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)

Pentamidine, recently released for clinical use, is effective in therapy for the hemolymphatic stage of Gambian trypanosomiasis, antimony-resistant leishmaniasis, and Pneumocystis carinii pneumonia. The mechanism of action is unclear and may differ for different organisms. Trypanosomes actively transport pentamidine intracellularly, and the drug may then interfere with DNA biosynthetics. However, pentamidine appears to kill nonreplicating P. carinii. The mechanism of killing is unexplained. The pharmacokinetics of pentamidine has been incompletely studied in humans. The estimated volume of distribution is 3 liters/kg. Levels in plasma of pentamidine range from 0.3-1.4 microgram/ml after standard 4 mg/kg dosing, with no appreciable increase in drug levels on successive dosing and no correlation between levels and creatinine clearance or adverse reactions. The drug appears to be concentrated in the kidney and excreted in the urine, with levels detectable six to eight weeks after cessation of therapy. Immediate adverse reactions have included hypotension, nausea, and vomiting. Local pain or abscess formation at an injection site, mild azotemia, leukopenia, abnormal findings from liver function tests, and hypoglycemia may also occur.
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PMID:Pentamidine: a review. 390 42

Study was made of the pharmacokinetics and toxicopathy of deoxynivalenol (DON, vomitoxin) given IV to swine. In the 24 hours after swine were given DON, clinical signs of vomiting, diarrhea, muscular weakness, tremors, and twilight coma were similar to those observed with other 12,13-epoxytrichothecenes. Hypoglycemia and pancreatic islet cell lesions were observed which indicated that DON-induced changes in intermediary metabolism may be an insidious aspect of DON intoxication. Histopathologic examination of all organ systems revealed pancreatic acinar and islet cell necrosis and mild lympholysis of the mesenteric lymph nodes. The renal excretion of DON was altered by IV infusion of saline solution. Pharmacokinetic findings may indicate that DON was both secreted and reabsorbed by the renal tubules. The half-life of DON ranged from 2.08 to 3.65 hours. Residues of DON were not found in skeletal muscle of swine at 24 hours after dosing.
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PMID:Preliminary study of the pharmacokinetics and toxicopathy of deoxynivalenol (vomitoxin) in swine. 397 Apr 24

Five patients aged 7 to 21 months are described who developed attacks of coma after a short prodromal illness with diarrhea or vomiting or both. Four had concomitant hypoglycemia, and all had hypoketonemia, with excessive urinary excretion of medium-chain dicarboxylic acids, medium-chain (omega-1)-hydroxyacids, suberylglycine, hexanoylglycine, and octanoylcarnitine. All patients accumulated octanoic acid, decanoic acid, and cis-4-decenoic acid in plasma. Fibroblasts from three patients showed a decreased rate of octanoate oxidation (10%, 12%, and 29% of control values, respectively). These findings suggest a deficiency of medium-chain acyl-CoA dehydrogenase, most probably an autosomal recessive inherited metabolic disorder. Two of the patients died during an acute attack, and a third had severe neurologic sequelae; the two remaining patients recovered. Plasma free carnitine levels were low, but total carnitine was normal. The three surviving patients underwent a fasting test, which did not lead to hypoglycemia, although hypoketonemia, dicarboxylic aciduria, and excessive mobilization of fatty acids did occur. The surviving patients were maintained on frequent carbohydrate-enriched meals.
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PMID:Octanoic acidemia and octanoylcarnitine excretion with dicarboxylic aciduria due to defective oxidation of medium-chain fatty acids. 403 35

Congenital methylmalonic acidaemia (MMA-aemia) was diagnosed in an 8-month-old girl who presented with severe metabolic acidosis, hypoglycaemia and hyperglycinaemia. Vomiting, failure to thrive and apathy first appeared when breast feeding was replaced by a cows' milk formula at the age of 3 months. The patient, unresponsive to OH-Cbl therapy, was successfully treated with dietary protein restriction and with Shohl's solution. Aged 4 years 9 months, she is in good health. Studies in cultured fibroblasts revealed a defect of the MMA-CoA mutase apoenzyme. Mutase activity in cell extracts was barely detectable both with and without added coenzyme (Ado-Cbl). Addition of OH-Cbl to the culture medium improved overall propionate metabolism in intact fibroblasts but had no effect on mutase activity in cell extracts. These observations point to the presence of a very labile mutant enzyme, suggesting that the patient reported here may be suffering from yet another variant of MMA-aemia.
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PMID:Methylmalonic acidaemia due to mutase apoenzyme defect: responsive to vitamin B12 in intact fibroblasts but not in vivo. 613 33

An 8-yr-old girl is presented who had periodic attacks of vomiting, psychotic depression, drowsiness, and hypertension (160/110 mm Hg) for a period of 16 months after head injury. At the initiation of the attack, serum ACTH and vasopressin levels were prominently increased (610 pg/ml and 41 microunits/ml, respectively), followed by hypercortisolemia, hyponatremia, and hypoosmolality in plasma. Serum PRL also was elevated (91 ng/ml). Responses of GH and cortisol to insulin-induced hypoglycemia and those of TSH to TRH were reduced. Urinary excretion of epinephrine and norepinephrine were increased, while dopamine (DA) excretion was reciprocally decreased, resulting in a marked elevation of the epinephrine plus norepinephrine to DA ratio during the episodes (0.4-4.5); this was normalized on attack-free days (0.08-0.25). During the attack, the concentration of homovanillic acid, a major metabolite of DA in the brain, also was reduced in cerebrospinal fluids from 70 to 23 ng/ml. The administration of methyl-dopa and reserpine effectively suppressed the recurrence of the episode. Although the exact cause of this syndrome is unknown, a periodic metabolic dysfunction of catecholamine in the central nervous system might be postulated.
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PMID:A syndrome of periodic adrenocorticotropin and vasopressin discharge. 627 29

A recently introduced rodenticide containing N-3-pyridylmethyl N'-p-nitrophenyl urea (PNU), Vacor, was accidently ingested by a 25-month-old child, resulting in acute vomiting, lethargy, seizures, and hypoglycemia, as well as chronic evidence of autonomic and peripheral neuropathy and glucose intolerance. Treatment with niacinamide (nicotinamide), may have been of benefit since all problems were resolved within three months of ingestion. This agent (PNU) is remarkably similar chemically and toxicologically to alloxan and streptozocin, both potent beta-cell toxins. These similarities are not only important in regard to the antodite for PNU, but they also suggest that the toxin m,y cause long-term endocrinologic, neurlogic, and oncologic problems.
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PMID:Accidental ingestion of Vacor rodenticide: the symptoms and sequelae in a 25-month-old child. 644 44

A case of central pontine myelinolysis (CPM) following rapid correction of hyponatremia was reported and literatures were reviewed. The case was 61-year-old nonalcoholic female who had taken an operation of craniopharyngioma 23 years ago. Fifteen years later, she received re-operation for the recurrent tumor, followed by replacement therapy of corticosteroid and clofibrate. She was otherwise well until two weeks before entry, when she noticed abrupt onset of high grade fever, nausea, vomiting and general malaise. She was admitted to an emergency hospital because of weakness, disorientation and a slight impairment of consciousness, but she was able to speak and to take some food per os. Laboratory studies disclosed urinary tract infection and showed a serum sodium level of 117 mEq/l, potassium 2.9 mEq/l, a serum osmolarity 232 mO sm/l and urine osmolarity 141 mEq/l. She was diagnosed to have an exacerbation of adrenal insufficiency with hyponatremia and hypotonic dehydration triggered by urinary tract infection. Intravenous administration of vitamin B complex, electrolytes including KCL, 5% glucose solution and physiological saline with a large amount of corticosteroid was performed aggressively. Serum sodium concentration was raised to 161 mEq/l in two days, and the increased level had been maintained more than five days, resulting in coma and flaccid quadriplegia. During this period, there was no episode of hypotension, hypoglycemia, hypoxia nor hepatic failure which could have caused brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine and extrapontine myelinolysis following rapid correction of hyponatremia--report of an autopsy case]. 646 6

The main purpose of this work was to study changes in the balance of fluids, electrolytes and blood metabolites in neonatal piglets with severe transmissible gastroenteritis. Six two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as normal controls. Blood samples were collected in heparin when the infected piglets were moribund. The following variables were measured: packed red cell volume, total plasma protein and bicarbonate, blood pH, blood urea nitrogen and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets and they were moribund one or two days later. Before becoming moribund, most of the piglets fell rapidly into a lethargic and comatose state. The most evident changes in their blood variables were an increase in packed cell volume, total protein, blood urea nitrogen, phosphorus and magnesium levels and a decrease in pH and bicarbonate concentration as well as a severe hypoglycemia. The results suggest that severe hypoglycemia coupled with metabolic acidosis and dehydration might be an important factor contributing to the high mortality rates caused by transmissible gastroenteritis in neonatal piglets. The hypoglycemia results from a combination of the inadequate glucose metabolism inherent to neonatal piglets and the acute maldigestion and malabsorption resulting from the diffuse and severe villous atrophy induced by the virus.
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PMID:Hypoglycemia: a factor associated with low survival rate of neonatal piglets infected with transmissible gastroenteritis virus. 647 97

A five-year-old-girl with a history of recurrent hypoglycemia presented with acidosis, intractable vomiting, and abdominal tenderness; the diagnosis of acute pancreatitis was made by abdominal ultrasonography and supportive biochemical studies. Urinary organic acid analysis revealed metabolites suggestive of HMG-CoA lyase deficiency, and subsequent enzyme assays of lymphocytes and fibroblasts confirmed this diagnosis. Acute pancreatitis, an uncommon condition in childhood, is seen with increased frequency in patients with Reye syndrome, a metabolic disorder with which HMG-CoA lyase deficiency may be confused. The pathogenesis of pancreatitis in Reye syndrome or in HMG-CoA lyase deficiency has not been determined.
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PMID:A child with acute pancreatitis and recurrent hypoglycemia due to 3-hydroxy-3-methylglutaryl-CoA lyase deficiency. 648 80

Two cases of triglyceride storage in liver, kidney, heart, and skeletal muscle are described in infants who died at the age of 1 1/2 years and 4 d, respectively. In the first patient, a previously normal girl, the clinical symptoms began two months before death with encephalopathy (vomiting, unconsciousness), liver enlargement, hypoglycemia, increase in serum transaminases. These signs disappeared within the following days. Some weeks later she died during the second attack. The 4-d-old boy, the second child of healthy consanguineous parents, showed at the third day of life an impaired sucking, muscular hypotonia, respiratory arrest and bradycardia. An intensive therapy was inefficient. At autopsy gross examination showed only a moderately enlarged yellow liver and an edematous brain in the first case and pale organs in the second one but no cause of death. The microscopial examination of all tissues of both cases showed fat storage within the four organs mentioned above. The common histochemical methods for neutral lipids were positive, the Schultz-reaction for cholesterol and cholesterol esters was negative. The lipid loaden cells did not show birefringence in polarized light. A predominance and strong fat storage of the type I fibres was found in the skeletal muscle. The storage of triglyceride could be confirmed by histochromatography, a thin-layer chromatography of tissue sections. The triglyceride accumulation in liver, heart, kidney, and skeletal muscle is a characteristic feature of systemic carnitine deficiency. The clinical symptoms of the first patient are in agreement with reports of this disease also. A carnitine deficiency in a newborn was not yet described. Family studies revealed a low carnitine concentration in the mother's serum in both cases, while the serum of father and brother resp. sister showed normal carnitine levels.
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PMID:[Metabolic triglyceride storage disorders. A report of 2 cases of systemic carnitine deficiency]. 652 56


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