Chelating Agents
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Direct answer
Chelating agents are antidotes that bind toxic metals into stable, excretable complexes. Dimercaprol treats arsenic, mercury and lead; calcium EDTA treats lead; succimer, the oral dimercaptosuccinic acid, handles lead, arsenic and mercury; D-penicillamine chelates copper in Wilson disease; deferoxamine binds iron, with oral deferasirox and deferiprone for chronic overload. Each chelator has a metal affinity profile and its own toxicity, and all lose selectivity at the extremes — mobilising essential metals when misused.
What you must remember
- Dimercaprol, or British anti-Lewisite, was designed against the arsenical war gas lewisite; its two sulphydryl groups bind arsenic, mercury, gold and lead — it is given intramuscularly in a peanut-oil vehicle, causes tachycardia, hypertension, salivation and lacrimation, and must never accompany iron or cadmium poisoning because the complexes formed are more toxic.
- Calcium disodium EDTA is the lead chelator; given intramuscularly or intravenously it is nephrotoxic, depletes zinc, and in lead encephalopathy it follows an initial dimercaprol dose rather than preceding it, to avoid raising brain lead.
- Succimer, oral DMSA, is the outpatient lead chelator for children with elevated blood levels and also serves arsenic and mercury; adverse effects are rash, transaminase elevation and neutropenia.
- Unithiol, or DMPS, is the water-soluble dimercaprol descendant used for mercury and arsenic where available.
- D-penicillamine is the oral copper chelator for Wilson disease, also serving lead, mercury and cystinuria; its toxicities — nephrotic proteinuria, bone marrow suppression, lupus-like syndrome and pyridoxine depletion — mandate supplementation with vitamin B6 and regular monitoring; trientine is the better-tolerated alternative, with zinc blocking copper absorption as maintenance.
- Deferoxamine, a siderophore-derived parenteral iron chelator, colours urine vin-rose and risks hypotension on rapid infusion, Yersinia and mucormycosis-promoting iron-dependent infection; oral deferasirox and deferiprone serve thalassaemia and transfusional overload, deferiprone causing neutropenia and agranulocytosis.
- Clinical anchors: acute lead encephalopathy gets dimercaprol then calcium EDTA; arsenic and mercury get dimercaprol or succimer; iron overdose gets deferoxamine; Wilson disease gets penicillamine or zinc long term.
Common confusion
The mercury-iron pairing is the classic error: dimercaprol with iron forms a toxic complex, so iron poisoning belongs exclusively to deferoxamine. Lead therapy is also commonly jumbled — oral succimer for stable children, but dimercaprol first in encephalopathy because calcium EDTA alone transiently raises brain lead concentrations.
Exam-focused takeaway
Theory answers should list each chelator with its metals, route and toxicity, closing with the lead-encephalopathy sequence. Viva examiners ask why dimercaprol is contraindicated with iron and what urine colour deferoxamine produces. MCQs test BAL against lewisite, succimer as oral lead therapy, penicillamine in Wilson disease with B6 supplementation, and deferoxamine for acute iron poisoning.
Frequently asked questions
Which chelator is used for lead poisoning with encephalopathy?
Dimercaprol intramuscularly first, followed by calcium EDTA — the sequence prevents EDTA from redistributing lead into the brain before clearance begins.
Why is dimercaprol contraindicated in iron overdose?
It forms a toxic iron-dimercaprol complex; iron poisoning is treated with deferoxamine instead.
What is the role of D-penicillamine?
It chelates copper in Wilson disease and aids lead, mercury and cystinuria therapy, with vitamin B6 given routinely and blood counts plus urinalysis monitored for marrow and renal toxicity.
What are the adverse effects of deferoxamine?
Rapid-infusion hypotension, vin-rose urine, and promotion of Yersinia and mucormycosis by supplying iron to iron-dependent organisms.
Which oral chelators treat chronic iron overload?
Deferasirox, given once daily, and deferiprone, which demands neutrophil monitoring for agranulocytosis — both sparing the parenteral deferoxamine route in thalassaemia.