Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 17-year-old girl presented with malaise, weakness, palpitations, dysphagia, myalgias, and weight loss of 1 month's duration. Within 24 hours of admission to the hospital, she had hypotension unresponsive to medical management, intractable congestive heart failure, and arrhythmias; she died. Several empty bottles of syrup of ipecac were later found among her belongings. Syrup of ipecac is commonly used to induce emesis in patients who had ingested toxic substances. The chief pharmacologic property of this agent is due to its alkaloid component, emetine. There have been many previous reports of death due to emetine poisoning in patients receiving ipecac fluid extract and in those treated for amoebic dysentery. However, the literature cites only three case reports of fatalities secondary to chronic ipecac use as a means of losing weight. This is the first report of a death due to chronic ipecac use in an adolescent patient with bulimia. Emetine persists in the body for long periods, and in patients who have ingested it chronically, emetine is extremely toxic, specifically to cardiac smooth and skeletal muscles. With an increased awareness of the importance of weight control in the adolescent age group, the physician must carefully evaluate these patients for the use of emetics.
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PMID:Death due to chronic syrup of ipecac use in a patient with bulimia. 287 30

A 69-year-old man was referred to our department because of acute onset nausea, vomiting, dysphagia, dysarthria and gait disturbance. He had a 50-day-history of amebic dysentery and had been treated with 1,500 mg metronidazole per day. Neurological examination revealed dysphagia, ataxic speech, ataxia of the left extremities and the trunk, and hyperactive deep tendon reflexes in all extremities. Sensory impairment of all modalities was apparent in a glove and stocking pattern, with mild paresthesia. Brain MRI showed T2 high signal lesions in the bilateral cerebellar dentate nuclei, more markedly on the left. On brain SPECT, obvious low blood perfusion was observed in the left cerebellar hemisphere. These findings well explained the ataxia of the left limbs. One month after discontinuing metronidazole, the cerebellar ataxia, dysphagia and MRI abnormalities completely cleared. Therefore, central nervous system damage induced by metronidazole is considered reversible. In spite of the presence of the MRI lesion in the right dentate nucleus, the patient had no ataxia of the right extremities and there was no hypoperfusion in the right cerebellar hemisphere. Thus, metronidazole does not appear to have a direct neurotoxic effect on the central nervous system. On the other hand, nerve conduction studies showed axonal polyneuropathy, which was not improved one month after cessation of the drug; thus metronidazole seems to exert more damage on peripheral nerves.
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PMID:[MRI and SPECT findings in a case of metronidazole-induced reversible acute cerebellar ataxia]. 1596 Jan 79