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Improvement in vehicle design may improve the delivery of drugs to the target site. A clinical trial was performed to evaluate an improved vehicle for topical benzoyl peroxide. Thirty-nine subjects participated in a split-face, double-blind trial of topical benzoyl peroxide 5 percent versus benzoyl peroxide 5 percent in 8 percent urea. All subjects had grade II or III acne as described by Pillsbury. Study solutions were randomly assigned to a selected side of the subject's face and applied twice a day to the appropriate side of the face for eight weeks. Total and inflammatory lesion counts were performed by the same investigator during the eight weeks of study at biweekly intervals. No overall differences in the response to the study preparations were observed when assessed objectively and subjectively.
Benzoyl peroxide (BP) has been a standard and effective topical treatment for acne vulgaris for the past 35 years. Previous studies and case reports have documented benzoyl peroxide to be a strong irritant and a weak allergen, with many cases of tolerance induced with repeat use of this irritant. While less common, numerous cases of BP-induced allergic contact dermatitis (delayed type hypersensitivity reaction) have been reported in the literature. We report here an individual with an incipient edematous reaction to topical BP used for acne therapy. This under-recognized presentation is discussed in the context of published literature on BP-induced hypersensitivity and irritation.
Benzoyl peroxide, a powerful organic oxidizing agent, was applied topically according to a carefully developed technique to cutaneous ulcers of different types. The healing time was shortened greatly by the rapid development of healthy granulation tissue and the quick ingrowth of epithelium. Exceptionally large pressure ulcers with deep cavities, undercut edges and sinus tracts were sucessfully treated, as were stasis ulcers of long duration resistant to all other therapy. There were only 13 treatment failures among the 133 cases. The slow, sustained release of oxygen by benzoyl peroxide was though to be responsible for the success. The only complications were contact irritant dermatitis in 3% and contact allergic dermatitis in 2% of patients treated.
BACKGROUND: Concerns have arisen over the development of antibiotic-resistant organisms due to the prolonged use of oral and topical antibiotics in acne vulgaris. We have previously demonstrated that benzoyl peroxide used in consort with a chemical with an accessible tertiary amine, such as an allylamine, increases radical activity and biological effect. OBJECTIVES: The purpose of this pilot study was to assess the efficacy of two nonantibiotic topical remedies for mild to moderate acne, with one of the agents being a combination of benzoyl peroxide with butenifine, an allylamine. METHODS: In an open-label, patient-satisfaction, 8-week comparative study, 23 patients demonstrating mild to moderate facial acne were given randomly either benzoyl peroxide in Proactiv Solution or the combination of benzoyl peroxide with an allylamine. RESULTS: The allylamine-benzoyl peroxide combination therapy outperformed Proactiv Solution during each 2-week stage of evaluation in terms of reduction of comedones, inflammatory lesions, and degree of oiliness. There was a marked preference for the allylamine-benzoyl peroxide combination in terms of patient satisfaction. CONCLUSIONS: Benzoyl peroxide used in consort with antimicrobial agents that contain an accessible tertiary amine, such as erythromycin, has previously been shown to increase radical activity and biological effect. Trials of short duration with small numbers of patients do not adequately inform practitioners about whether the combination of allylamines with benzoyl peroxide is a viable alternative to topical antibiotic therapy for acne. Nevertheless, the higher satisfaction with the allylamine-benzoyl peroxide combination certainly warrants further investigation.
Benzoyl peroxide (BP) is shown to be a weak allergen. Of 25 guinea pigs, only 5 were sensitized in the TINA test. Before treatment, only 2 of 172 acne patients gave a positive patch test with 1% BP, but not with 0.1% BP. The following results suggest that BP is a strong irritant. The irritant potential ID50 in rabbits was 2.52%, and the IT50 was 2.31 days with 5% BP, 4.34 days with 1% and 8.35 days with 0.1% BP. 29% of acne patients and non-exposed controls had a positive patch test with 5% BP. However, only 11 of 155 acne patients had clinical signs of intolerance, which settled despite continued use in 10 cases. The possible reasons for this dichotomy are explored. Neither the irritant nor allergenic properties of BP impaired its clinical use.
Benzoyl peroxide (BP) is commonly used for topical acne treatment and has long been known to be a weak allergen and a strong irritant. We report a case of a 26-year-old woman, who presented with an itchy erythematous reaction and strong oedema localized to the face. Two weeks before angioedema, the patient had started a new topical treatment with a gel containing 10% BP for acne. She was patch tested to European Standard Series, including BP 1% in white petrolatum, and to the 10% BP-containing gel previously used by herself, showing positivity on day 2 to BP 1% and to the 10% BP-containing gel. Factors that suggested an association between the severe angioedematous reaction and BP topical application include the strong reaction to BP in the patch-test, the temporal relationship, the complete resolution of symptoms after the drug was withdrawn and the absence of other identified explanations.
Benzoyl peroxide (BzPO) is both a tumor promoter and progressor in mouse skin; however, BzPO is neither an initiator nor a complete carcinogen in this tissue. Although not mutagenic, BzPO has been observed to produce strand breaks in DNA of exposed cells. These actions are presumed to be mediated by free-radical derivatives of BzPO. Previous studies suggested that the metabolism of BzPO in keratinocytes proceeds via the initial cleavage of the peroxide bond, yielding benzoyloxy radicals which, in turn, can either fragment to form phenyl radicals and carbon dioxide or abstract H atoms from biomolecules to yield benzoic acid. Benzoic acid is the major stable metabolite of BzPO produced by keratinocytes. In the present study we have investigated the role of BzPO and its metabolites in the generation of strand scissions in a cell-free system using phi X-174 plasmid DNA. In this system BzPO produced DNA damage that was dose-dependent over a concentration range of 0.1-1 mM and required the presence of copper but not other transition metals. By contrast, benoic acid did not produce DNA damage in this system, either in the presence or in the absence of copper. The inclusion of spin trapping agents, such as N-tert-butyl-alpha-phenylnitrone (PBN), 3,5-dibromo-4-nitrosobenzenesulfonate, and nitrosobenzene, in incubations was found to significantly reduce the extent of DNA damage generated via the copper-mediated activation of BzPO. Electron paramagnetic resonance spectroscopy studies suggested that the primary radical trapped by PBN following copper-mediated decomposition of BzPO was the benzoyloxy radical.(ABSTRACT TRUNCATED AT 250 WORDS)
Benzoyl peroxide (BP), used widely in dermatologic therapy and by the food industry, is considered a tumor promoter in chemically induced skin. Tumor promoters of both the phorbol and non-phorbol type interact with protein kinase C (PKC). This enzyme, therefore, is regarded as the intracellular receptor for a number of tumor promoters. BP bears some structural resemblance to diacylglycerol (DAG) and thus may exert its action through the PKC system. Based on these observations, we have investigated the effect of BP on PKC from mouse skin. Our data show that unlike phorbol esters, which stimulate PKC (in vivo and in vitro), BP inhibits PKC. Concentration-dependent inhibition by BP is observed when PKC is stimulated by phorbol esters, diacylglycerol, phosphatidyl serine (PS), or a combination of the latter two. BP also inhibits PKC stimulated by (-) Indolactam V, a nonphorbol compound resembling the teleocidins. 3H-phorbol ester binding experiments reveal that inhibition by BP may be due to its interference with the phorbol ester binding site and consequently diacylglycerol binding. The binding data and the inability of BP to inhibit either cyclic AMP-dependent protein kinase I or II imply that BP interacts with PKC, and not with the histone substrate. Results presented here clearly indicate that unlike phorbol and certain non-phorbol type of tumor promoters BP does not stimulate PKC in vitro.
Benzoyl peroxide (BzPO) is a free radical generating compound that acts as a tumor promoter and progressor in mouse skin. BzPO is cleaved in the presence of copper to produce benzoyloxyl and phenyl radicals. Treatment of mutation reporter plasmids with BzPO and copper yields predominantly single-strand breaks and G-->T transversion mutations. To explore the role of base modifications in the possible mammalian mutagenicity of BzPO the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) within the DNA of cultured murine keratinocytes was investigated. Treatment with 10 microM BzPO produced a maximum 3-fold increase in levels of 8-OHdG versus vehicle controls within 1-2 h, with significant levels of 8-OHdG persisting 6 h after initial exposure to BzPO. Pretreatment with the copper chelator bathocuproine disulfonic acid reduced the levels of 8-OHdG generated by BzPO to near background. However, treatment with the iron chelator desferal did not. The stable metabolic product of BzPO benzoic acid was ineffective in producing 8-OHdG. Depletion of cellular glutathione with L-buthionine-(S,R)-sulfoximine increased the amount of BzPO-generated 8-OHdG, while supplementation with glutathione monoethyl ester reduced the number of 8-OHdG molecules formed. Collectively, these results suggest that BzPO at non-cytotoxic concentrations undergoes copper-dependent activation to a reactive product to generate 8-OHdG within cultured murine keratinocytes.
BACKGROUND: Topical clindamycin and benzoyl peroxide have each demonstrated clinical efficacy in the treatment of acne vulgaris. When used in combination, they promise greater efficacy than either individual agent used alone and the combined use of benzoyl peroxide with topical antibacterial has been shown to decrease the emergence of antibacterial resistant species. OBJECTIVE: The objective was to determine the efficacy and safety of a combination benzoyl peroxide plus clindamycin in a gel formulation compared with each of its 2 active constituents in gel vehicle, and gel vehicle given alone in the treatment of acne vulgaris. METHODS: In this 10-week, multicenter, double-blind trial, 480 patients with moderate to moderately severe acne were randomized to receive twice-daily treatment with 5% benzoyl peroxide plus 1% clindamycin, 5% benzoyl peroxide, 1% clindamycin, or vehicle. RESULTS: Significantly greater reductions in the number of inflammatory and total lesions were demonstrated in patients using combination therapy compared with those using any of its 3 individual components. Likewise, both physicians' and patients' global evaluations showed significantly greater improvements with the combination therapy than with its individual components. The most frequent adverse effect, dry skin, occurred to a similar extent in the combination and benzoyl peroxide treatment groups. CONCLUSION: The improved efficacy obtained with the combination therapy was accompanied by a tolerability profile similar to that of benzoyl peroxide alone, making this new combination product an alternative antimicrobial therapy for acne vulgaris.
Acne vulgaris is a common, inflammatory disease of the pilosebaceous duct. Propionibacterium acnes proliferated in sebum, produces chemotactic factors followed by phagocytosis and this process results in the production of reactive oxygen species which contribute to the inflammatory reaction in papulopustular type acne. Benzoyl peroxide (BP) and BP combination with erythromycin (BP/E) are effective topical medications for the treatment of mild and moderate acne vulgaris. In the present study, the effects of BP and BP/E on antioxidant defence enzymes in 40 patients with papulopustular type acne were evaluated. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), and also thiobarbituric acid reactive substance (TBARS) levels were determined in peripheral blood leukocytes in all patients, as well as in tissues of a small group of patients before and at the end of 4 weeks of treatment. No difference was detected in leukocyte antioxidant enzyme activities and TBARS levels due to BP treatment. However, SOD, CAT and GSH-Px activities in leukocytes decreased and TBARS levels increased in BP/E-treated patients (p < 0.05). There was no statistically significant difference between pretreatment and posttreatment enzyme activities in tissue samples. The results of this preliminary study may be attributable to in vivo conditions and possible stability problems while compounding the mixture of the BP/E. Influence of the other ingredients of the formulations applied in the study must also be considered.
A double-blind, controlled clinical trial with 60 patients was employed in order to study the relative merits of two treatment schedules in acne vulgaris. One therapy comprised the topical application of a cream containing a combination of miconazole 2% and benzoylperoxide 5% (Acnidazil, Janssen) twice a day. In the other therapy, we applied a cream containing only benzoylperoxide 5%. Both groups of patients showed large and statistically significant reduction in the number of comedones, papules, and pustules during 12 weeks of therapy. Acnidazil, however, was found to have definitely better therapeutical results than benzoylperoxide alone: The lesions improved significantly faster, tolerance was better, and the patients overall evaluation clearly favored Acnidazil. 86,2% of the patients treated with Acnidazil rated the results good to very good, in contrast to 63% of the patients treated with benzoylperoxide only (p = 0.037).
62-65% reduction in the number of lesions was obtained in the treatment of 52 patients with acne vulgaris in this randomized single-blind study comparing a 5% benzoyl peroxide/2% miconazole cream (BPO-MCZ) with a 5% benzoyl peroxide gel (BPO). While BPO gel was equally effective in male and female patients (66 and 73% reduction of lesions), the BPO-MCZ cream was significantly more effective in the latter (50 vs. 74% mean reduction of lesions). Tolerance was significantly better with the BPO/MCZ cream preparation, particularly in females.
BACKGROUND: Topical clindamycin and benzoyl peroxide have each demonstrated clinical efficacy in the treatment of acne vulgaris. When used in tandem, they promise greater efficacy than either individual agent through their antibacterial and anti-inflammatory effects. OBJECTIVE: To determine the efficacy and safety of combination benzoyl peroxide/ clindamycin compared with benzoyl peroxide or benzoyl peroxide/erythromycin in the treatment of acne. METHODS: In this randomized, 10-week, multicenter, single-blind trial, 492 patients with moderate to moderately severe acne were treated twice daily with 5% benzoyl peroxide/1% clindamycin, 5% benzoyl peroxide, or 5% benzoyl peroxide/3% erythromycin and assessed every 2 weeks. RESULTS: Compared with benzoyl peroxide, benzoyl peroxide/clindamycin demonstrated significantly greater reductions in inflammatory lesions (p = 0.04) and significantly greater overall improvement as assessed by physicians (p < or = 0.04) and patients (p < 0.001). Benzoyl peroxide/clindamycin demonstrated a nonsignificant trend for greater efficacy compared to benzoyl peroxide/erythromycin. Dry skin was the most frequent (< or = 7.3%) adverse event with all three therapies. CONCLUSION: Benzoyl peroxide/clindamycin demonstrated improved efficacy and similar tolerability; to benzoyl peroxide used alone and was similar to benzoyl peroxide/ erythromycin, making this combination product an effective alternative antimicrobial therapy for acne.
A topical gel combining 5% benzoyl peroxide and 1% clindamycin as phosphate was evaluated in a 10-week randomized double-blind trial involving 287 patients with moderate to moderately severe acne. The combination agent demonstrated significantly greater reductions in inflammatory lesions than either of its active constituents (5% benzoyl peroxide and 1% clindamycin) or vehicle when used alone. Significantly greater reductions in comedos and improvements, as measured by both physicians' and patients' global evaluations, were obtained with the combination agent than with clindamycin or vehicle. The reduction in comedos and the global improvements were similar between the combination agent and benzoyl peroxide. The combination agent was well tolerated; the incidence of dry skin was similar to that found with benzoyl peroxide, and other adverse events were similar to that with vehicle. The improved efficacy obtained with combination therapy was accompanied by a safety profile similar to that of either constituent used alone.
Alkaline elution was used to examine DNA single-strand breaks in cultured normal and carcinogen-altered mouse keratinocytes exposed to 12-O-tetradecanoyl phorbol-13-acetate and benzoyl peroxide. Seven cell lines derived from carcinogen-induced mouse skin papillomas and three cell lines derived from N-methyl-N'-nitro-N-nitrosoguanidine-treated non-tumor bearing mouse skin were resistant to phorbol ester-mediated DNA strand breaks after 6 or 24 h. Normal keratinocytes sustained strand breaks after 24 h but not after 6 h. Benzoyl peroxide induced extensive strand breaks in normal keratinocytes at both 6 and 24 h, and this was associated with marked cytotoxicity. In contrast, 9 of 10 cell lines showed complete or partial resistance to strand breaks following benzoyl peroxide exposure. It is proposed that differential resistance to DNA strand breaks and cytotoxicity among normal and carcinogen-altered keratinocytes provides the biological basis for the promoting action of benzoyl peroxide. Furthermore, sublethal DNA damage in preneoplastic or neoplastic keratinocytes may account for the potency of benzoyl peroxide in causing malignant conversion.
Benzoyl peroxide (BP) is an initiator of polymerisation used in the synthesis of methyl methacrylate dental materials, and is a known allergen that causes allergic contact dermatitis during occupational exposure, especially in dentists and dental personnel. The eyes of dental technicians, dentists and even patients with an allergic history are the first level of exposure, and therefore complaints of allergic reactions of the eyes are usually noted. In this article the authors used a modification direct cell culture testing method to assess the cytotoxic potential of BP. L929 mouse fibroblasts as well as cells from human limbal eye rings were exposed to BP vapours in the experiments. The MTT and crystal violet assays were also employed to determine cell numbers and viability. Results indicated that there is an exponential decrease in cell viability. After exposure of five minutes, cell viability had already decreased by 20 and 40% for vapours derived from either a 10 or 20 microliters aliquot of BP, respectively. After a further five minutes, cell viability decreased by a further 10% with a statistical difference form the control of p < 0.01. Results indicated that BP vapours are cytotoxic to mouse L929 and human eye fibroblasts. Furthermore, the authors concluded that the permanent L929 mouse fibroblast cell line can provide valuable information regarding the cytotoxic effects of dental products and associated compounds that form toxic vapours.