“…As shown in figure 5, sulfamethoxazole has a chemical structure similar to dapsone, which would be the drug of choice in the treatment of a variety of inflammatory dermatoses [18,19]. Thus, it is understand able that sulfamethoxazole shows action mechanisms similar to dapsone.…”
The patient described here had all the clinical features (itchy red papules and reticular pigmentation) as well as the histological findings (lichenoid tissue reactions) of prurigo pigmentosa, a little-known disorder of unknown etiology, and responded well to sulfamethoxazole treatment. In order to investigate the mode of action of this drug and thus the underlying pathogenesis of this dermatosis, the effect of sulfamethoxazole on the production of oxygen intermediates (OIs) was examined both in the cell-mediated system and in the xanthine-xanthine oxidase system. It was found that therapeutic doses of the drug significantly reduced the hydroxyl radical levels, one of the most potent oxidants that might cause tissue injury. These findings suggest the possibility that OIs produced by infiltrated cells are involved in the inflammatory process of prurigo pigmentosa and that sulfonamides exert their anti-inflammatory effects by affecting OI generation which results in protection against lichenoid tissue reaction.
“…As shown in figure 5, sulfamethoxazole has a chemical structure similar to dapsone, which would be the drug of choice in the treatment of a variety of inflammatory dermatoses [18,19]. Thus, it is understand able that sulfamethoxazole shows action mechanisms similar to dapsone.…”
The patient described here had all the clinical features (itchy red papules and reticular pigmentation) as well as the histological findings (lichenoid tissue reactions) of prurigo pigmentosa, a little-known disorder of unknown etiology, and responded well to sulfamethoxazole treatment. In order to investigate the mode of action of this drug and thus the underlying pathogenesis of this dermatosis, the effect of sulfamethoxazole on the production of oxygen intermediates (OIs) was examined both in the cell-mediated system and in the xanthine-xanthine oxidase system. It was found that therapeutic doses of the drug significantly reduced the hydroxyl radical levels, one of the most potent oxidants that might cause tissue injury. These findings suggest the possibility that OIs produced by infiltrated cells are involved in the inflammatory process of prurigo pigmentosa and that sulfonamides exert their anti-inflammatory effects by affecting OI generation which results in protection against lichenoid tissue reaction.
“…As DDS-NOH is inevitably formed during dapsone therapy, all these adverse effects are obligatory and vary only in intensity. These hematologic side effects of dapsone have long been recognized and have been reviewed by various authors [11, 101, 125, 136, 165, 173, 178]. Therefore, they will not be dealt with in detail in this survey.…”
Dapsone (4,4′-diaminodiphenylsulfone) is an aniline derivative belonging to the group of synthetic sulfones. In 1937 against the background of sulfonamide era the microbial activity of dapsone has been discovered. Shortly thereafter, the use of dapsone to treat non-pathogen-caused diseases revealed alternate antiinflammatory mechanisms that initially were elucidated by inflammatory animal models. Thus, dapsone clearly has dual functions of both: antimicrobial/antiprotozoal effects and anti-inflammatory features similarly to non-steroidal anti-inflammatory drugs. The latter capabilities primarily were used in treating chronic inflammatory disorders. Dapsone has been investigated predominantly by in vitro methods aiming to get more insights into the effect of dapsone to inflammatory effector cells, cytokines, and/or mediators, such as cellular toxic oxygen metabolism, myoloperoxidase-/halogenid system, adhesion molecules, chemotaxis, membrane-associated phospholipids, prostaglandins, leukotrienes, interleukin-8, tumor necrosis factor α, lymphocyte functions, and tumor growth. Moreover, attention has been paid to mechanisms by which dapsone mediates effects in more complex settings like impact of lifespan, stroke, glioblastoma, or as anticonvulsive agent. Additionally, there are some dermatological investigations in human being using dapsone and its metabolites (e.g., leukotriene B4-induced chemotaxis, ultraviolet-induced erythema). It could be established that dapsone metabolites by their own have anti-inflammatory properties. Pharmacology and mechanisms of action are determining factors for clinical use of dapsone chiefly in neutrophilic and/or eosinophilic dermatoses and in chronic disorders outside the field of dermatology. The steroid-sparing effect of dapsone is useful for numerous clinical entities. Future avenues of investigations will provide more information on this fascinating and essential agent.
“…This suggests that under pathological conditions, this substance may be available to the dermis and could be an important mediator of cutaneous inflammation. In this regard it is provocative that dapsone, a compound used in the treatment of several dermatological disorders [7], was effective against rIL-lfl-induced inflammation in our model.…”
A single, 10 ng intradermal injection of human recombinant interleukin-1 beta (rIL-1 beta) into rat ears produced acute inflammation. Tissue wet weight (edema) and total myeloperoxidase activity (PMN accumulation), peaked at 3 hours and returned to base line at 3 days. Given orally, 1 hour prior to rIL-1 beta injection, cyproheptadine, dexamethasone, conventional NSAID's, or mixed cyclooxygenase/lipoxygenase inhibitors were potent antagonists of edema and moderate antagonists of PMN accumulation. In addition, the putative DMARD's, auranofin, dapsone, and levamisole were effective inhibitors of rIL-1 beta induced inflammation.
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