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)

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
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PMID:Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital. 81 31

The clinical spectrum of juvenile head trauma syndromes was derived from an analysis of 50 attacks in 25 patients. Attacks were grouped into four clinical types: (1) hemiparesis; (2) somnolence, irritability, and vomiting; (3) blindness; and (4) brain stem signs. Our evidence shows that these four types are different manifestations of a common underlying process. All attacks followed mild head trauma after a latent interval, generally of one to ten minutes. Forty of the 50 attacks occurred in patients under 14 years of age. Full recovery occurred after a variable time in all but one instance. This patient, and one other, had an angiographically demonstrable occlusion of a branch of the middle cerebral artery. In clinical and laboratory features, these attacks resemble classical migraine and presumably have a similar underlying mechanism.
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PMID:Juvenile head trauma syndromes and their relationship to migraine. 118 Jul 41

Two cases are described presenting a clinical picture of sudden headache, fever and vomiting, accompanied by unilateral ophthalmoplegia and acute deterioration of visual acuity. In one this amounted to monocular blindness with a field defect in the other, indicative of chiasmal compression. Necrotic pituitary adenoma material was removed by the transphenoidal route in both cases. Recovery of eye movements was obtained and considerable improvement of visual acuity, which in one patient, was restored completely.
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PMID:Trans-sphenoidal surgical approach in pituitary apoplexy. 126 21

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Recognition of adrenal atrophy during a review of autopsy findings in two sisters who died at 8 months and 3 1/2 years prompted estimation of very long chain fatty acids, phytanic acid and pristanic acid on wet liver fixed in formalin for 12 years. These were shown to be markedly increased and defects in multiple peroxisomal functions and decrease in particulate catalase were shown in cultured fibroblasts, confirming an abnormality of peroxisomal biogenesis. The patients had presented with failure to thrive, recurrent diarrhoea and vomiting, poor mental development, retinal pigmentation, blindness and in the older patient deafness, with only mild dysmorphic features. Autopsy in the older patient showed adrenal atrophy, cirrhosis, and foamy histiocytes in multiple organs. The brain showed no demyelination, little cytoarchitectural abnormality, occasional perivascular histiocytes in the grey matter and meninges and prominent Purkinje cells in the molecular layer of the cerebellum. In the younger patient the changes were very subtle in spite of the marked clinical similarity. Despite the young age at death the clinicopathological features are most suggestive of infantile Refsum disease. In many situations anatomical pathology can be very useful in the recognition and study of peroxisomal disorders.
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PMID:Autopsy findings in two siblings with infantile Refsum disease. 137 19

2 AIDS patients are described who had cryptococcal meningitis accompanied by increased intracranial pressure (ICP) and visual complications, a finding thought to be relatively rare in AIDS. Of the 2-6% of AIDS patients who develop cryptococcal meningitis, many have disseminated and recurrent infections. The 1st case was a 45-year old Ugandan woman who presented with stiff neck, and right VIth cranial nerve palsy. She was treated with amphotericin B and flucytosine with some improvement, but on the 9th day she awoke with headache, drowsiness, and total blindness, although no papilledema. Her CSF pressure was 40 cm H20. She recovered after a month of intravenous chemotherapy and acetazolamide, but remained blind. Her sudden blindness was thought to be due to bilateral optic nerve infarction. The 2nd case was a 32-year old male homosexual, admitted with headache, vomiting, confusion, and drowsiness. He had stiff neck, and a CSF of 40 cm containing Cryptococcus neoformans. He was given amphotericin B, flucytosine, and has CSF drained every other day. On day 21 papilledema was seen in the right eye, and acetazolamide was started to lower CSF pressure. This patient recovered without loss of vision. 3 published series of cryptococcus meningitis in AIDS patients remarked about the low incidence of raised ICP, while 1 reported 9 of 27 with neurological and ophthalmic complications. The visual complications and increased ICP in these patients was thought to be due to inflammatory arachnoiditis or direct cryptococcal infiltration.
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PMID:Raised intracranial pressure and visual complications in AIDS patients with cryptococcal meningitis. 156 10

Two cases of acute quinine toxicity are presented, one from self-poisoning and the other from an unidentified source. Both patients presented with acute bilateral blindness. They also experienced the classic symptoms of cinchonism, including nausea, vomiting, and tinnitus. Prolongation of the Q-T interval developed in both patients. Serum quinine levels of 5.3 mg/L and 13 mg/L were measured. Although their visual acuity improved, both patients had some residual deficit at follow-up. A review of the literature, including clinical presentation and emergency medicine diagnosis and management, is also presented.
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PMID:Cinchonism: two case reports and review of acute quinine toxicity and treatment. 162 42

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

Fludarabine phosphate (NSC 312878), an adenosine deaminase resistant analogue of 9-beta-D-arabinofuranosyladenine, has entered clinical trials. Eleven patients with acute leukemia in relapse received 14 courses of fludarabine phosphate as a 5-day continuous infusion administered at doses of 40 to 100 mg/m2/day. Toxicity was characterized by uniform myelosuppression, as well as occasional nausea, vomiting, and hepatotoxicity. Three episodes of metabolic acidosis and lactic acidemia were noted. In addition, three patients suffered neurotoxicity. Two of these three patients had a severe neurotoxicity syndrome characterized by blindness, encephalopathy, and coma. Neither patient recovered neurological function. Neuropathological findings at autopsy were characterized by a diffuse, necrotizing leukoencephalopathy which was most severe in the occipital lobes. The medullary pyramids and posterior columns were also severely affected. This sporadic fatal neurotoxicity was observed only at doses greater than 40 mg/m2/day. The maximum tolerated dose for a 5-day infusion of fludarabine phosphate is thus 40 mg/m2/day.
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PMID:Fludarabine phosphate (NSC 312878) infusions for the treatment of acute leukemia: phase I and neuropathological study. 242 88

Vitamin A deficiency is a serious problem throughout the developing world. An estimated 25-50 million children may well suffer the physiologic consequences of vitamin A deficiency; 5 million develop xerophthalmia, of whom 250,000 to 500,000 go blind every year; and untold numbers are at increased risk of diarrhea, respiratory disease, and death. Even mild vitamin A deficiency has been associated with a 14- to 10-fold increase in mortality, and controlled field trials have demonstrated vitamin A supplementation can reduce childhood death rates by 30%-70%. Three general intervention strategies exist for improving vitamin A status of high-risk, rural, economically deprived populations. These include nutrition education leading to increased dietary intake; vitamin A fortification of centrally processed, widely consumed dietary items; and periodic administration of large doses of vitamin A. At present, the latter is far and away the most widely employed intervention activity, because of its immediate impact, and because it can be implemented through the existing (and specialized) health care infrastructure. Vitamin A is a fat-soluble vitamin stored in the liver, so that a large dose of 200,000 IU (100,000 IU for children under 1 year of age) every 6 months reduces mortality, stimulates growth, and prevents xerophthalmia and nutritional blindness. Recent data suggest more frequent administration, every 3 to 4 months, may be desirable. Side effects have been minimal, with mild nausea, vomiting, and headaches in less than 1% to 4% of recipients. Care should be taken, however, that doses above 10,000 IU not be administered to women during the first trimester of pregnancy because of potential teratogenic effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Large dose vitamin A to control vitamin A deficiency. 250 5


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