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)

Hyperammonemia associated with inherited disorders of amino acid and organic acid metabolism is usually manifested by irritability, somnolence, vomiting, seizures, and coma. Although the majority of these patients present in the newborn period, they may also present in childhood, adolescence, and adulthood with failure to thrive, persistent vomiting, developmental delay, or behavioral changes. Persistent hyperammonemia, if not treated rapidly, may cause irreversible neuronal damage. After the diagnosis of hyperammonemia is established in an acutely ill patient, certain diagnostic tests should be performed to differentiate between urea cycle defects and other causes of hyperammonemic encephalopathy. In a patient with a presumed inherited metabolic disorder, the aim of therapy should be to normalize blood ammonia levels. Recent experience has provided treatment guidelines that include minimizing endogenous ammonia production and protein catabolism, restricting nitrogen intake, administering substrates of the urea cycle, administering compounds that facilitate the removal of ammonia through alternative pathways, and, in severe cases, dialysis therapy. Initiation of dialysis in the encephalopathic patient with hyperammonemia is indicated if the ammonia blood level is greater than three to four times the upper limit of normal. Hemodialysis is the most effective treatment for rapidly reducing blood ammonia levels. Continuous hemofiltration and peritoneal dialysis are also effective modalities for reducing blood ammonia levels. An improved understanding of the metabolism of ammonia and neurological consequences of hyperammonemia will assist the nephrologist in providing optimal care for this high-risk patient population.
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PMID:Hyperammonemia in urea cycle disorders: role of the nephrologist. 1132 92

Glutamine is used to supplement intravenous and enteral feeding. Although there have been many human studies of its efficacy, there have been very few studies with safety as a primary goal. This article analyzes the literature on the safety of glutamine and also examines the available information on high intakes of total protein and other amino acids, so that additional indicators of potentially adverse effects can be suggested. Four studies that specifically addressed glutamine safety were identified, from which it was concluded that glutamine is safe in adults and in preterm infants. However, the published studies of safety have not fully taken account of chronic consumption by healthy subjects of all age groups. To help identify potential undetected hazards of glutamine intake, the literature on adverse effects of high dietary intake of protein and other amino acids was examined. High protein is reputed to cause nausea, vomiting and ultimately death in adults, and has been shown to result in neurological damage in preterm infants. Individual amino acids cause a variety of adverse effects, some of them potentially fatal, but neurological effects were the most frequently observed. Because glutamine is metabolized to glutamate and ammonia, both of which have neurological effects, psychological and behavioral testing may be especially important.
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PMID:Assessment of the safety of glutamine and other amino acids. 1153 13

A postprandial ammonia tolerance test (PPATT) was performed on normal dogs and dogs with signs that suggested they may have liver disease. All dogs underwent transcolonic scintigraphy, liver biopsy, or both and were assigned to extrahepatic disease, primary hepatocellular, and congenital portosystemic vascular anomalies (PSVA) groups. Each dog was fed a chicken and rice diet providing 25% of its estimated daily metabolizable energy requirement (MER) as an ammonia challenge. This is practical in patients with liver disease because ammonium chloride administration often causes vomiting or ammonia toxicity. Venous ammonia concentrations were measured before feeding and every 2 hours after feeding for 8 hours. No difference in mean ammonia concentrations between dogs with extrahepatic disease and control dogs was found. Therefore, the specificity of the PPATT was 100%. Dogs with hepatocellular disease showed no change in mean ammonia concentration at any time point, before or after feeding, but sensitivity was greatest when venous ammonia was measured 6 hours after feeding (sensitivity before feeding, 28%, and after feeding, 36%). Among dogs with congenital PSVA, mean ammonia concentrations were higher than the reference range at all time points before and after feeding, and peak mean ammonia concentration occurred 6 hours after feeding. In this group, the sensitivity of the PPATT was 81% before feeding and 91% 6 hours after feeding. This study demonstrates that the measurement of venous ammonia concentration is a useful test to detect congenital PSVA, and the sensitivity of the test may be improved by sampling 6 hours after feeding. The PPATT has poor sensitivity in detecting primary hepatocellular disease.
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PMID:Postprandial venous ammonia concentrations in the diagnosis of hepatobiliary disease in dogs. 1159 33

A 23-year-old Japanese man was admitted to our hospital because of acute generalized muscle weakness and frequent vomiting. He had been diagnosed as having hypokalemic periodic paralysis, since he had recurrent episodes of transient generalized muscle weakness with a hypokalemia. Laboratory studies have revealed a severe hypokalemic hyperchloremic metabolic acidosis, elevated serum levels of creatine phosphokinase and ammonia. The urinary level of the hippuric acid, a metabolic product of toluene, was found to be extremely high, suggesting that he had been exposed to toluene. With intravenous supplement of potasium, his muscle strength improved. Chronic exposure to toluene induces various neurological disorders, such as encephalopathy, cerebellar and pyramidal signs, peripheral neuropathy. In addition, it should be kept in mind that hypokalemic muscle weakness can be induced by the renal tubular acidosis resulting from chronic toluene exposure, and that it is by no means easy to distinguish hypokalemic periodic paralysis if it occurs recurrently.
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PMID:[Generalized muscle weakness mimicking periodic paralysis in a patient with toluene abuse]. 1205 13

A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen. On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. Urinalysis revealed an elevated specific gravity and numerous muddy granular casts. Hepatitis A, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1258 38

Hepatic encephalopathy is a frequent complication of cirrhosis. Abnormalities of 5-hydroxytryptamine (5-HT) and its metabolites are recognized and may contribute to its pathogenesis. We therefore studied the effect of an oral tryptophan load (6-18 g) upon psychometric test scores and analyzed EEG's in alcoholic cirrhotic patients. Eight patients had had previous encephalopathic episodes related to variceal bleeds and one patient was awaiting a liver transplant. Five out of the 10 patients had at least one abnormal baseline psychometric test. Following tryptophan challenge there were no changes in blood ammonia but plasma tryptophan levels were elevated approximately 10-fold (p < 0.01 x 10(-7)). Nevertheless, there were no statistically significant changes in psychometric testing or analyzed EEG frequency distribution. All patients reported nausea or vomiting while one patient developed a short-lived serotonin like syndrome. We conclude that in this group of patients, an oral tryptophan load does not induce or worsen subclinical hepatic encephalopathy. If the high blood levels of tryptophan seen in these studies are able to influence cerebral neurotransmitter synthesis, the results do not support a primary role for abnormalities of 5-HT neurotransmission in hepatic encephalopathy.
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PMID:Oral tryptophan challenge studies in cirrhotic patients: no evidence of neuropsychiatric changes. 1456 68

Methionine tablets are used as urinary acidifiers for pets and to decrease damage from dog urine to lawns. A 39-kg Labrador Retriever ingested approximately 350 tablets containing 150 mg methionine/tablet and was presented after repeated episodes of vomiting. The only abnormality was posterior ataxia suggestive of spinal cord injury. The animal was treated with i.v. fluids, steroids and gastrointestinal protectants. Approximately 4.5 h after entering the clinic the dog had a single seizure episode lasting 2-3 min which was treated with phenobarbital. Serum ammonia at that time was normal (0.19 mg/dL). The animal did not show further CNS abnormalities and awoke apparently normal. A musty odor to the breath was noticed through the course of the day, possibly due to volatile mercaptans produced from methionine metabolism. The animal made an uneventful recovery and was discharged the next day.
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PMID:Overingestion of methionine tablets by a dog. 1464 Apr 82

Ammonia, normally produced from catabolism of amino acids, is a deadly neurotoxin. As such, the concentration of free ammonia in the blood is very tightly regulated and is exceeded by two orders of magnitude by its physiologic derivative, urea. The normal capacity for urea production far exceeds the rate of free ammonia production by protein catabolism under normal circumstances, such that any increase in free blood ammonia concentration is a reflection of either biochemical or pharmacologic impairment of urea cycle function or fairly extensive hepatic damage. Clinical signs of hyperammonemia occur at concentrations > 60 micromol/L and include anorexia, irritability, lethargy, vomiting, somnolence, disorientation, asterixis, cerebral edema, coma, and death; appearance of these findings is generally proportional to free ammonia concentration, is progressive, and is independent of the primary etiology. Causes of hyperammonemia include genetic defects in the urea cycle ("primary") or organic acidemias ("secondary"), as well as genetic or acquired disorders resulting in significant hepatic dysfunction. Thus, because of the neurotoxic implications of hyperammonemia and the typical absence of other specific laboratory abnormalities, appearance of the clinical signs should trigger an emergent search for elevated blood ammonia concentration.
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PMID:Hyperammonemia, bane of the brain. 1549 74

Since 1993, the New York State Department of Health, funded by the Agency for Toxic Substances and Disease Registry, has collected data about non-petroleum hazardous substances releases through the Hazardous Substances Emergency Events Surveillance (NYHSEES) project. This study investigates risk factors for hazardous substances releases that may result in public health consequences such as injury or reported health effects. The 6428 qualifying events that occurred during the 10-year-period of 1993-2002 involved 8838 hazardous substances, 842 evacuations, more than 75,419 people evacuated, and more than 3120 people decontaminated. These events occurred both at fixed facilities (79%) and during transport (21%). The causative factors most frequently contributing to reported events were equipment failure (39%) and human error (33%). Five of the 10 chemicals most frequently associated with injuries were also among the 10 chemicals most frequently involved in reported events: sulfuric acid, hydrochloric acid, ammonia, sodium hypochlorite, and carbon monoxide. The chemical categories most frequently associated with events, and with events with adverse health effects were volatile organic compounds (VOCs) and solvents, and acids. Events with releases of hazardous substances were associated with injuries to 3089 people including employees (37%), responders (12%), the general public (29%) and students (22%). The most frequently reported adverse health effects were respiratory irritation, headache, and nausea or vomiting. Most of the injured were transported to the hospital, treated, and released (55%) or treated at the scene (29%). These data have been used for emergency response training, planning, and prevention activities to reduce morbidity and mortality from future events.
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PMID:New York hazardous substances emergency events surveillance: learning from hazardous substances releases to improve safety. 1551 63

Valproic acid has been widely used for the treatment of epilepsy. Although it is usually well tolerated, it has been associated with some side effects. A poor studied side effect is the hyperammonemia, which independs from the drug hepatotoxic action. The hyperammonemia may occurs just after the beginning or during the treatment and is characterized by vomiting, progressive impairment of consciousness, focal neurologic signs and increased seizure frequency. We report boy a 6 year-old boy who presented with hyperammonemia during the use of valproic acid within the therapeutic range. Complementary investigation was negative for aminoacidopathy, organic acidemia and urea cycle disorders. The hypothesis of secondary effect to the valproic acid was reinforced by the normalization of ammonia levels after drug withdrawal. The pathogenesis of valproate-induced hyperammonemia have been discussed. We conclude that routine monitoring of ammonia blood concentration are strongly recommended in patients under valproic acid treatment.
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PMID:[Hyperammonemia secondary to the use of valproic acid: case report]. 1610 Sep 94


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