Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Medical records of 107 consecutive patients with a diagnosis of phencyclidine (PCP) intoxication were reviewed and in 27 of these the diagnosis was confirmed by positive urine assay. In the 27 confirmed cases, the most common abnormalities present on physical examination were mental/behavioral (89%) and nystagmus (85%). Elevations in blood pressure, temperature, and heart rate that were statistically significant when compared with an age-matched control group also were noted. Review of available medical records disclosed that 13 of these patients had been evaluated previously at our institution for PCP intoxication. Toxicological screening tests including blood alcohol level, hypnotic screen, and urine test for alkaloids, were performed on 11 patients and found positive in four. The most common serious medical complication requiring hospitalization was rhabdomyolysis which occurred on three patients, two of whom developed acute renal failure. This complication may occur more frequently than previously recognized and should be excluded in patients with PCP intoxication.
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PMID:Phencyclidine intoxication: clinical experience in 27 cases confirmed by urine assay. 722 72

Lilies are considered nephrotoxic only to domestic cats, which belong to the family Felidae of the suborder Feliformia. However, a 7-month-old female meerkat, belonging to the family Herpestidae of the suborder Feliformia, presented with oliguria, seizure, tachypnea, self-biting, and nystagmus after it ingested lilies. The meerkat died approximately 40 hr after lily ingestion. Gross and histopathologic lesions consistent with acute renal failure were conspicuous in the animal. The renal lesions were acute tubular necrosis, corresponding to the typical pathological changes of lily toxicosis in cats. In addition, massive hepatocyte necrosis and pulmonary congestion/edema were observed. These findings suggest that lily toxicosis in meerkats is characterized by pulmonary and hepatic failure, in addition to the renal failure observed in domestic cats.
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PMID:Suspected lily toxicosis in a meerkat (Suricata suricatta): a case report. 2931 34