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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bismuth encephalopathy, characterized by the constant association of acute confusion, myoclonus, severe ataxia and dysarthia has reached "epidemic" proportion since its first description in 1974. The clinical aspects the pathogenic hypothesis, the diagnostic criteria as well as the report of a typical case are described by the authors, who stress the similarities with encephalopathies induced by other metals.
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PMID:Bismuth encephalopathy. 100 97

A 68 year old man with a creatinine clearance rate of only 15 ml/min took twice the recommended dose of tripotassium dicitrato bismuthate (TDB) as DeNol liquid; 10 ml qds; a total of 864 mg bismuth daily for two months. Whole blood bismuth concentrations rose to 880 micrograms/l and he developed global cerebral dysfunction with hallucinations, ataxia, and an abnormal EEG. Renal clearance of bismuth rose from 0.24 to 2.4 ml/min when the heavy metal chelator 2-3 dimercapto-1 propane sulphonic acid (DMPS) was given by mouth. Bismuth was measured by a novel method involving inductively coupled plasma source mass spectrometry. Fifty days after stopping TDB, whole blood bismuth concentrations fell to 46 micrograms/l and the patient's EEG returned to normal. His mental function also recovered completely. The case serves as a timely reminder that TDB should not be administered to patients with renal disorders, as stated in the data sheet.
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PMID:Bismuth induced encephalopathy caused by tri potassium dicitrato bismuthate in a patient with chronic renal failure. 221 Apr 58

Bismuth subsalicylate preparations are over-the-counter products for gastrointestinal complaints. Bismuth toxicity causes delirium, psychosis, ataxia, myoclonus, and seizures and is reversible over several weeks or months, when bismuth intake is stopped. We report a 54-year-old man with a 6-week history of progressive confusion and memory difficulty and a 2-3-week history of involuntary movements and gait impairment. His encephalopathy was further characterized by marked multifocal myoclonic jerks, coarse postural tremors, postural instability, and gait ataxia. He gradually improved. Extensive toxic, metabolic, and infectious workup demonstrated bismuth toxicity. Spinal tap and brain magnetic resonance scan were normal. Electroencephalography showed bihemispheric slowing. As his encephalopathy cleared, he reported using bismuth subsalicylate long term (daily intake of 8 oz). Bismuth levels 5 weeks after cessation of bismuth were elevated and normalized after 12 weeks. He followed a typical course for bismuth toxicity with subacute progressive encephalopathy and gradual recovery. Creutzfeldt-Jakob was strongly considered due to his rapidly progressive encephalopathy, multifocal myoclonus, and ataxia. Due to its rarity, bismuth toxicity is often overlooked. We hope this presentation will increase recognition of bismuth toxicity. We believe more detailed labeling of bismuth products is needed to avoid similar toxicity from this readily available product.
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PMID:Bismuth subsalicylate toxicity as a cause of prolonged encephalopathy with myoclonus. 775 66

The industrial use of bismuth is increasing. In medicine, bismuth compounds have long been used in the treatment of gastrointestinal disorders, recently in combination with antibiotics for the treatment of Helicobacter pylori-associated peptic ulcers. Bismuth-induced encephalopathy is a known side-effect. One of the symptoms of bismuth encephalopathy is ataxia, suggesting possible cerebellar involvement. The introduction of autometallography (AMG) for tracing BiS/BiSe nanocrystals has provided histochemical evidence supporting the cerebellum being involved in bismuth encephalopathy, but the effect of bismuth on the neuron number in the cerebellum has never been evaluated. In vitro studies have indicated that CA1 neurons may be targets for bismuth intoxication, but results have been conflicting. Recently, the loss of dorsal root ganglion cells was reported after moderate bismuth exposure. This raises the question whether the use of another neurotoxic stimulus, such as hypoxia, amplifies the toxic effects of bismuth. Despite AMG-detectable bismuth accumulations, stereological examinations revealed no statistically significant decrease in the number of Purkinje, CA1 or CA3 neurons or in the volume of the cerebellar granule layer. Surprisingly, intermittent hypoxia led to a statistically significant loss of Purkinje cells without affecting the hippocampus. Bismuth neither ameliorated nor exacerbated the hypoxic effects on the cerebellum.
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PMID:Influence of bismuth on the number of neurons in cerebellum and hippocampus of normal and hypoxia-exposed mouse brain: a stereological study. 1601 41