150 mg/kg-dosed dogs and the 180- and 600 mg/kg-dosed rats had a slight increase in the number of renin-containing granules in the renal juxtaglomerular cells. No other compound-related microscopic changes were observed. These data are similar to data reported for Captopril and suggest that in the dog and rat the toxicity of ACE inhibitors is not dependent upon the presence or absence of a sulfhydryl group.
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PMID:Acute and subchronic toxicity of a nonsulfhydryl angiotensin-converting enzyme inhibitor. 300 64

Two incidents of toxin-type food poisoning in N.E. Scotland associated with the consumption of red whelks (Neptunea antiqua) are described. Four patients developed symptoms within 1 h of consuming whole whelks. These included visual disturbances--double vision and difficulty in focusing--tingling of the fingers, prostration and in one subject nausea, vomiting, diarrhoea and ataxia. In all cases recovery was complete in 24 h. Using a newly developed analytical technique the concentration of the causative toxin, tetramine, in the salivary glands of the whelks consumed was estimated at 0.07%, equivalent to a content of 3.75 mg/100 g of the shellfish.
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PMID:Food poisoning due to the consumption of red whelks (Neptunea antiqua). 318 22

Antimonial preparations (Pentostam, Neostibosan, stibophen, and tartar emetic) have occasionally been used in the treatment of onchocerciasis without very promising results. The advent of the preparations TWSb (stibocaptate) and MSbE (Friedheim) of allegedly reduced toxicity made it desirable to test them against Onchocerca volvulus.The action of both preparations on the parasites was found to vary from one patient to another, ranging from complete elimination of all parasites in a few cases to no detectable action in others. A microfilaricidal action was detectable in many patients, particularly after treatment with TWSb, which was used at higher doses than MSbE. A lethal or sterilizing action on some or all adult female worms was observed in some patients. However, toxic reactions to the drugs were common and distressing, and often it was necessary to stop treatment on this account. Anorexia, nausea, vomiting and prostration were the most common manifestations, and there was one fatality from coincident yellow fever, which may well have been aggravated by antimony treatment.The uncertain action of these preparations on O. volvulus and the toxic manifestations that accompany their use render them unsuitable for the treatment of onchocerciasis, and it is probable that the effects of antimony on O. volvulus are produced only at or above the normal level of human tolerance.
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PMID:The effects of drugs on Onchocerca volvulus. 2. The antimonial preparations TWSb and MSbE. 488 Oct 67


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