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Rapid acne regression using photopneumatic therapy
POSTER DISCUSSION SESSION 491—ACNE P101 Heat-killed Propionibacterium acnes are capable of inducing inflammatory responses Peter Lyte, Johnson & Johnson, Skillman, NJ, United States; Marion Barry, Johnson & Johnson, Skillman, NJ, United States; Olivia Linton, Johnson & Johnson, Skillman, NJ, United States; Jue-Chen Liu, Johnson & Johnson, Skillman, NJ, United States Acne vulgaris is a common multifactorial disorder of the pilosebaceous follicles, involving sebaceous hyperplasia, follicular hyperkeratinization, bacterial infection, and immune hypersensitivity. Part of the inflammation seen in acne is the result of the host response to Propionibacterium acnes. P acnes responses appear to be mediated by the activation of Toll receptors found on numerous cell types within the skin. Many current treatments for acne have focused on heating the bacteria within acne lesions, presumably to induce a bactericidal process. However, it appears that although heat treatment is sufficient to reduce bacteria, it is unclear to what extent the technique is effective as a means of reducing the appearance of acne. Indeed, studies of other Gram-positive bacteria have demonstrated that cellular membrane components of dead bacteria can still trigger an inflammatory reaction. Therefore, we sought to determine whether heat treatment would affect P acnes viability and subsequently determine whether heat-treated P acnes could induce an inflammatory response. We found that direct heat treatment of P acnes bacteria cultures resulted in a temperature-dependent decrease in P acnes viability. Treatment of P acnes bacteria cultures with temperatures ranging from 508C to 708C reduced viability by 22% and 93%, respectively. We next examined the effect of heat-treated P acnes on macrophages and primary cultures of human keratinocytes. Inoculating macrophages with live P acnes resulted in a significant release of nitric oxide. Heat treatment of P acnes before inoculation did not decrease the amount of released nitric oxide as compared to live P acnes. In a similar manner, co-culturing human keratinocytes with live P acnes resulted in an increased release of proinflammatory cytokines, interleukin (IL)-8, and IL-1RA. However, treating human keratinocytes with heat-compromised P acnes did not correlate with a similar reduction in the release of proinflammatory cytokines. Treating P acnes bacteria cultures up to 708C, which reduced P acnes viability by more than 90%, only resulted in a 21% and 57% decrease in IL-1RA and IL-8 cytokine release, respectively, suggesting that heat-killed P acnes are still capable of inducing significant inflammatory responses in skin. Taken together, these results indicate that heat is not an effective treatment for reducing P acneseinduced inflammation.
P109 Early signs and frequency of inflammatory lesions—Can we predict the next pimple? Theresa Chen, PhD, Neutrogena Corporation, Los Angeles, CA, United States; Yohini Appa, PhD, Neutrogena Corporation, Los Angeles, CA, United States Acne consists of both noninflammatory lesions and inflammatory lesions. But an acne sufferer is much more concerned about the latter. Moreover, for a person with acne prone skin, the biggest frustration is not knowing where the next pimple will surface. However, noninflammatory lesions (ie, closed comedones and open comedones) have been known to transform into inflammatory lesions. It has also been suggested that closed comedones are more likely to transform into inflammatory lesions than open comedones. At the same time, clinical observations suggest that inflammatory lesions can also appear de novo. Combining a specially developed image analysis software with a multi-modal imaging system that can visualize subsurface acne (ie, not yet visible on the skin surface) and a hyperspectral imaging system that uses discrete spectral bands to identify and measure specific chromaphores (oxy-hemoglobin, deoxy-hemoglobin, and melanin) in the skin, we have tracked the pleomorphic progression of acne lesions from follicular plugs to microcomedones to comedones to full-fledged inflammatory lesions on study subjects. The image analysis results show that more inflammatory lesions arise out of closed comedones than open comedones, but some also arise de novo. Furthermore, our evaluations reveal subsurface signs that may indicate predisposition of a microcomedone or a comedone to become an inflammatory lesion. 100% sponsored by Neutrogena Corporation.
100% is sponsored by Johnson & Johnson.
P105 Detection of TNF-a in inflammatory and noninflammatory acneiform lesions Brian Berman, MD, PhD, University of Miami, Miami, FL, United States; Oliver Perez, MD, University of Miami, Miami, FL, United States; Ran Huo, University of Miami, Miami, FL, United States; Martha Viera, MD, University of Miami, Miami, FL, United States
P102 Rapid acne regression using photopneumatic therapy Girish Munavalli, MD, MHS, Dermatology, Laser, and Vein Institute of the Carolinas, Charlotte, NC, United States Background: A multicenter study was performed to evaluate the safety and efficacy of an FDA-approved, vacuum-assisted pulsed light device in the treatment of active acne. Study design and materials: 15 subjects with Fitzpatrick skin types I to IV with comedonal, inflammatory papulo-pustular, or nodulocystic acne were treated with a series of 4 full-face treatments, performed at 1 to 4 week intervals. Treatment protocols employed multiple passes (2-4) with varying levels of vacuum and fluence with evaporative cooling. No treatment lasted more than 20 minutes. Standardized clinical photography was obtained at baseline, before each treatment, and 1 month following the final treatment. Acne severity was graded on a standardized scale, and blinded physician photographic assessment was performed. Results: Reduction of acne lesions began after 2 treatments. Overall reduction of acne activity included: cystic papules 65%, pustules 70%, and comedones 70% reduction. Reduction in facial oiliness was also reported. Pain was judged as minimal by immediate posttreatment survey. No blistering or pigmentation changes were observed. Conclusions: Rapid regression of active acne was observed following short treatment times with this relatively painless, novel pulsed light and vacuum device. 50% sponsored by Aesthera.
FEBRUARY 2008
Background: Acneiform lesions can be noninflammatory or inflammatory. Tissue necrosis factor-alpha (TNF-a) is a pivotal cytokine involved in inflammation. Studies have shown increased in vitro production of TNF-a by macrophages and keratinocytes after stimulation by Propionibacterium acnes. However, in vivo studies have not been performed to determine TNF-a concentrations in inflammatory and noninflammatory acneiform lesions and the possible effect of concomitant sulfamethoxazole/trimethoprim (SMX/TMP) therapy on TNF-a concentrations. Purpose: To detect levels of TNF-a in clinically inflammatory and noninflammatory acneiform lesions and possible effect of concomitant SMX/TMP therapy on TNF-a concentrations. Materials and methods: After informed consent was obtained, samples from 19 acneiform lesions from the face of 6 subjects were collected and characterized during office visits. Each sample was weighed, normalized to 600 mg of acneiform material per mL, and analyzed by enzyme-linked immunosorbent assay to determine the concentration of TNF-a. Results: Noninflammatory acneiform lesions (n ¼ 3) from subjects who were not receiving SMX/TMP therapy had a mean TNF-a concentration of 0.55 pg/mL, while inflammatory lesions (n ¼ 9) from the same subjects had a mean TNF-a concentration of 1.80 pg/mL (P ¼ .59). Noninflammatory acneiform lesions (n ¼ 2) from patients who were receiving SMX/TMP therapy had a mean TNF-a concentration of 8.36 pg/mL, while inflammatory lesions (n ¼ 5) from the same subjects were nonstatistically significantly lower (P ¼ .12) at 1.16 pg/mL. Conclusions: TNF-a was detected in clinically inflammatory and noninflammatory acneiform lesions. It appears that treatment with SMX/TMP subjects failed to significantly reduce TNF-a levels below that in untreated subjects. In light of SMX/TMP being solely an antibiotic, future studies are needed to determine whether other classes of antibiotics possessing antiinflammatory activities (macrolides, tetracyclines) are able to reduce TNF-a concentrations in acneiform lesions. Supported in part by research sponsorship by Collagenex.
J AM ACAD DERMATOL
AB1
P109 Early signs and frequency of inflammatory lesions—Can we predict the next pimple? Theresa Chen, PhD, Neutrogena Corporation, Los Angeles, CA, United States; Yohini Appa, PhD, Neutrogena Corporation, Los Angeles, CA, United States Acne consists of both noninflammatory lesions and inflammatory lesions. But an acne sufferer is much more concerned about the latter. Moreover, for a person with acne prone skin, the biggest frustration is not knowing where the next pimple will surface. However, noninflammatory lesions (ie, closed comedones and open comedones) have been known to transform into inflammatory lesions. It has also been suggested that closed comedones are more likely to transform into inflammatory lesions than open comedones. At the same time, clinical observations suggest that inflammatory lesions can also appear de novo. Combining a specially developed image analysis software with a multi-modal imaging system that can visualize subsurface acne (ie, not yet visible on the skin surface) and a hyperspectral imaging system that uses discrete spectral bands to identify and measure specific chromaphores (oxy-hemoglobin, deoxy-hemoglobin, and melanin) in the skin, we have tracked the pleomorphic progression of acne lesions from follicular plugs to microcomedones to comedones to full-fledged inflammatory lesions on study subjects. The image analysis results show that more inflammatory lesions arise out of closed comedones than open comedones, but some also arise de novo. Furthermore, our evaluations reveal subsurface signs that may indicate predisposition of a microcomedone or a comedone to become an inflammatory lesion. 100% sponsored by Neutrogena Corporation.
100% is sponsored by Johnson & Johnson.
P105 Detection of TNF-a in inflammatory and noninflammatory acneiform lesions Brian Berman, MD, PhD, University of Miami, Miami, FL, United States; Oliver Perez, MD, University of Miami, Miami, FL, United States; Ran Huo, University of Miami, Miami, FL, United States; Martha Viera, MD, University of Miami, Miami, FL, United States
P102 Rapid acne regression using photopneumatic therapy Girish Munavalli, MD, MHS, Dermatology, Laser, and Vein Institute of the Carolinas, Charlotte, NC, United States Background: A multicenter study was performed to evaluate the safety and efficacy of an FDA-approved, vacuum-assisted pulsed light device in the treatment of active acne. Study design and materials: 15 subjects with Fitzpatrick skin types I to IV with comedonal, inflammatory papulo-pustular, or nodulocystic acne were treated with a series of 4 full-face treatments, performed at 1 to 4 week intervals. Treatment protocols employed multiple passes (2-4) with varying levels of vacuum and fluence with evaporative cooling. No treatment lasted more than 20 minutes. Standardized clinical photography was obtained at baseline, before each treatment, and 1 month following the final treatment. Acne severity was graded on a standardized scale, and blinded physician photographic assessment was performed. Results: Reduction of acne lesions began after 2 treatments. Overall reduction of acne activity included: cystic papules 65%, pustules 70%, and comedones 70% reduction. Reduction in facial oiliness was also reported. Pain was judged as minimal by immediate posttreatment survey. No blistering or pigmentation changes were observed. Conclusions: Rapid regression of active acne was observed following short treatment times with this relatively painless, novel pulsed light and vacuum device. 50% sponsored by Aesthera.
FEBRUARY 2008
Background: Acneiform lesions can be noninflammatory or inflammatory. Tissue necrosis factor-alpha (TNF-a) is a pivotal cytokine involved in inflammation. Studies have shown increased in vitro production of TNF-a by macrophages and keratinocytes after stimulation by Propionibacterium acnes. However, in vivo studies have not been performed to determine TNF-a concentrations in inflammatory and noninflammatory acneiform lesions and the possible effect of concomitant sulfamethoxazole/trimethoprim (SMX/TMP) therapy on TNF-a concentrations. Purpose: To detect levels of TNF-a in clinically inflammatory and noninflammatory acneiform lesions and possible effect of concomitant SMX/TMP therapy on TNF-a concentrations. Materials and methods: After informed consent was obtained, samples from 19 acneiform lesions from the face of 6 subjects were collected and characterized during office visits. Each sample was weighed, normalized to 600 mg of acneiform material per mL, and analyzed by enzyme-linked immunosorbent assay to determine the concentration of TNF-a. Results: Noninflammatory acneiform lesions (n ¼ 3) from subjects who were not receiving SMX/TMP therapy had a mean TNF-a concentration of 0.55 pg/mL, while inflammatory lesions (n ¼ 9) from the same subjects had a mean TNF-a concentration of 1.80 pg/mL (P ¼ .59). Noninflammatory acneiform lesions (n ¼ 2) from patients who were receiving SMX/TMP therapy had a mean TNF-a concentration of 8.36 pg/mL, while inflammatory lesions (n ¼ 5) from the same subjects were nonstatistically significantly lower (P ¼ .12) at 1.16 pg/mL. Conclusions: TNF-a was detected in clinically inflammatory and noninflammatory acneiform lesions. It appears that treatment with SMX/TMP subjects failed to significantly reduce TNF-a levels below that in untreated subjects. In light of SMX/TMP being solely an antibiotic, future studies are needed to determine whether other classes of antibiotics possessing antiinflammatory activities (macrolides, tetracyclines) are able to reduce TNF-a concentrations in acneiform lesions. Supported in part by research sponsorship by Collagenex.
J AM ACAD DERMATOL
AB1