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Advances in Acne Vulgaris and Acne Rosacea Treatment

Advances in Acne Vulgaris and Acne Rosacea Treatment

Acne vulgaris and acne rosacea are both complex conditions that often have different etiologies but possible similar immunologic responses. Acne vulgaris may have a variety of clinical presentations including non-inflammatory papules, open and closed comedones, inflammatory pustules and cysts. 

Acne vulgaris is thought to have at least 5 different precipitating factors. These include a genetic predisposition, follicular epithelial proliferation with follicular plugging,1 often an increase in sebum production, a proliferation of the bacterium Propionibacterium acnes2 and a concomitant inflammatory response.3 Acne rosacea has many presentations including erythematotelangiectatic (this is the red flushing type of rosacea), papulopustular (this is the classic type with acne lesions), papular and phymatous or hyperplastic type (this has thickened skin such as the W.C. Fields nose). There is also an ocular type that affects the eyes, causing redness and inflammation. The ocular type may occur alone or in conjunction with other types of rosacea. 

Acne rosacea has an unknown etiology.4,5 Oxidative damage from ferritin,6 vascular endothelial growth factor overexpression,7 the LL-37 peptide form of cathelicidin8 and possible foods and environmental exposures may all play a role in the etiology of rosacea. Therefore, regardless of the complex etiology of both acne vulgaris and acne rosacea, there are many common immunologic responses contributing to the clinical disorder.

[Related: For more articles on Acne visit the Acne Medical Resource Center here.]

Treatment Options

The historic treatments of acne vulgaris include topical treatments such as retinoids, benzoyl peroxide and topical antibiotics. Systemic antibiotics are also commonly used.9 Oral spironolactone, with its anti-androgen effect has been reported to be useful.10 Oral isotretinoin has been used for more severe cases. Many potential treatments for acne rosacea have been suggested including topical treatments such as corticosteroids, azeleic acid, sulfacetamide and metronidazole, which have all been tried with limited to moderate responses. Oral antibiotics, oral retinoids, dapsone, beta-blockers and oral contraceptives have also been used in order to try to control rosacea.11

Lasers, such as the 1450 nm lasers,12 and phototherapy using red light13 or blue light in conjunction with photodynamic therapy14 have been reported as potential treatments for acne. In an attempt to treat the vascular component found in rosacea, high-dosed 595 nm pulsed dye lasers,  532 nm KTP lasers, 810 nm diode lasers, 755 nm long-pulsed Alexandrite lasers and 1064 nm long-pulsed Nd:YAG lasers have all been used.15-17

Clinical Experience

In our clinic we have been using the Regenlite Pulsed Dye Laser, from Chromogenex, which has 2 treatment modes: pulse modes and a vascular mode called Smartpulse. The pulse mode — the traditional thermal mode — has a pulse profile that has low energy initially and builds to a higher level. For skin rejuvenation, the laser delivers low fluency visible yellow light at 585 nm with Smartpulse technology. This design of a traditional laser pulse is used to accumulate energy in a target leading to damage, either of a blood vessel or of collagen tissue. 

The second pulse mode is called Smartpulse, and has the opposite pulse characteristics. There is high energy initially, with a gradual tapering of the pulse energy. This allows gentle heating of a blood vessel.18 When a microscopic blood vessel is gently heated, a repair process is initiated without destruction. Many cytokines may be released but transforming growth factor beta (TGF- β) is the most prominent factor reported. This has been measured with an increase of up to 500% after a single treatment, with this augmented presence noted as early as 3 hours after the laser irradiation.19,20

TGF-β is part of a large family of growth factors that have many effects in the body. It has been shown that TGF-β is important in tumor surveillance, skin repair and proliferation and many immune processes.19 

There is a general anti-inflammatory response followed by a repair phase leading to improvement in acne lesions. There is also a stimulation of  T-regulatory cells that have the potential to provide long-lasting immunity.20-22

Our clinical experience has shown this process is effective in treating inflammatory acne vulgaris (Figures 1 and 2) and acne rosacea (Figures 3 and 4). Patients were treated with the Regenlite laser, 7mm spot-size, with an energy density ranging from 2.5 and 3.0 J/cm2.  The entire face was treated with a single pass with minimal overlap. 

Figures 1 and 2. A low fluence pulsed dye laser was used to treat inflammatory acne vulgaris in this female patient.Patients were treated with the Regenlite laser, 7 mm spot-size, with an energy density ranging from 2.5 and 3.0 J/cm2.

The entire face was treated with a single pass with minimal overlap.

 

 

Figures 3 and 4. Acne rosacea treatments with the low fluence pulsed dye laser.

 

These patients’ acne resolved even after there was no response to oral antibiotics and topical treatments. Therefore, our hypothesis is that an increase in the TGF-β influences an anti-inflammatory response including a long-lasting T-regulatory response that leads to a prolonged resolution of acne vulgaris and acne rosacea. 

Overall, this laser appears to be an effective and long-lasting treatment for both acne vulgaris and acne rosacea. n

 

Dr. Eubanks is in practice with The Dermatology & Laser Center at Harvard Park in Denver, CO.

 

Disclosure: The author is a paid speaker for Chromogenex.

 

References

1. Norris JF, Cunliffe WJ. A histological and immunocytochemical study of early acne lesions. Br J Dermatol. 1988;118(5):651-659.

2. Webster GF. Inflammatory acne represents hypersensitivity to Propionibacterium acnes. Dermatology. 1998;196(1):80-81.

3. Kim J, Ochoa MT, Krutzik SR, et al. Activation of toll-like receptor 2 in acne triggers inflammatory cytokine responses. J Immunol. 2002;169(3):1535-1541.

4. Wilkin J, Dahl M, Detmar M, et al. Standard classification of rosacea: report of the National Rosacea Society expert committee on the classification and staging of rosacea. J Am Acad Dermatol. 2002;46(4):584-587.

5. Crawford GH, Pelle MT, James WD. Rosacea: I. Etiology, pathogenesis, and subtype classification. 

J Am Acad Dermatol. 2004;51(3):327-341.

6. Tisma VS, Basta-Juzbasic A, Jaganjac M, et al. Oxidative stress and ferritin expression in the skin of patients with rosacea. J Am Acad Dermatol. 2009;60(2):270-276.

7. Laquer V, Hoang V, Nguyen A, Kelly KM. Angiogenesis in cutaneous disease: part II. J Am Acad Dermatol. 2009;61(6):945-958.

8. Schauber J, Gallo RL. Antimicrobial peptides and the skin immune defense system. J Allergy Clin Immunol. 2008;122(2):261-266.

9. Strauss JS, Krowchuk DP, Leyden JJ, et al. Guidelines of care for acne vulgaris management. J Am Acad Dermatol. 2007;56(4):651-663.

10. Shaw JC. Low-dose adjunctive spironolactone in the treatment of acne in women: a retrospective analysis of 85 consecutively treated patients. J Am Acad Dermatol. 2000;43(3):498-502.

11. Pelle MT, Crawford GH, James WD. Rosacea II. Therapy. J Am Acad Dermatol. 2004;51(4):499-512.

12. Jih MH, Friedman PM, Goldberg LH, Robles M, Glaich AS, Kimyai-Asadi A. The 1450-nm diode laser for facial inflammatory acne vulgaris: Dose response and 12 month follow-up study. 

J Amer Acad Dermatol. 2006;55(1):80-87.

13. Cunliffe WJ, Goulden V. Phototherapy and acne vulgaris. Br J Dermatol. 2000;142(5):855-856.

14. Papageorgiou P, Katsambas A, Chu A. Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris. Br J Dermatol. 2000;142(5):973-978.

15. Bassichis BA, Swamy R, Dayan SH. Use of the KTP laser in the treatment of rosacea and solar lentigines. Facial Plast Surg. 2004;20(1):77-83.

16. Neuhaus I, Zane LT, Tope WD. Comparative efficacy of nonpurpuragenic pulsed dye laser and intense pulsed light for erythematotelangiectatic rosacea. Dermatol Surg. 2009;35(6):920-928.

17. Kozarev J. Use of long pulse Nd:YAG 1064 nm laser for treatment of rosacea telangiectatica. 

J Laser Health Acad. 2011;1:33-36.

18. Omi T, Kwana S, Sato S, et al. Cutaneous immunological activation elicited by a low-fluence pulsed dye laser. Br J Dermatol. 2005;153(suppl 2):57-62.

19. Gorelik L, Flavell RA. Transforming growth factor-beta in T-cell biology. Nat Rev Immunol. 2002;2(1):46-53.

20. Seaton ED, Charakia A, Mouser PE, Grace I, Clement RM, Chu AC. Pulsed-dye laser treatment for inflammaotry acne vulgaris: randomised controlled trial. Lancet. 2003;362(9393):1347-1352.

21. Seaton ED, Mouser PE, Charakia A, Alam S, Seldon PM, Chu AC. Investigation of the mechanism of action of nonablative pulsed-dye laser therapy in photorejuvenation and inflammatory acne vulgaris. British J Derm. 2006;155(4):748-755.

22. Wan YY, Flavell RA. TGF-beta and regulatory T cell in immunity and autoimmunity. J Clin Immunol. 2008;28(6):647-659.

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