Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case report is presented describing a worker who was splashed with arsenic acid in an industrial accident and subsequently developed symptoms of systemic arsenicalism and peripheral neuropathy. This is the only report, to the authors' knowledge, of a single episode of cutaneous absorption of arsenic resulting in peripheral neuropathy. Previous reports of arsenical neuropathy and rationale for BAL therapy early in the treatment of systemic arsenicalism are discussed.
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PMID:Arsenical neuropathy: residual effects following acute industrial exposure. 19 18

A 47-year-old man had an episode of severe respiratory failure after acute intoxication with arsenic. Features of the initial clinical presentation included nausea, vomiting, and diarrhea, acute psychosis, diffuse skin rash, and marked pancytopenia. A peripheral neuropathy then developed which resulted in severe weakness of all muscles of the limbs, the shoulder and pelvis girdles, and the trunk. The neuropathy continued to progress despite treatment with dimercaprol (BAL in oil). Five weeks after the initial exposure, the patient was no longer able to maintain adquate ventilation and required mechanical ventilatory support. Improvement in the patient's neuromuscular status permitted successful weaning from the ventilator after one month of mechanical ventilation. Long-term follow-up revealed no further respiratory difficulty and slow improvement in the strength of the peripheral muscles.
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PMID:Acute respiratory failure following severe arsenic poisoning. 22 46

A 29-year-old man was found unresponsive a few minutes after self-injecting undetermined amounts of potassium cyanide and sodium arsenite intravenously in a suicide attempt. Treatment with the Lilly Cyanide Antidote kit rapidly resolved the initial coma, despite a whole blood cyanide level of 4.4 micrograms/mL. A 12-hour urine arsenic collection begun on admission showed 10,065 micrograms arsenic/12 hr. The patient received intramuscular BAL initially, which was followed by two ten-day courses of oral D-penicillamine. Complications included upper gastrointestinal tract bleeding requiring transfusion, transient elevations of liver function tests, self-limited complaints of decreased vision with conjunctival hyperemia and photophobia, and an abscess at the injection site. Although specific antidote therapy completely resolved the cyanide toxicity, early and prolonged arsenic chelation did not prevent a mild sensory peripheral neuropathy from developing with onset about 17 days after self-injection.
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PMID:Cyanide and arsenic poisoning by intravenous injection. 253 98

We describe a case with neurologic disease manifested as encephalopathy, generalized muscle fasciculations, and peripheral neuropathy occurring in a patient treated with therapeutic doses of gold for presumed rheumatoid arthritis. The illness remitted promptly during chelation therapy with dimercaprol (BAL). A review of the limited experience in the literature with the central nervous system toxicity of gold is given.
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PMID:Gold induced encephalopathy: case report. 632 82

Symptomatic arsenic poisoning is not often seen in occupational exposure settings. Attempted homicide and deliberate long-term poisoning have resulted in chronic toxicity. Skin pigmentation changes, palmar and plantar hyperkeratoses, gastrointestinal symptoms, anemia, and liver disease are common. Noncirrhotic portal hypertension with bleeding esophageal varices, splenomegaly, and hypersplenism may occur. A metallic taste, gastrointestinal disturbances, and Mee's lines may be seen. Bone marrow depression is common. 'Blackfoot disease' has been associated with arsenic-contaminated drinking water in Taiwan; Raynaud's phenomenon and acrocyanosis also may occur. Large numbers of persons in areas of India, Pakistan, and several other countries have been chronically poisoned from naturally occurring arsenic in ground water. Toxic delirium and encephalopathy can be present. CCA-treated wood (chromated copper arsenate) is not a health risk unless burned in fireplaces or woodstoves. Peripheral neuropathy may also occur. Workplace exposure or chronic ingestion of arsenic-contaminated water or arsenical medications is associated with development of skin, lung, and other cancers. Treatment may incklude the use of chelating agents such as dimercaprol (BAL), dimercaptosuccinic acid (DMSA), and dimercaptopanesulfonic acid (DMPS).
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PMID:Chronic arsenic poisoning. 1186 18

Clinically evident lead poisoning is rare in Indian children but is more common than in adults. In children, lead poisoning may appear as fever, seizures, anemia, or abdominal pain, while in adults it is more likely to manifest as chronic minor peripheral neuropathy or gum pigmentation. Children with acute lead poisoning can be treated with chelators such as EDTA and BAL, but many are left with permanent brain damage. The most common sources of acute lead poisoning in Indian children are inhalation of fumes from burned car batteries, ingestion of flaking paint, consuming food cooked in cheap aluminum or brass utensils, and eating contaminated soil. The sources of chronic lead poisoning are water from lead pipes and fumes from industrial or automotive exhaust. Another common source in India is application of "kajjal" to children's eyes. Sources of lead in Western countries, such as drinking water, canned food, residential paint, automotive fuel, and ambient air quality, are regulated by law. None of these are regulated in India.
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PMID:Environmental lead hazard to children. 1231 56