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)

A 3 year old boy who had glutaric aciduria diagnosed at 22 months of age was admitted with a history of lethargy, vomiting, and fever. He had been receiving glucose polymers as part of his dietary management. He was severely hypernatraemic, but after resuscitation and rehydration made a good recovery. The possible aetiology of his hypernatraemia is discussed.
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PMID:Glucose polymer regimens and hypernatraemia. 224 22

A phase I trial of 2-beta-D-ribofuranosylthiazole-4-carboxamide (NCS 286193, tiazofurin) was conducted using a 5-day i.v. bolus schedule, every 21 days. Thirty one patients with advanced cancer were entered on the trial. A total of 106 cycles were administered with doses ranging from 550 to 2750 mg/m2. Concomitant administration of Allopurinol was necessary to prevent hyperuricemia. Tiazofurin was difficult to evaluate and many side effects were variable and sporadic. The dose limiting toxicities were nonhematologic consisting particularly of myalgias, headaches and general malaise. Other toxicities included nausea, vomiting, stomatitis, lethargy, sleeping difficulty, sinus bradycardia, skin rash, desquamation of the palms and soles, photophobias and burning of the eyes. Hematologic toxicity was mild and not dose related though it led to a neutropenic septic death in one patient at 2750 mg/m2. Anemia was documented in 60% of cycles. Biochemical abnormalities consisted of mild hyperglycemia, hyperuricemia and elevated skeletal creatinine phosphokinase levels which did not correlate with the incidence or degree of myalgias. Though some patients were able to tolerate higher doses, the recommended dose for phase 2 study is 1650 mg/m2. Further studies will be required to achieve a better understanding of this interesting drug.
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PMID:Phase I study of tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC 286193). 238 15

The ingestion of hydrogen peroxide is usually benign. However, the ingestion of greater than 10% hydrogen peroxide can result in significant pathology. Two fatalities are reported in the literature involving children who ingested 27% and 40%. We report a case involving the ingestion of one mouthful of 35% hydrogen peroxide by a 26-month-old female. The child vomited spontaneously. In the Emergency Department the child was lethargic and had an episode of bright red emesis. Several hours later the child experienced a fainting episode followed by a brief respiratory arrest after which she began drooling bright red blood. The initial oral evaluation was negative. Endoscopic evaluation performed 16 hours postingestion revealed erosion of the cardia of the stomach, erythema of the lower esophageal sphincter, and an additional gastric burn. The child was observed for six days and discharged. Follow-up endoscopy performed 12 days postingestion showed only minimal hyperemia in the cardia of the stomach. Exposures to concentrated hydrogen peroxide should be managed aggressively.
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PMID:Ingestion of 35% hydrogen peroxide. 238 Oct 26

Although consequences of zinc deficiency have been recognized for many years, it is only recently that attention has been directed to the potential consequences of excessive zinc intake. This is a review of the literature on manifestations of toxicity at several levels of zinc intake. Zinc is considered to be relatively nontoxic, particularly if taken orally. However, manifestations of overt toxicity symptoms (nausea, vomiting, epigastric pain, lethargy, and fatigue) will occur with extremely high zinc intakes. At low intakes, but at amounts well in excess of the Recommended Dietary Allowance (RDA) (100-300 mg Zn/d vs an RDA of 15 mg Zn/d), evidence of induced copper deficiency with attendant symptoms of anemia and neutropenia, as well as impaired immune function and adverse effects on the ratio of low-density-lipoprotein to high-density-lipoprotein (LDL/HDL) cholesterol have been reported. Even lower levels of zinc supplementation, closer in amount to the RDA, have been suggested to interfere with the utilization of copper and iron and to adversely affect HDL cholesterol concentrations. Individuals using zinc supplements should be aware of the possible complications attendant to their use.
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PMID:Zinc toxicity. 240 97

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

A case of pituitary apoplexy causing pituitary hemorrhage with extension into the third ventricle is reported. The patient was a 73-year-old, obese female admitted with sudden onset of vomiting and impaired consciousness. Neurological examination revealed that she was stuporous, with marked neck stiffness and a dilated left pupil. A plain skull X-ray showed sellar enlargement and destruction of the dorsum sellae. Computed tomography demonstrated a high-density area in the third and lateral ventricles and a round, high-density mass in the suprasellar cistern. The patient died the next day. Autopsy revealed a large tumor in the sellar and suprasellar areas. The tumor and the hematoma within it compressed the floor of the third ventricle and passed through the lamina terminalis and the hypothalamic region. Histological examination disclosed a basophilic adenoma. The pituitary hemorrhage appeared to be the result of ischemia and necrosis within the pituitary adenoma caused by its acute expansion. The extension of the hematoma into the third ventricle was attributable to the large size of the tumor and its close adhesion to the floor of third ventricle.
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PMID:[Pituitary hemorrhage extending into the third ventricle. Case report]. 248 40

In a randomized prospective trial of radiotherapy in 29 patients. Comparing 24 Gy in six fractions is two to three weeks with a single treatment of 8 Gy in the palliative treatment of bone metastasis no differences could be detected in daily subjective pain scores for one month or monthly objective scores for six months. Of the single treatment group 25% required retreatment. Daily subjective record of nausea/vomiting, diarrhoea, skin reaction and lethargy for one month showed no difference between the two groups. Palliative radiotherapy for metastatic bone pain using a single treatment is recommended.
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PMID:A randomized trial of a single treatment versus conventional fractionation in the palliative radiotherapy of painful bone metastases. 248 89

Inpatient and community-based care can be complementary in relation to the management of HIV disease. Medical records from 200 inpatients of Chikankata Hospital near Lusaka, Zambia and 200 home based patients were examined and compared for the common symptoms of presentation of HIV disease, associated opportunistic infections, and treatment protocols. Drug costs of both groups were also compared. The most common respiratory symptoms in the 2 groups are cough, chest pains, weight loss, and hemoptysis. Treatment employed for these symptoms were cortimoxazole, penicillin V, erthromycin, and tetracycline. Acetyl saliclic acid and paracetamol were used for pain relief in both groups. Gastointestinal system symptoms for both groups were diarrhea, weight loss, abdominal pain, and vomiting. Cotrimoxazole and metronidazole were used in treating diarrhea. Additional treatment protocol for the 2 patient samples included oral rehydration therapy for dehydration, antacid or bismuth subsalicylate for diarrhea and enteritis, and mycostatin for oral candidiasis. Central nervous system symptomatology included headache, dementia, neckace, and lethargy. Chloramphenicol was employed in treating bacterial meningitis. Diazepam and chlorpromazine were effective for restless patients. Genito-urinary system symptomatology for the 2 groups included dysuria, genital ulcers, hematuria, viral warts, and buboes. Antibodies were used for sexually transmitted diseases and infections. Skin symptomatology included rash and dermatitis, herpes zoster, abscess, kaposi's sarcoma, ulcers, furunculosis, and discharging anal sinus. In treating these symptoms, hospital based care and home based care were similar. Overall, it was found that hospital treatment protocols were detailed, expensive, and time consuming. Furthermore, hospital treatment for HIV positive patients is more expensive than HIV negative patients; hospital costs for 50 HIV negative patients totaled US$415.94 compared to US$1204.98 HIV positive/PTB negative patients and US$1705.62 for HIV positive/PTB positive patients. Drug cost/patient admission is increased by 469% if HIV positive. (author's modified).
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PMID:Clinical care as part of integrated AIDS management in a Zambian rural community. 248 94

Toxicosis caused by Anabaena spiroides was diagnosed in 7 of 26 finishing hogs in a farrow-to-finish operation in Kentucky. Several sick pigs in the herd had the following clinical signs: vomiting, dull appearance, lethargy, anorexia, muscle tremors, frothing at the mouth, coughing, sneezing, dyspnea, and bloody diarrhea. Of the 7 dead pigs, 2 were necropsied. Tissue speciments and stomach contents were obtained for microscopic, microbiologic, and toxicologic evaluations. In addition, vomitus from sick pigs and pond water samples were collected for laboratory analysis. Direct microscopic examination of pond water, vomitus, and stomach contents revealed nearly pure A spiroides, a toxic blue-green algae. The possible involvement of bacterial toxins in these pigs was not established; however, the laboratory and field data suggested that the clinical signs and death losses were attributable to the consumption of pond water mixed with the bloom of the alga, A spiroides.
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PMID:Blue-green algae (Anabaena spiroides) toxicosis in pigs. 250 12

Medium-chain acyl-CoA dehydrogenase deficiency is a recently described inborn error of metabolism characterized by episodes of coma and hypoketotic hypoglycaemia in response to prolonged fasting. Secondary carnitine deficiency has been documented in these patients as well as the excretion in the urine of medium-chain-length acyl carnitine esters, such as octanoylcarnitine. Based on the potential toxicity of medium-chain fatty acid metabolites and the beneficial responses of patients with other inborn errors of metabolism and secondary carnitine deficiency, oral carnitine has been proposed as treatment for children with medium-chain acyl-CoA dehydrogenase deficiency. We report the results of carefully monitored fasting challenges of an infant with this deficiency both before and after 3 months of oral carnitine therapy. Carnitine supplementation failed to prevent lethargy, vomiting, hypoglycaemia and accumulation of free fatty acids in response to fasting despite normalization of plasma carnitine levels and a marked increase in urinary excretion of acyl-carnitine esters. Potentially toxic medium-chain fatty acids accumulated in the plasma in spite of therapy. Based on this study of one patient, we stress that avoidance of fasting and prompt institution of glucose supplementation in situations when oral intake is interrupted remain the mainstays of therapy for medium-chain acyl-CoA dehydrogenase deficient patients.
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PMID:Medium-chain acyl-CoA dehydrogenase deficiency: metabolic effects and therapeutic efficacy of long-term L-carnitine supplementation. 250 71


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