Removal of the inciting agent is the goal of treatment. Correcting fluid and electrolyte losses and rectifying any nutritional imbalances (vitamin-rich diets, vitamin-B complex) are of utmost importance in the treatment of the disease.
The chelating agent meso 2,3-dimercaptosuccinic acid has been shown to be the preferred treatment modality. It can almost completely prevent methylmercury uptake by erythrocytes and hepatocytes.
In the past, dimercaprol (British antilewisite; 2,3-dimer-capto-l-propanol) and D-penicillamine were the most popular treatment modalities. Disodium edetate (Versene) was also used. Neither disodium edetate nor British antilewisite has proven reliable. British antilewisite has now been shown to increase CNS levels and exacerbate toxicity. N -acetyl-penicillamine has been successfully given to patients with mercury-induced neuropathies and chronic toxicity, although it is not approved for such uses. It has a less favorable adverse effect profile than meso 2,3-dimercaptosuccinic acid. 
Hemodialysis with and without the addition of L-cysteine as a chelating agent has been used in some patients experiencing acute renal failure from mercury toxicity.
Peritoneal dialysis and plasma exchange also may be of benefit.
Tolazoline (Priscoline) has been shown to offer symptomatic relief from sympathetic overactivity.
Antibiotics are necessary when massive hyperhidrosis, which may rapidly lead to miliaria rubra, is present. This can easily progress to bacterial secondary infection with a tendency for ulcerating pyoderma.
Long-term disability has been noted. Some patients have been shown to have lower intelligence test scores and abnormal electroencephalographic tracings, indicating possible organic damage to the CNS.