Only special multi-wawelength oximeters (CO-oximeters) can detect methemoglobinemia directly. When there is a "saturation gap" between a low ordinary pulse oximeter reading and a high arterial blood gas analysis result, methemoglobinemia may be suspected. Liver
Toxic hepatitis and cholestatic jaundice have been reported by the manufacturer. These toxic reactions may also occur as part of the dapsone hypersensitivity syndrome (a form of SCARs-see above) or dapsone syndrome (see below). Dapsone is metabolized by the Cytochrome P450 system, specifically isozymes CYP2D6, CYP2B6, CYP3A4, and CYP2C19. Dapsone metabolites produced by the cytochrome P450 2C19 isozyme are associated with the methemoglobinemia side effect of the drug. Skin
When used topically, dapsone can cause mild skin irritation, redness, dry skin, burning, and itching. When used together with benzoyl peroxide products, temporary yellow or orange skin discolorations can occur. Dapsone hypersensitivity syndrome
Hypersensitivity reactions occur in some patients. This reaction may be more frequent in patients receiving multiple-drug therapy.The reaction always involves a rash, may also include fever, jaundice, and eosinophilia, and is likely to be one manifestation of the SCARs reaction viz., the DRESS syndrome (see above). In general, these symptoms will occur within the first six weeks of therapy or not at all, and may be ameliorated by corticosteroid therapy. Other adverse effects
Other adverse effects include nausea, headache, and rash (which are common), and insomnia, psychosis, and peripheral neuropathy. Effects on the lung occur rarely and may be serious, though are generally reversible.
Further investigation into the involved chemicals opened the way to sulfa drug and sulfone therapy, first with the discovery of sulfanilamide, the active agent of prontosil, by Daniel Bovet and his team at Pasteur Institute (1935), then with that of dapsone independently by Ernest Fourneau in France and Gladwin Buttle in the United Kingdom. Proposed use in antimalarial drugs
The spread of drug-resistant malaria in Africa has encouraged the development of new, low-cost antimalarial drugs. Plasmodium falciparum, one of the Plasmodium species that causes malaria, has developed resistance both to chloroquine and sulfadoxine/pyrimethamine, two of the most common treatments for malaria. Artemisinin, another antimalarial drug, had been developed in the 1980s but was too expensive for large-scale use. This led GlaxoSmithKline to develop Lapdap, a combination drug consisting of chlorproguanil and dapsone. Lapdap was licensed in the United Kingdom starting in October 2003.One advantage of Lapdap was that chlorproguanil and dapsone are both low-cost drugs. Another was that by virtue of being a combination drug, it was less likely to cause drug resistance. However, because dapsone causes hemolytic anemia in patients with G6PD deficiency, and because G6PD deficiency affects 10-25% of the population of sub-Saharan Africa, it was discovered that Lapdap is not safe for use in Africa. It was available in many African countries for four years before GlaxoSmithKline took it off the market in February 2008. Dapsone gel
Dapsone had been reported in a few cases to effectively treat acne, but the risk of hemolytic anemia kept it from being widely used for this purpose.