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)

To date, seven inborn errors of mitochondrial fatty acid oxidation have been identified. A total of about 100 patients in the world have been reported. Clinically the beta-oxidation defects are more often characterized by episodic hypoglycaemia leading to a coma mimicking Reye's syndrome. The hypoglycaemia is non-ketotic since the synthesis of ketone bodies is deficient. Periods of decompensation occur when carbohydrate supply is poor, e.g. prolonged fasting, vomiting, or increased caloric requirements, as and when lipid stores are used. Defects in beta-oxidation have also been reported to be one cause of sudden infant death syndrome. The diagnosis of these inborn errors is by biochemical investigation since where symptoms suggest such a defect, the precise aetiology cannot be assessed. The biochemical diagnosis is based firstly on identification of abnormal plasma and of urinary metabolites during acute attacks. Derivatives of the omega-oxidation and omega-1-oxidation of medium chain fatty acids have been identified, as well as acylglycine and acylcarnitine conjugates. These metabolites are nearly always absent when patients are in good clinical condition. Secondly, the diagnosis must be based on the identification of the enzymatic defects: this involves global assays which allow a localization of the 'level' of the defect (i.e. the oxidation of long, medium or short chain fatty acids) and specific measurement of enzyme activities (acyl-CoA dehydrogenases and electron carriers: ETF and ETF-DH). The diagnosis of these disorders is of prime importance because of the severity of the clinical symptoms. These can be prevented, in some cases, by an appropriate diet (a high carbohydrate, low fat diet, sometimes supplemented with L-carnitine). In other cases, genetic counselling can be offered.
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PMID:The inborn errors of mitochondrial fatty acid oxidation. 311 38

The etiology, pathophysiology, clinical features, diagnosis, and medical treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are reviewed. SIADH is a common cause of hyponatremia in hospitalized patients. Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Symptoms generally occur only when hyponatremia is severe (less than or equal to 125 meq/L) and may include anorexia, vomiting, and confusion, followed by seizures, coma, and death. SIADH may result from a variety of diseases, as well as from the use of drugs such as chlorpropamide, carbamazepine, diuretics, and some antineoplastic agents. Diagnosis of SIADH is confirmed by demonstration of a high urine osmolality with a low plasma osmolality, in the absence of diuretic use. Immediate treatment of the symptomatic patient with SIADH includes intravenous furosemide and 3% sodium chloride injection to produce a negative free-water balance. If the underlying cause of SIADH cannot be corrected, the treatment of choice for chronic SIADH is fluid restriction. If this is not tolerated by the patient, demeclocycline can be used to induce a negative free-water balance. Urea, lithium, phenytoin, and loop diuretics have been reported to be effective, but there are few data to support their use. Future research into the treatment of SIADH must be directed at developing effective antagonists of ADH. Treatment of SIADH consists of elimination of underlying causes and restriction of fluid intake; if these measures are unsuccessful or poorly tolerated, long-term drug therapy may be indicated.
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PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

Of 61 cases of ibuprofen overdosage reported consecutively to the Rocky Mountain Poison and Drug Center from September 1985 through April 1986, 16 were excluded because of incomplete follow-up or concurrent medication ingestion. A toxic reaction developed in 7 (16%) of the remaining 45 patients. Nausea, vomiting, abdominal cramps, mild central nervous system depression, coma, tachycardia, apnea, metabolic acidosis with or without respiratory alkalosis, hematemesis, and oliguric renal failure were noted. Two of six adults had a toxic reaction, and one died. Among pediatric patients, 5/39 (13%) had a toxic reaction. Of patients whose ibuprofen ingestion was less than 104 mg per kg, none became ill. All patients in whom the time of ingestion was known (six of seven) and who had a toxic reaction did so within four hours of ingestion. An ibuprofen overdose, although usually benign, can occasionally produce serious toxicity.
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PMID:Ibuprofen overdose--a prospective study. 317 71

Extradural haematoma (EDH) is generally a condition of young adult males. It represents only a small percentage of the total number of head injuries admitted to a neurosurgical service, but it must be differentiated from simple concussion, and this means that it is considered in a large number of patients. EDH has the potential for a low mortality rate because of its extraaxial location, but in practice it is approximately 10%. Our results show that about 40% of EDH present with vomiting or nausea and no focal neurological signs. Skull X-ray does not aid in the diagnosis as approximately 35% are reported as being normal. There is a place for conservative treatment of EDH but only if the shift of the midline is minimal (less than 5 mm). A score has been developed to predict accurately a patient's outcome after suffering an EDH. This score includes the Glasgow Coma Scale, pupillary reaction and initial CT scan appearance, and has an accuracy of 88%.
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PMID:Outcome prediction in extradural haematomas. 322 7

The authors describe an intoxication by Atractylis gummifera in a 7-year old boy who drunk an extract made from the plant's root as traditional medicine. He was admitted to the Hospital 2 days after ingestion, in coma stage II, with epigastric pain, vomiting and general anxiety. Laboratory findings showed severe hepatocellular damage and acute renal failure. In spite of all treatment and therapeutic efforts, the boy died 8 days after admission. A postmortem histopathological study of the liver confirmed the panlobular hepatic necrosis and allowed the differential diagnosis of the intoxication from Reye syndrome.
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PMID:Hepatotoxicity due to Atractylis gummifera-L. 323 May 99

The toxicities of antimalarial drugs vary because of the differences in the chemical structures of these compounds. Quinine, the oldest antimalarial, has been used for 300 years. Of the 200 to 300 compounds synthesised since the first synthetic antimalarial, primaquine in 1926, 15 to 20 are currently used for malaria treatment, most of which are quinoline derivatives. Quinoline derivatives, particularly quinine and chloroquine, are highly toxic in overdose. The toxic effects are related to their quinidine-like actions on the heart and include circulatory arrest, cardiogenic shock, conduction disturbances and ventricular arrhythmias. Additional clinical features are obnubilation, coma, convulsions, respiratory depression. Blindness is a frequent complication in quinine overdose. Hypokalaemia is consistently present, although apparently self-correcting, in severe chloroquine poisoning and is a good index of severity. Recent toxicokinetic studies of quinine and chloroquine showed good correlations between dose ingested, serum concentrations and clinical features, and confirmed the inefficacy of haemodialysis, haemoperfusion and peritoneal dialysis for enhancing drug removal. The other quinoline derivatives appear to be less toxic. Amodiaquine may induce side effects such as gastrointestinal symptoms, agranulocytosis and hepatitis. The main feature of primaquine overdose is methaemoglobinaemia. No cases of mefloquine and piperaquine overdose have been reported. Overdose with quinacrine, an acridine derivative, may result in nausea, vomiting, confusion, convulsion and acute psychosis. The dehydrofolate reductase inhibitors used in malaria treatment are sulfadoxine, dapsone, proguanil (chloroguanide), trimethoprim and pyrimethamine. Most of these drugs are given in combination. Proguanil is one of the safest antimalarials. Convulsion, coma and blindness have been reported in pyrimethamine overdose. Sulfadoxine can induce Lyell and Stevens-Johnson syndromes. The main feature of dapsone poisoning is severe methaemoglobinaemia which is related to dapsone and to its metabolites. Recent toxicokinetic studies confirmed the efficacy of oral activated charcoal, haemodialysis and haemoperfusion in enhancing removal of dapsone and its metabolites. No overdose has been reported with artemesinine, a new antimalarial tested in the People's Republic of China. The general management of antimalarial overdose include gastric lavage and symptomatic treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and management of poisoning due to antimalarial drugs. 330 66

Literature data on current methods of induced abortion during the 2nd trimester are reviewed with special emphasis on the use of intraamniotic administration of hypertonic saline solution. A 20% saline is injected during amniocentesis either intra-abdominally or through the vagina; the optimum time period for pregnancy termination is 21-23 weeks of gestation. In the majority of patients, miscarriage occurs within 24-36 hours. The incidence of complications after administration of 20% saline ranges from 1.7-2.18%. Complications include hypernatremia, hemolysis, anuria, coma, seizures, incomplete abortion, hemorrhage, and inflammatory pelvic disease. Contraindications for pregnancy termination using hypertonic saline include cardiovascular diseases, central nervous system diseases, kidney diseases, late pregnancy toxemias, presence of postoperative cicatrix on the uterus, and placenta previa. The mechanism of abortifacient action of hypertonic saline may be associated with stimulation of the synthesis of endogenous prostaglandins (PG). The findings that PG can stimulate uterine contractions prompted clinical trials of PG as abortifacient agents. Longterm iv administration of PGF2 alpha and PGE during 2nd trimester was found to be associated with serious complications (nausea, vomiting, diarrhea, phlebitis at the site of vein puncture). For this reason, the method of iv administration of PG was abandoned. Intra-amniotic administration of PGF2 alpha (40-50 mg) was shown to induce abortion in 82-91% of the patients within 48 hours after injection. The incidence of hemorrhage and rupture of the cervix uteri after PG administration was significantly greater than that after saline injection. The intramuscular and vaginal administration of synthetic PG alone or in combination with Laminaria was shown to provide the most effective and safe method of induced abortion during the 2nd trimester.
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PMID:[Artificial termination of pregnancy in late periods]. 332 84

Cerebral symptoms were registered in a multicenter study including 64 patients with severe hypertension, diastolic blood pressure (DBP) greater than or equal to 135 mmHg, and more or less pronounced hypertensive encephalopathy. The symptoms were: headache (70%), dizziness (35%), consciousness disturbances (28%), nausea (27%), paresis (23%), blurred vision (22%), paraesthesia (21%) and vomiting (14%). None had convulsions or coma. Initial treatment was furosemide i.v., and if DBP was greater than or equal to 125 mmHg after one hour, patients were randomized to treatment with either i.v. diazoxide (bolus injections of 75-150 mg) or i.m. dihydralazine (bolus injections of 6-12.5 mg). A gradual fall in blood pressure (BP) was obtained in all three groups. Along with BP reduction a substantial regression of neurological symptoms was registered. After 5 hours only minor cerebral symptoms were present without significant difference between diazoxide and dihydralazine. None developed cerebral complications. The study failed to show a significant correlation between BP reduction and regression of neurological symptoms graded semiquantitatively. Reduction of BP by titration using small repeated bolus injections is recommended, but oral treatment should be considered in the patients who are able to ingest peroral medication in spite of neurological symptoms.
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PMID:Reversibility of cerebral symptoms in severe hypertension in relation to acute antihypertensive therapy. Danish Multicenter Study. 353 94

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

The authors analyse 115 cases of acute fatty liver of pregnancy, proven histologically. Characteristics of the condition is the finding of central nuclei in the hepatocytes containing microvesicular droplets. The disease occurs more frequently in primiparous women (54 per cent) and usually occurs in the third trimester of the pregnancy. A pre-icteric phase usually precedes the jaundice and during that time there is usually vomiting and/or nausa with abdominal pain or anarexia. In 92 per cent of case there is transient loss of consciousness with hepatic encephalopathy. Further tests show that there is more defective liver function than would be expected from the extent of cell lysis; and there is defective renal function. The worst complications are intestinal haemorrhages (48 per cent of cases)--genital bleeding (43 per cent of cases)--shock--diffuse intravascular coagulation and complications associated with coma. Maternal mortality at present runs at 25 per cent and fetal mortality at 60 per cent. The condition does not recur. Early evacuation of the uterus is recommended by most authors and does probably improve the outlook. The various hypotheses concerning the aetiology are discussed.
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PMID:[Acute fatty liver of pregnancy]. 354 2


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