[What do we know today about diaminodiphenylsulfone?].

INTRODUCTION Diaminodiphenylsulfone or dapsone is a chemical analogue of sulfapyridine, synthesized in 1908. Dapsone is a bacteriostatic agent that proved to be efficient in treating leprosy and malaria, but today it is used in treating dermatologic noninfectious inflammatory diseases. PHARMACOLOGY Dapsone is orally used in a dose of 50-400 mg per day in treatment of dermatologic diseases, and also in a dose of 50-100 mg per day in leprosy treatment. Dapsone is mainly eliminated from the body by urine and smaller part by faeces. Pharmacological interaction was reported when it is used with rifampicin and probenecid. MECHANISM OF ACTION The bacteriostatic effect of dapsone is well known. It involves inhibition of folic acid synthesis in susceptible organisms. The anti-inflammatory effect of dapsone, which proves to be efficient in treating noninfectious inflammatory diseases, has not been explained completely yet. There are some pieces of evidence that anti-inflammatory action is not connected with its antibacteriological action. CLINICAL USE Based on previous studies about therapy efficiency of dapsone in treating some diseases, there are two groups of diseases: the group responding well to dapsone (leprosy, malaria, DH, linear IgA-dermatosis, erythema elevatum diutinum, bullous systemic lupus erythematosus) and a group responding with average good response to dapsone (pyoderma gangrenosum, bullous and cicatricial pemphigoid, acne conglobata, discoid cutaneous lupus erythematosus, subcorneal pustulosis dermatosis, granuloma faciale, rheumatoid arthritis, polychondritis, leucocytoclastic vasculitis). ADVERSE EFFECTS Adverse effects depend on the dose and they rarely occur at doses less than 100 mg per day. They are mainly shown on skin, nervous system, digestive system, hepatobiliary system, and kidney and hematologic system. The most important adverse effects are hemolytic anaemia and methemoglobinemia. Hemolysis usually occurs at doses of 200 mg and more per day. In patients with glucose-6-phosphate dehydrogenase deficiency, hemolysis may be provoked by a dose less than 50 mg per day. For prevention, before using dapsone in therapy, clinical examination with history, blood parameters, liver and renal parameters and determination of glucose-6-phosphate dehydrogenase level are recommended. CONCLUSION The use of dapsone is absolutely indicated in DH treatment and erythema elevatum diutinum. Because of anti-inflammatory effects, dapsone can also be used in treating other inflammatory noninfectious dermatoses when one should take care about "therapy efficiency/adverse effect" balance using the correct dose, monitoring relevant clinical and laboratory parameters and educating patients.

[1]  A. Wolff.  Systemic therapy , 2001, Current opinion in oncology.

[2]  M. Mcguigan.  Acute dapsone intoxication: A pediatric case report , 1997, Pediatric emergency care.

[3]  T. Kündig,et al.  [Dapsone in granulomatous rosacea]. , 1997, Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete.

[4]  S. Bombardieri,et al.  International survey on the management of patients with SLE. I. General data on the participating centers and the results of a questionnaire regarding mucocutaneous involvement. , 1996, Clinical and experimental rheumatology.

[5]  L. Sigal,et al.  Dapsone in rheumatoid arthritis. , 1996, Seminars in arthritis and rheumatism.

[6]  J. Gardiner,et al.  The Effect of Acetylation and Deacetylation on the Disposition of Dapsone and Monoacetyl Dapsone Hydroxylamines in Human Erythrocytes In‐vitro † , 1996, The Journal of pharmacy and pharmacology.

[7]  H. J. Smith,et al.  A Dapsone‐induced Blood Dyscrasia in the Mouse: Evidence for the Role of an Active Metabolite , 1996, The Journal of pharmacy and pharmacology.

[8]  Y. Tay,et al.  Bullous systemic lupus erythematosus--a case report and review. , 1995, Annals of the Academy of Medicine, Singapore.

[9]  S. Pani,et al.  Dapsone agranulocytosis in a leprosy patient. , 1994, Leprosy review.

[10]  A. Breckenridge,et al.  The use of cimetidine as a selective inhibitor of dapsone N-hydroxylation in man. , 1990, British journal of clinical pharmacology.

[11]  B. Wiholm,et al.  The incidence of agranulocytosis during treatment of dermatitis herpetiformis with dapsone as reported in Sweden, 1972 through 1988. , 1990, Archives of dermatology.

[12]  K. Yancey,et al.  Selective inhibition of human neutrophil chemotaxis to N-formyl-methionyl-leucyl-phenylalanine by sulfones. , 1986, Journal of immunology.

[13]  J. Callen,et al.  Dapsone‐induced Peripheral Neuropathy , 1986, International journal of dermatology.

[14]  R. Cowan,et al.  Dapsone and severe hypoalbuminaemia in dermatitis herpetiformis , 1981, The British journal of dermatology.

[15]  K. Tomecki,et al.  Dapsone hypersensitivity. The sulfone syndrome revisited. , 1981, Archives of dermatology.

[16]  W. Strober,et al.  Dermatitis herpetiformis: the skin and the gut. , 1980, Annals of internal medicine.

[17]  R. Dutta.  Erythema multiforme bullosum due to dapsone. , 1980, Leprosy in India.

[18]  C. Dahlgren,et al.  The inhibition of polymorphonuclear leukocyte cytotoxicity by dapsone. A possible mechanism in the treatment of dermatitis herpetiformis. , 1978, The Journal of clinical investigation.

[19]  M. Frank,et al.  Effect of sulfones on complement deposition in dermatitis herpetiformis and on complement-mediated guinea-pig reactions. , 1976, The Journal of investigative dermatology.

[20]  V. P. Barranco.  Inhibition of lysosomal enzymes by dapsone. , 1974, Archives of dermatology.

[21]  P. T. Gammon,et al.  Dapsone acetylation in dermatitis herpetiformis , 1974, The British journal of dermatology.

[22]  S. G. Browne.  Antileprosy drugs. , 1971, British medical journal.

[23]  E. Fromm,et al.  Derivate des p‐Nitrothiophenols , 1908 .