Dimercaprol for

Examples of this mechanism of action include the administration of BAL (Dimercaprol) for the treatment of arsenic, copper, lead, or mercury intoxication. BAL is usually administered in a does of 3-5 mg/kg intramuscularly every 4 hours for 2 days, then every 4-6 hours for an additional 2 days, then every 4-12 hours for... 

Inhalation and dermal absorption mustards no antidote. For lewisite and ewisite/ mustard lmixtures British Anti-Lewisite (BAL or Dimercaprol) IM (rarely available). Thermal burn therapy supportive care (respiratory support and eye care). 

Decontaminate the casualty ensuring that all the vesicants have been removed. Rapid decontamination of any exposure is essential. If vesicants have gotten into the eyes, irrigate the eyes with water or 0.9% saline solution for at least 15 minutes. BAL (British-anti-Lewisite, dimercaprol) solution or ophthalmic ointment may be beneficial if administered promptly. Irrigate open wounds with water or 0.9% saline solution for at least 10 minutes. 

BAL British Anti-Lewisite. Dimercaprol, a treatment for toxic inhalations. 

Treatment—Patients should be decontaminated immediately prior to treatment using the decontamination method presented in Section 7.3.2. British Anti-Lewisite (BAL) dimercaprol antidote will alleviate some effects. It is available as a solution in oil for intramuscular administration to counteract systemic effects. It is not manufactured currently in the forms of skin and eye ointments.2... 

The treatment of metal poisoning is to administer a compound that binds the metal ion more strongly than does the group in the active centre of the enzyme. These compounds are known as chelating agents. For lead, the compound ethyl-enediaminetetraacetic acid (EDTA) is used. For mercury, dimercaptopropanol (dimercaprol) is used. 

Dimercaprol (BAL, British Anti-Lewisite) was developed in World War 11 as an antidote against vesicant organic arsenicals (B). It is able to chelate various metal ions. Dimercaprol forms a liquid, rapidly decomposing substance that is given intramuscularly in an oily vehicle. A related compound, both in terms of structure and activity, is di-mercaptopropanesulfonic acid, whose sodium salt is suitable for oral administration. Shivering, fever, and skin reactions are potential adverse effects. 

Patients who have received calcium EDTA with or without dimercaprol may use succimer for subsequent treatment after an interval of 4 weeks. Data on the concomitant use of succimer with calcium EDTA with or without dimercaprol are not available, and such use is not recommended. 

Several chelators can effectively lower the child s blood lead level. These include dimercaprol, ede-tate calcium disodium (CaNazEDTA) and suc-cimer. Protocols are available for using the chelators depending upon the severity of symptoms. 

Lead poisoning (with encephalopathy) IM Initially, dimercaprol 4 mg/kg then give dimercaprol 4 mg/kg and calcium EDTA 250 mg/m then 4 hr later and q4h for 5 days. 

For the treatment of poisoning, a selective antidote (which antagonises the action) may be given e.g., nalorphine and naloxone in case of morphine poisoning, atropine in case of anticholinergic drugs, dimercaprol in mercury and penicillamine in lead poisoning, etc. 

Succimer has also been effective in animal models and has a higher therapeutic index than dimercaprol. However, because it is available in the United States only for oral administration, its use may not be advisable in the initial treatment of acute arsenic poisoning, when severe gastroenteritis and splanchnic edema may limit absorption by this route. 

Chemical structures of several chelators. Ferroxamine (ferrioxamine) without the chelated iron is deferoxamine. It is represented here to show the functional groups the iron is actually held in a caged system. The structures of the in vivo metal-chelator complexes for dimercaprol, succimer, penicillamine, and unithiol (see text) are not known and may involve the formation of mixed disulfides with amino acids. 

Dimercaprol is FDA-approved as single-agent treatment of acute poisoning by arsenic and inorganic mercury and for the treatment of severe lead poisoning when used in conjunction with edetate calcium disodium (EDTA see below). Although studies of its metabolism in humans are limited, intramuscularly administered dimercaprol appears to be readily absorbed, metabolized, and excreted by the kidney within 4-8 hours. Animal models indicate that it may also undergo biliary excretion, but the role of this excretory route in humans and other details of its biotransformation are uncertain. 

When used in therapeutic doses, dimercaprol is associated with a high incidence of adverse effects, including hypertension, tachycardia, nausea, vomiting, lacrimation, salivation, fever (particularly in children), and pain at the injection site. Its use has also been associated with thrombocytopenia and increased prothrombin time—factors that may limit intramuscular injection because of the risk of hematoma formation at the injection site. Despite its protective effects in acutely intoxicated animals, dimercaprol may redistribute arsenic and mercury to the central nervous system, and it is not advocated for treatment of chronic poisoning. Water-soluble analogs of dimercaprol—unithiol and succimer—have higher therapeutic indices and have replaced dimercaprol in many settings. 

For example, the elucidation of the mechanism of action of the war gas Lewisite (Fig. 1.2), which involves interaction with cellular sulfhydryl groups, allowed the antidote, British anti-Lewisite or dimercaprol (Fig. 1.2), to be devised. Without the basic studies performed by Sir Rudolph Peters and his colleagues, an antidote would almost certainly not have been available for the victims of chemical warfare. 

Tolerance to heavy metals, specifically mercury and cadmium, has been associated with the induction of kidney metallothionein, a protein rich in sulfhydryl groups which protects by chelation (102). The synthetic antidote dimercaprol, introduced after World War I for arsenic-containing gases, works by a similar mechanism (103). 

They act on the kidney by depressing the mechanisms that govern the active reabsorption of sodium and chloride ions. They are rapidly excreted by the kidney but their use is hazardous because their action is believed to be due to inorganic mercury ions released by rupture of the carbon-to-mercury bond, probably followed by the firm attachment of the mercury ion to a sulphydryl group of a renal enzyme. The administration of dimercaprol (SO), a strong chelating agent for mercury, removes mercury from the kidney and terminates the diuretic action. It is of interest that Paracelsus used calomel (mercurous chloride) as a diuretic. 

The first chelating agent developed as an antidote to a heavy metal poison was 2,3-dimereaptopropanol (dimercaprol, British Anti-Lewisite, BAL). Originally intended for use on victims of the arsenical vesicant poison gas Lewisite52, it has since proved efficacious in the treatment of antimony, gold and mercury poisoning as well as... 

Treatment of acute arsenic poisoning includes removal from the exposure source, supportive measures for loss of fluids, and chelation therapy (Ibrahim et al., 2006). Chelators that can be used include dimercaprol or 2,3-dimercaptosuccinic acid. In cases of renal failure, hemodialysis should be considered. 

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