Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 45-year-old white man ingested approximately two cups of boric acid crystals dissolved in water in a suicide attempt. Nausea, vomiting, greenish diarrhea, and dehydration occurred shortly thereafter. Two days later, he presented to the hospital with hypotension, metabolic acidosis, oliguric renal failure, a generalized erythematous rash, and several superficial skin abrasions. His condition failed to improve despite intravenous fluids and vasopressors. He later developed atrial fibrillation with a rapid ventricular response and could not be converted to a sinus rhythm. This rhythm deteriorated to electromechanical dissociation, and the patient died 17 hours after admission. The urine and whole blood boric acid concentrations approximately 52 hours after ingestion were 160 and 42 mg/dL, respectively. These results are equivalent to urine and blood boron concentrations of 28 and 7 mg/dL, respectively. A postmortem urine boron concentration was 29.4 mg/dL. The autopsy report listed boron toxicity as the cause of death. This is the only adult reported to die from acute boric acid ingestion in recent years and may be atypical since the patient was untreated for 3 days and presented with dehydration and renal function impairment. This case suggests that lack of adequate urine flow and dehydration increases the risk of boron toxicity.
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PMID:Fatal ingestion of boric acid in an adult. 138 80

Paroxetine is a new selective serotonin reuptake inhibitor which has been extensively evaluated as an antidepressant in clinical trials and a large computerized safety database has been accumulated. A comprehensive review of data on dosage supports the recommendation that 20 mg paroxetine daily is the optimal therapeutic dose for most patients. When compared to active controls--mainly tricyclic antidepressants--paroxetine was found to have a different adverse-event profile with fewer anticholinergic, cardiovascular and nervous system events but more gastrointestinal events, particularly nausea. However, these events were not severe and did not usually lead to discontinuation of treatment. The adverse events reported with paroxetine were most likely to occur early in the course of treatment and there was no evidence of any increase in events in the elderly or with longer-term treatment. Paroxetine was not associated with excess of death from any cause, suicides, suicide attempts or serious life-threatening events. No clinically significant drug-related abnormalities were reported in laboratory monitoring, including liver function tests, in short- or long-term use. Finally, and importantly for an antidepressant, paroxetine appears relatively safe in overdose.
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PMID:Paroxetine: an overview of dosage, tolerability, and safety. 143 Oct 15

We experienced a case of a 44 year old man who had ingested potassium bromate solution for suicide attempt. Soon after the ingestion, nausea, vomiting, abdominal pain and diarrhea developed in him. Several hours later, he began to complain of auditory disturbance and, in addition, anuric acute renal failure occurred. Direct hemoperfusion and hemodialysis was performed on the patient for the treatment purpose. Five weeks later, he was released from hemodialysis procedure. Gradually, on the other hand, progressing anemia was observed until 90th hospital day, which slowly improved thereafter. Further, pruritus, lower leg pain, headache, tinnitus and loss of sense of taste, etc. were observed in the clinical course. Renal biopsy was performed on the 119th hospital day and the specimen showed the regenerative stage of acute tubular necrosis. In our case, acute renal failure was reversible and, many other clinical manifestations were observed. However slight anemia and irreversible severe auditory disturbance remained unimproved.
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PMID:[A case of acute potassium bromate intoxication]. 222 63

The literature was reviewed for cases of cutaneous pigmentation induced by rifampicin overdosage. 29 examples have been described, in which 2 general groups of individuals were observed. The first consisted of older individuals (average age 27.1 years) who attempted suicide. A prior history of suicide attempts, depression and substance abuse was a predominant factor in these patients. The second group included generally younger patients (average age 2.9 years) in whom misformulation of rifampicin preparations for treatment of Haemophilus influenzae Type B resulted in bright reddish-orange discoloration to the skin. The time to clinical appearance of skin discoloration was approximately 2.2 hours after administration. Periorbital or facial oedema occurred in 72.4% of the patients, pruritus in 62.1% and either nausea, vomiting or diffuse abdominal tenderness in 51.7%. Limited laboratory data are available but these indicate that all patients had elevated levels of total bilirubin. Histological examination in selected individuals revealed rifampicin crystal deposits in the nasopharynx, gastrointestinal tract and lining of the aorta. In adults, it appears that a dose of at least 14 g of rifampicin is necessary before cardiovascular-pulmonary arrest occurs. Other than general supportive measures, very few methods are described in the literature for the treatment of acute intoxications with this drug. A differential diagnosis of other causes of reddish-orange pigmentation is discussed, together with clinical information to differentiate these cases from toxic rifampicin ingestion.
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PMID:A review of the Redman syndrome and rifampicin overdosage. 268 37

Acetaminophen is a remarkably safe agent when used in therapeutic doses. Most reported overdoses of acetaminophen are the result of suicide attempts. The clinical course of patients with toxic blood levels follows four distinct stages. Symptoms of nausea, vomiting, diaphoresis, and anorexia usually begin within seven to 14 hours after ingestion. After 24 to 48 hours, these symptoms may diminish, but SGOT, SGPT, bilirubin, and prothrombin time begin to rise. Peak hepatotoxicity occurs at 72 to 96 hours, and SGOT levels of 20,000 I.U. are not unusual. Oral N-acetylcysteine is the drug of choice for acetaminophen overdose. Intravenous use of N-acetylcysteine is advocated in England, Europe, and elsewhere, but it is not available in the United States. Clinical studies of oral and intravenous N-acetylcysteine clearly demonstrate that the drug has a profound effect on reducing morbidity and mortality if it is administered during the first 16 hours after the overdose. In addition, data from these studies have shown that alcohol taken simultaneously with an overdose of acetaminophen is actually hepatoprotective. Therefore, patients who have consumed alcohol at the time of overdose, or those who are chronic alcoholics, should be managed in the same way as patients with no exposure to alcohol. However, study results also reveal that overdose in children under 10 to 12 years of age follows a distinctly different pattern. These children demonstrate a lesser degree of hepatotoxicity and have only minor increases in transaminase levels.
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PMID:Acetaminophen overdose. 635 59

A case of acute Dapsone intoxication due to voluntary ingestion of 3 g of this drug as a suicide attempt is described. A severe methemoglobinemia developed, accompanied by intense cyanosis, dyspnea, headache, and nausea. Subsequently, significant sulfhemoglobinemia responsible for prolonged cyanosis was observed, as well as mild hemolytic anemia. Relapses of methemoglobinemia after methylene blue treatment required repeated administration of the reducing agent. The need of a careful follow-up for several days in this type of intoxication is emphasized.
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PMID:Delayed sulfhemoglobinemia after acute dapsone intoxication. 715 40

A 36-year-old man with a history of depression presented to the emergency department after ingesting approximately 3,000 mL of ethylene glycol antifreeze in a suicide attempt. The patient's ethylene glycol concentration, 1,889 mg/dL, was higher than any level previously documented in the medical literature. Although his course was complicated by nausea, emesis, lethargy, metabolic acidosis, and kidney failure, the patient survived without persistent kidney failure or other chronic problems. Sustained hemodialysis and ethanol infusion were instituted in the ED, on the basis of the patient's history, before laboratory confirmation of the ingestion was obtained.
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PMID:Emergency department hemodialysis in a case of severe ethylene glycol poisoning. 986 97

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

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.
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PMID:Human health effects of sodium azide exposure: a literature review and analysis. 1285 Nov 50

In a European, multicenter, double-blind study, 244 adolescents, 13 to 18 years old, with major depression were randomized to treatment with citalopram (n = 124) or placebo (n = 120). One third of the patients in both groups withdrew from the study. No significant differences in improvement of scores from baseline to week 12 between citalopram and placebo were found. The response rate was 59% to 61% in both groups according to the Schedule for Affective Disorders and Schizophrenia for school-aged children-Present episode version (Kiddie-SADS-P) (depression and anhedonia scores < or =2) and Montgomery Asberg Depression Rating Scale (MADRS) (> or =50% reduction). Remission (MADRS score < or =12) was achieved by 51% of patients with citalopram and 53% with placebo. A post hoc analysis revealed that more than two thirds of all patients received psychotherapy during this study. For those patients not receiving psychotherapy, there was a higher percentage of Kiddie-SADS-P responders with citalopram (41%) versus placebo (25%) and a significantly higher percentage of MADRS responders and remitters with citalopram (52% and 45%, respectively) versus placebo (22% and 19%, respectively). Mild to moderate treatment-emergent adverse events were reported in 75% citalopram and 71% of placebo patients, most commonly headache, nausea, and insomnia. Serious adverse events occurred in 14% to 15% in both groups. Suicide attempts, including suicidal thoughts and tendencies, were reported by 5 patients in the placebo group and by 14 patients in the citalopram group (not significant) with no pattern with respect to duration of treatment, time of onset, or dosage. In contrast, the suicidal ideation (Kiddie-SADS-P) single item showed worsening more frequently in the placebo (18%) than in the citalopram group (8%).
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PMID:A randomized, double-blind, placebo-controlled study of citalopram in adolescents with major depressive disorder. 1750 98


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