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)

Four normal adult dogs received two consecutive weekly cycles of human recombinant interleukin-2 (IL-2) by continuous infusion for 4 days/week. The dose of IL-2 given to each dog was 3 x 10(6) units m-2 day-1. Toxicities consisted of mild vomiting, diarrhea, and lethargy to varying degrees in all the dogs. These side-effects were reversed when the treatment was discontinued. Fever, tachypnea, and weight gain were not seen. A marked lymphocytosis and eosinophilia developed in all dogs after completion of each course of IL-2 (resulting in a more than sevenfold increase in each cell type) and persisted for more than 1 month in some. Fresh peripheral blood lymphocytes (PBL) obtained during this lymphocytosis mediated enhanced in vitro lysis of a natural-killer-cell-sensitive canine tumor cell line (CTAC). The in vitro proliferative responses of these same PBL to IL-2 could be detected earlier, progressed faster, and involved more cells than PBL tested prior to IL-2 infusion. Thus, a relatively well-tolerated regime of IL-2 in dogs can induce dramatic increases in lymphocyte numbers and activation, which is associated with augmentation of their in vitro antitumor reactivity. The clinical effectiveness of this immunotherapeutic approach remains to be tested in tumor-bearing dogs where it could serve as a relevant large-animal model for immunotherapy of cancer with IL-2.
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PMID:Clinical and immunological effects of human recombinant interleukin-2 given by repetitive weekly infusion to normal dogs. 804 33

We report a patient with methylmalonic acidemia who developed an acute extrapyramidal disorder after severe ketoacidosis. The neurologic findings resulted from bilateral destruction of the globus pallidus. A 10-year-old girl was the term product of an uncomplicated pregnancy and delivery. Poor feeding and vomiting were noted after one month. She was hospitalized at 6 months of age with vomiting, coma and tachypnea. Analysis of urinary organic acids revealed a massive amount methylmalonic acid. She was not vitamin B 12-responsive and was maintained on a low-protein diet. At 33 months of age, she was able to walk and speak, but she developed acute severe ketoacidosis. Involuntary movements and spastic paraplegia became evident two days after admission. Subsequently, the patient has had metabolic ketoacidosis once or twice a year. Her intelligence quotient was 47. Neurologic examination revealed spastic paraplegia and generalized hypotonicity with mild dystonia. Some relief from dystonic symptoms has been obtained through the use of L-dopa. A brain CT scan at 5 years of age disclosed bilaterally symmetric lucencies of the globus pallidus. T2-weighted brain MRI at 8 years of age showed bilateral symmetric high intensities of the globus pallidus.
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PMID:[Methylmalonic acidemia with bilateral MRI high intensities of the globus pallidus]. 826 Feb 10

The features of toxic shock syndrome in burned children have been described in a review of seven patients (J. D. Frame et al., Burns 1985; 11, 234). These include a 'prodromal' 24-48 h period with diarrhoea, vomiting, general malaise, pyrexia, tachycardia and tachypnoea. The white cell count and haemoglobin concentration fall prior to the 'shock' phase, which occurs 3-4 days postburn. Once 'shock' has occurred the mortality of the condition is approximately 50 per cent; in the absence of 'shock' it is much reduced. We have undertaken a retrospective review of six burned children who were admitted in a 2-year period to the Mount Vernon NHS Trust Burns Unit with a clinical diagnosis of toxic shock syndrome. The evidence from our patients suggests that reliable early diagnostic signs are a rapidly developing severe pyrexia of 39.5 degrees C or above, and a simultaneously increasing tachycardia and tachypnoea to high levels. There is a sudden profound fall in the white cell count and haemoglobin concentration over a period of hours between 1 and 3 days from injury. Specific treatment should be instituted before the onset of 'shock'. The name staphylococcal toxaemia might promote earlier diagnosis and treatment of this condition and so reduce its mortality.
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PMID:Early diagnosis of staphylococcal toxaemia in burned children. 835 73

From January 1984 to May 1994, 17 of 239 children under 15 years old stung by Tityus serrulatus (15.1%) or Tityus bahiensis (84.9%) presented severe envenoming. Of these 17 patients (1-11 years old; median = 2 yr) 14 were stung by T. serrulatus and three by T. bahiensis. All of them received scorpion antivenom i.v. at times ranging from 45 min. to 5 h after the accident (median = 2 h). On admission, the main clinical manifestations and laboratory and electrocardiographic changes were: vomiting (17), diaphoresis (15), tachycardia (14), prostration (10), tachypnea (8), arterial hypertension (7), arterial hypotension (5), tremors (5), hypothermia (4), hyperglycemia (17), leukocytosis (16/16), hypokalemia (13/17), increased CK-MB enzyme activity (> 6% of the total CK, 11/12), hyperamylasemia (11/14), sinusal tachycardia (16/17) and a myocardial infarction-like pattern (11/17). Six patients stung by T. serrulatus had depressed left ventricular systolic function assessed by means of echocardiography. Of these, five presented pulmonary edema and four had shock. A child aged two-years old presented severe respiratory failure and died 65 h after being stung by T. serrulatus. Severe envenomations caused by T. serrulatus were 26.2 times more frequent than those caused by T. bahiensis (p < 0.001).
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PMID:A comparative study of severe scorpion envenomation in children caused by Tityus bahiensis and Tityus serrulatus. 859 62

Death from ferric chloride poisoning has never been reported in Taiwan. We report a fatality from the suicidal ingestion of ferric chloride solution used as an etching agent for printed circuitry. A 25-y-old woman presented with vomiting after ingestion of 200 ml ferric chloride solution (pH 1.0). She had hypoxemia and severe metabolic acidosis with respiratory alkalosis initially. Three hours after her ingestion she presented with drowsy consciousness, tachycardia, tachypnea and protracted vomiting. Laboratory studies showed leukocytosis, elevated glucose, aspartate aminotransferase, amylase, lactate dehydrogenase, and total bilirubin, coagulation defect and hemolysis. Aspiration pneumonia and vision loss were also noted. Four hours after ingestion cardiopulmonary arrest suddenly occurred after severe vomiting and she expired. Toxicological studies showed marked elevation of serum iron (2440 micrograms/dl); the estimated oral dose of ferric chloride was equivalent to 11.52 g (230 mg/kg) of elemental iron. This patient did not receive deferoxamine due to rapid deterioration and a late diagnosis. Deferoxamine should be given in any symptomatic patient or in the presence of anion gap metabolic acidosis with a history of ferric chloride ingestion.
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PMID:A fatal case of acute ferric chloride poisoning. 946 7

A single dose toxicity study of magnesium sulfate by intravenous administration was conducted in rats and dogs. The results are summarized in the following. Magnesium sulfate was administered once at dose levels of 90, 130, 200, 300 and 450 mg/kg to Crj:CD(SD) rats at 6 weeks of age. Deaths occurred in the 200 mg/kg and above groups in both sexes. The LD50 values were 206 mg/kg for males and 174 mg/kg for females. In the surviving animals, in the 130 mg/kg and above groups, tonic convulsions, abnormal gait and tachypnea were seen. However, these signs disappeared gradually and all animals returned to a normal state by 15 min after dosing. There were no treatment-related changes in the body weight or gross pathology. Magnesium sulfate was infused for 6 hr at dose levels of 75, 300 and 1200 mg/kg (12.5, 50 and 200 mg/kg/hr) to female beagle dogs at 6 months of age. No deaths were observed in any of the dose groups and it was considered that the lethal dose level would be higher than 1200 mg/kg(200 mg/kg/hr). In the 1200 mg/kg group, vomiting, decreased spontaneous movement, staggering gait, prone position and flush of the conjunctiva and ear auricles were seen. However, these signs disappeared gradually and animals returned to a normal state by 1 hr after dosing. There were no treatment-related changes in the body weight, food consumption or gross pathology.
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PMID:[A single dose toxicity study of magnesium sulfate in rats and dogs]. 961 34

Dirofilariasis was diagnosed in 2 cats with spontaneous pneumothorax. One cat had a 3-week history of a cough, and the other had an 11-month history of vomiting and tachypnea. Pneumothorax was managed in cats by thoracocentesis and supportive care. Diagnosis of dirofilariasis was made on the basis of heartworm antigen and antibody test results and radiographic findings. Clinical signs of heartworm infection improved after treatment with corticosteroids. Cats had good extended outcomes. Heartworm disease should be one of the differential diagnoses considered in cats with spontaneous pneumothorax.
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PMID:Pneumothorax secondary to Dirofilaria immitis infection in two cats. 965 31

Twenty cases of zinc phosphide (Zn3P2) ingestion (self-poisoning) were seen during the last 5 years (January 1992-December 1996). Poisoning was rare before 1986. Profuse vomiting (100%), pain in abdomen (100%), palpitation and sweating (80%), dyspnea and tachypnea (75%), metabolic acidosis (60%), shock (40%), and hypotension (40%) were the most common presenting features. Five patients (25%) died. The toxic effects were due to liberation of toxic phosphine (PH3) gas which was detected by qualitative silver nitrate paper test in majority of cases.
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PMID:Zinc phosphide intoxication symptoms: analysis of 20 cases. 970 58

Recent advances in the diagnosis and treatment of inborn errors of metabolism have improved substantially the prognosis for many of these conditions. This makes it essential that the practicing pediatrician be familiar with the clinical presentation of these disorders. A practical clinical approach to the recognition of inborn errors of metabolism in the young infant is presented in this review. Indications for specific laboratory studies are discussed. Guidelines are provided for the stabilization and emergency treatment of critically ill infants. This approach will identify those infants who will benefit from additional evaluation and specific treatment. Many of the inborn errors of metabolism, including urea cycle defects, organic acidemias, and certain disorders of amino acid metabolism, present in the young infant with symptoms of an acute or chronic metabolic encephalopathy. Typical symptoms include lethargy, poor feeding, apnea or tachypnea, and recurrent vomiting. Metabolic acidosis and/or hyperammonemia are observed in many of these conditions, but there are notable exceptions, including nonketotic hyperglycinemia and molybdenum co-factor deficiency. Therefore, appropriate laboratory testing for metabolic disorders should be performed in any infant who exhibits these findings. Although sepsis may be the initial consideration in a neonate with these symptoms, inborn errors of metabolism should always be in the differential diagnosis, particularly in a full-term infant with no specific risk factors. Hypoglycemia may be the predominant finding in a number of inborn errors of metabolism, including glycogen storage disorders, defects in gluconeogenesis, and fatty acid oxidation defects. The latter disorders, among the most common encountered, exhibit marked clinical variability and also may present as a sudden death, a Reye's-like episode, or a cardiomyopathy. Jaundice or other evidence of hepatic dysfunction is the mode of presentation of another important group of inborn errors of metabolism including galactosemia, hereditary tyrosinemia, neonatal hemochromatosis, and a number of other conditions. A subset of lysosomal storage disorders may present very early with coarse facial features, organomegaly, or even hydrops fetalis. Specific patterns of dysmorphic features and congenital anomalies characterize yet another group of inherited metabolic disorders, such as Zellweger syndrome and the Smith-Lemli-Opitz syndrome. Each of these symptom complexes, and the appropriate evaluation of the affected infants, is discussed in more detail in this review.
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PMID:Inborn errors of metabolism in infancy: a guide to diagnosis. 983 97

During the 1995 outbreak of Ebola hemorrhagic fever in the Democratic Republic of the Congo, a series of 103 cases (one-third of the total number of cases) had clinical symptoms and signs accurately recorded by medical workers, mainly in the setting of the urban hospital in Kikwit. Clinical diagnosis was confirmed retrospectively in cases for which serum samples were available (n = 63, 61% of the cases). The disease began unspecifically with fever, asthenia, diarrhea, headaches, myalgia, arthralgia, vomiting, and abdominal pain. Early inconsistent signs and symptoms included conjunctival injection, sore throat, and rash. Overall, bleeding signs were observed in <45% of the cases. Typically, terminally ill patients presented with obtundation, anuria, shock, tachypnea, and normothermia. Late manifestations, most frequently arthralgia and ocular diseases, occurred in convalescent patients. This series is the most extensive number of cases of Ebola hemorrhagic fever observed during an outbreak.
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PMID:Ebola hemorrhagic fever in Kikwit, Democratic Republic of the Congo: clinical observations in 103 patients. 998 55


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