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)

To determine the pattern of emergency department (ED) utilization by renal dialysis (RD) patients, a prospective study was conducted of dialysis patients presenting to the ED of a regional dialysis center. The most common presenting complaints were shortness of breath (SOB), chest pain, abdominal pain, and vomiting; the most common diagnoses were congestive heart failure, chest wall pain, and electrolyte abnormalities. Interventional dialysis (ID), defined as emergent dialysis required to treat the patient's presenting complaint, was required for 30 patients, with the most common presenting complaints of these patients being shortness of breath, weakness, and chest pain. Only SOB was statistically significant in predicting the need for ID (P less than 0.001), with a positive predictive value of 0.63 and a negative predictive value of 0.85. Prehospital implications of these data suggest that RD patients with a chief complaint of SOB should be transported directly to a facility capable of dialysis on an emergent basis.
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PMID:Emergency department presentation of renal dialysis patients: indications for EMS transport directly to dialysis centers. 205 Sep 72

Stool specimens from 127 adults with gastrointestinal disorders, 357 persons engaged in a livestock farming in the district of Leningrad were examined for Cryptosporidium oocysts with the Ziehl-Neelson routine. Five positive cases were established among the latter cohort. Besides, the study conducted at the hospitals of Leningrad that enrolled 373 children aged under 7 years revealed oocysts in 10 of them. Two of the latters had high temperature (39-40 degrees C) during 3 and 5 days, respectively. Common clinical symptoms of cryptosporidiosis were vomiting, profuse diarrhea and weakness. Accompanied with the normalization of the stool the mean recovery time was 7.4 days. One child recovered 15 days after the disease onset. For the first time human cryptobiosis was detected in the USSR (Leningrad). Its sources and the routes of transmission still remain unknown.
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PMID:[The detection of human cryptosporidiosis in Leningrad]. 214 94

In 1988-1989 two outbreaks of trichinosis were recorded. The first case was group disease developed in 3 members of the family. The source of infection was rissoles rolled in cabbage leaves [correction of goloubets] stuffed with minced pork. The second outbreak affected 13 persons who had eaten home-made pork sausage and fat. All the patients displayed fever, weakness, muscular pain, subcutaneous fat edema, predominantly of the face. The patients suffered from dry mouth, thirst, deteriorated appetite, exanthema, eosinophilia, more occasionally, nausea, vomiting, abdominal pain and diarrhea. Trichinosis was confirmed serologically. Vermox therapy (300 mg per day) was performed for 7 to 12 days. The disease was severe, moderate and mild in 5, 7 and 4 patients, respectively. A brief abstract from a case record of a patient with severe trichinosis complicated by allergic myocarditis is presented. The severity of the disease was associated with the infecting dose and the time at which etiotropic therapy was started. Vermox had a good therapeutic effect and caused no adverse events.
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PMID:[The clinical characteristics of 2 outbreaks of trichinelliasis]. 214 73

Hereditary tyrosinemia results from an inborn error in the final step of tyrosine metabolism. The disease is known to cause acute and chronic liver failure, renal Fanconi's syndrome, and hepatocellular carcinoma. Neurologic manifestations have been reported but not emphasized as a common problem. In this paper, we describe neurologic crises that occurred among children identified as having tyrosinemia on neonatal screening since 1970. Of the 48 children with tyrosinemia, 20 (42 percent) had neurologic crises that began at a mean age of one year and led to 104 hospital admissions. These abrupt episodes of peripheral neuropathy were characterized by severe pain with extensor hypertonia (in 75 percent), vomiting or paralytic ileus (69 percent), muscle weakness (29 percent), and self-mutilation (8 percent). Eight children required mechanical ventilation because of paralysis, and 14 of the 20 children have died. Between crises, most survivors regained normal function. We found no reliable biochemical marker for the crises (those we evaluated included blood levels of tyrosine, succinylacetone, and hepatic aminotransferases). Urinary excretion of delta-aminolevulinic acid, a neurotoxic intermediate of porphyrin biosynthesis, was elevated during crises but also during the asymptomatic periods. Electrophysiologic studies in seven patients and neuromuscular biopsies in three patients showed axonal degeneration and secondary demyelination. We conclude that episodes of acute, severe peripheral neuropathy are common in hereditary tyrosinemia and resemble the crises of the neuropathic porphyrias.
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PMID:Neurologic crises in hereditary tyrosinemia. 215 31

A 17-year-old boy who had mitochondrial encephalomyopathy with focal deficiency of cytochrome c oxidase (CCO) activity is described. He experienced 3 episodes of muscle weakness, fatigability, nausea, vomiting and concomitant increase of serum creatine kinase activity, at the age of 13, 15 and 17 years. During interval there was no muscle weakness and the serum creatine kinase activity was within normal range. Increased levels of lactic acid and pyruvic acid were observed in the blood and cerebrospinal fluid. After an aerobic exercise test, lactic acid and pyruvic acid in the blood increased to an abnormally high level, and the arterial blood became acidic (pH 7.297). On EEG, occasional intermittent irregular theta activities were observed in the anterior region, but there were no abnormalities on CT and MRI in the central nervous system. In the biopsied muscle, ragged-red fibers comprised 20% on modified Gomori-trichrome staining and a number of fibers with no CCO activity were scattered throughout. The CCO activity in the mitochondria isolated from the biopsied muscle was reduced to 49.2 nmol/min/mg protein (normal range 144.7-355.8), while other mitochondrial enzyme activities in the electron transport system were normal. From these data, the patient was considered to have a unique form of mitochondrial encephalomyopathy. By the administration of a large amount of coenzyme Q10, episodes of muscle weakness and nausea, and an increase of lactic acid and pyruvic acid in the blood after aerobic exercise test were no longer observed.
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PMID:[Mitochondrial encephalomyopathy (focal cytochrome c oxidase deficiency) with transient episodes of muscle weakness and elevation of serum creatine kinase activity]. 216 88

Review of all reports involving anthelmintics in dogs and cats to the IAPIC between January 1, 1986 and August 10, 1988, revealed that ivermectin (extra-label use) and piperazine accounted for over 50% of the calls assessed as toxicoses and suspected toxicoses. Both ivermectin and piperazine are gamma-aminobutyric acid (GABA) agonists and their major effects appear to be on the central nervous system. Ivermectin toxicoses at estimated doses of greater than or equal to 100-less than 500 micrograms/kg were reported more than once only in the collies (n = 25) and Australian shepherds (n = 10); these two breeds accounted for 46% (69 of 150) of the toxicoses and suspected toxicoses calls in dogs. Ataxia, behavioral disturbances, tremors, mydriasis, weakness/recumbency, apparent blindness, hypersalivation/drooling (dogs only), and coma were the most commonly reported clinical signs in dogs and cats with suspected ivermectin toxicoses. Shock, dyspnea, vomiting, and ataxia were the most common clinical signs attributed to the microfilaricidal activity of ivermectin. Piperazine was the anthelmintic with the greatest number of reports of toxicoses and suspected toxicoses in cats. Piperazine neurotoxicity in cats and dogs usually was manifested by muscle tremors, ataxia, and/or behavioral disturbances within 24 hours after estimated daily dose(s) between 20 and 110 mg/kg.
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PMID:Ivermectin and piperazine toxicoses in dogs and cats. 218 Jan 89

A 14-year-old male presented with a one week history of weakness, lightheadedness and vomiting. Bilateral pleural effusions were evident on chest radiography; electrocardiogram revealed decreased voltages. Echocardiogram, abdominal ultrasound and magnetic resonance imaging revealed a mass in an hepatic vein and the inferior vena cava extending up to and filling the right atrium. Under deep hypothermia and extracorporeal circulation the mass was removed en bloc. It originated from the hepatic vein. Pathology revealed a smooth muscle tumour intermediate between benign and malignant (atypical leiomyoma). This is the first reported pediatric primary leiomyoma of the hepatic vein. It caused the Budd-Chiari syndrome, a rare pediatric entity.
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PMID:Atypical hepatic vein leiomyoma extending into the right atrium: an unusual cause of the Budd-Chiari syndrome. 218 75

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

Patients may be intolerant of zidovudine for several reasons, the most prominent being hematologic toxicity. In vitro studies demonstrate that zidovudine is toxic to the myeloid and erythroid precursors in the bone marrow; at concentrations of zidovudine near those associated with the optimal antiviral effect in vitro, the proliferative capability of these progenitor cells is reduced 50%-70%. The clinical manifestations of anemia and leukopenia generally are time- and dose-dependent. Strategies for alleviating the hematologic toxicity of zidovudine include the use of hematopoietic growth factors, such as erythropoietin, granulocyte colony-stimulating factor, or granulocyte-macrophage colony-stimulating factor. Myopathy, a recently recognized toxic effect of zidovudine, also appears to be time-dependent. Patients often complain of muscle weakness and discomfort and exhibit an associated elevation in creatine phosphokinase level; dose reduction or discontinuation of therapy generally is required. Some patients have experienced high fever, nausea, and vomiting; however, these effects are unusual and of unclear etiology. The substantial proportion of patients with AIDS or AIDS-related complex receiving zidovudine who experience hematologic or muscular toxicity may benefit from treatment with new antiviral agents, such as dideoxyinosine, with toxicity profiles different from that of zidovudine.
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PMID:Zidovudine intolerance. 220 Oct 71

An accidental poisoning due to drinking methyl alcohol in Chaoyang county is reported, analysing the accident. The poison came from the "retail white spirit" which was contaminated with methyl alcohol. Twenty-nine persons drank the wine, fourteen of them died, two of them became blind. After drinking this "retail white spirit" the drinkers showed symptoms of vertigo, headache, weakness, vomiting, night sweat, dyspnea and blurring of vision etc. within 6-120 hours. On examining the remaining spirit, we found the content of methyl alcohol to be between 16.6 and 40.69 g/100 ml. Some of the patients' urine and blood also contained methyl alcohol. We reckoned that each one of the twenty patients had taken more than 27 g of methyl alcohol and each of the ten dead drank more than 40 ml of the alcohol.
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PMID:[Accidental methyl alcohol poisoning]. 225 26


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