Allergic Contact Dermatitis to Preservatives and ... - Skin Therapy Letter

Volume 16 • Number 4 • April 2011 Indexed by the US National Library of Medicine and PubMed

Allergic Contact Dermatitis to Preservatives and Fragrances in Cosmetics Tatyana Hamilton, MD, PhD and Gillian C. de Gannes, MD, FRCPC Department of Dermatology and Skin Science, University of British Columbia, Vancouver, BC, Canada

ABSTRACT Cosmetics are an important cause of allergic contact dermatitis (ACD). Fragrances and preservatives are the two most clinically relevant allergens found in cosmetic products. Patch testing remains the gold standard for identification of causative allergens. Common cosmetic allergens are reviewed. Practical methods of allergen avoidance are also discussed. Key words: allergic contact dermatitis, fragrance, preservative, skin care

Introduction The term “cosmetic” is used synonymously with “make-up” in the general population. However, it has a much broader definition and includes personal care products, hair care, nail products, and sunscreens. There is an impressive array of cosmetic products available on the market today, with an even greater number of individual ingredients. The number of new products continues to increase and the rates of adverse cutaneous reactions are expected to rise. Therefore, given the widespread use of cosmetics, it is important to monitor their side-effects. It is estimated that the average woman uses 12 personal care products daily, which comprise 168 unique ingredients. The average man uses six personal care products each day with 85 unique ingredients.1 Skin care products have been found to account for the majority of cases of allergic contact dermatitis (ACD) to cosmetics, followed by hair care and nail cosmetics.2-5 The most common responsible cosmetic allergens are fragrances and preservatives.6 Epidemiology The prevalence of cosmetic allergy is estimated at less than 1% in the general population.7-9 However, since most people do not seek medical consultation for mild adverse reactions, the actual rates are likely much higher. Pooled data of seven different studies involving 30,207 patients patch tested for suspected contact dermatitis revealed that 9.8% of positive reactions were due to cosmetic allergens.10 A recent Danish study showed that the prevalence of ACD to cosmetic allergens has doubled between 1990 and 1998.11 The

majority of patients affected with ACD to cosmetic products are women between the ages of 20 and 55.2,7-9 In addition, a study of 794 patients showed that 34% of patients would have been missed if they were only tested with NACDG (North American Contact Dermatitis Group) screening series of 65 allergens.12 A European analysis of 5911 cosmetic-allergic patients found that one-third reacted only to a personal product and no other allergen. 13 Thus, while the optimal number of allergens for patch testing to cosmetics is not firmly established, testing for additional allergens using a specialized cosmetic series and the patient’s own personal products would capture about 30% of additional patients that otherwise would have been missed. Clinical Features of ACD ACD may have acute and chronic forms. Acutely, it presents with pruritic papules, vesicles, and bullae. Chronic forms are more common and present with pruritic, scaly papules and plaques distributed in areas of most contact with the offending allergen. The distribution provides very useful clinical clues about the possible causative agent. Occasionally, ACD may produce autoeczematization resulting in a widespread or generalized cutaneous eruption. Allergens may also be transferred from other persons or even pets, resulting in “connubial” or “consort” dermatitis.14-16 The main differential diagnostic possibilities for ACD are exacerbation of atopic dermatitis or irritant contact dermatitis, both of which are far more common than allergic contact reactions.

ALSO IN THIS ISSUE: Alcohol and Skin Disorders: With a Focus on Psoriasis (page 5) & Update on Drugs (page 8)

Classes of Allergens Responsible for ACD Cosmetic ingredients can be classified into several categories: fragrances, preservatives, antioxidants, vehicles, ultraviolet absorbers, humectants, emollients, emulsifiers, acrylates, hair dyes, nail polish components, and others. Preservatives and fragrances are the most frequently detected culprits; therefore, this review will primarily deal with these two classes of allergens. Preservatives Preservatives were identified as the most common cosmetic contact allergens in several recent studies. 6,17,18 They can be classified into three broad categories: antimicrobials, antioxidants, and ultraviolet light absorbers. The antimicrobial agents can be further divided into formaldehyde preservatives, formaldehyde-releasers, and non-formaldehyde-releasing preservatives. Formaldehyde-releasing preservatives (FRP) include quaternium-15, diazolidinyl urea, imidazolidinyl urea, 2-bromo-2-nitropropane-1,3-diol, and DMDM hydantoin. Non-formaldehyde-releasing preservatives include parabens,

methylchloroisothiazolinone-methylisothiazolinone (MCI-MI), methyldibromoglutaronitrile-phenoxyethanol (MDBGN-PE), and iodopropynyl butylcarbamate. Individuals allergic to formaldehyde may also be allergic to any of the FRPs. Formaldehyde-sensitized individuals may experience a flare of ACD with a number of foods, including cod fish, caviar, coffee, shiitake mushrooms, smoked ham, maple syrup, and aspartame.19 Table 1 lists the top 20 NACDG screening allergens associated with cosmetic source in females.17 For comparison, Tables 2a and 2b list the top 10 allergens from the North American Contact Dermatitis Group (NACDG) and the Mayo Clinic Contact Dermatitis Group (MCCDG) identified in all patients presenting for patch testing. It is evident that many of the top allergens are from cosmetic sources. Fragrances There are over 3000 different fragrances used in cosmetics today.20 Not surprisingly, fragrances represent the second most common group of cosmetic allergens. Available tools to assess for fragrance allergy are fragrance mix I (FMI), fragrance mix II (FMII), No. of allergic reactions

% Females with allergy to cosmetic source, N = 1582

% Reactions in females associated with cosmetic source, N = 2920

Quaternium-15 2%

323

20.4

11.1

2/3

Myroxylon pereirae (balsam of Peru) 25%

302

19.1

10.3

2/3

Fragrance mix 8%

302

19.1

10.3

4

p-Phenylenediamine 1%

247

15.6

8.5

5

Methyldibromoglutaronitrile/phenoxyethanol 2%

131

8.3

4.5

6

Formaldehyde 1%

108

6.8

3.7

7

Tosylamide formaldehyde resin 10%

97

6.1

3.3

8

Cocamidopropyl betaine 1%

84

5.3

2.9

9

Glyceryl thioglycolate 1%

83

5.3

2.8

10/11

Diazolidinyl urea 1%

79

5.0

2.7

10/11

Diazolidinyl urea 1%

79

5.0

2.7

12

DMDM hydantoin 1%

77

4.9

2.6

13

Lanolin alcohol 30%

71

4.5

2.4

14/15

Imidazolidinyl urea 2%

70

4.4

2.4

14/15

Methylchloroisothiazolinone/methylisothiazolinone 100 ppm*

70

4.4

2.4

16

Methyl methacrylate 2%

65

4.1

2.2

17

Amidoamine 0.1%

63

4.0

2.2

18

Propylene glycol 30%

61

3.9

2.1

19

DMDM hydantoin 1%

58

3.7

2.0

20

Imidazolidinyl urea 2%

51

3.2

1.8

Rank 1

Allergen

Table 1: Top 20 NACDG screening allergens associated with cosmetics in females * Not in petrolatum; all others are 2

• Editor: Dr. Stuart Maddin • Volume 16, Number 4 • April 2011

10 Most Common Allergens NACDG Nickel sulfate Neomycin Balsam of Peru Fragrance mix Thimerosal Gold sodium thiosulfate Quaternium-15 Formaldehyde Bacitracin Cobalt chloride Table 2a: Top 10 list of common contact allergens from NACDG 10 Most Common Allergens MCCDG Nickel sulfate Balsam of Peru Gold sodium thiosulfate Neomycin Fragrance mix Thimerosal Cobalt chloride Formaldehyde Benzalkonium chloride Bacitracin Table 2b: Top 10 list of common contact allergens from MCCDG and balsam of Peru. The components of these screening allergens are listed below: Fragrance Mix I (8.0% in petrolatum) • Amyl cinnamic alcohol 1.0% • Cinnamic alcohol 1.0% • Eugenol 1.0% • Cinnamic aldehyde 1.0% • Hydroxycitronellal 1.0% • Geraniol 1.0% • Isoeugenol 1.0% • Oak moss absolute 1.0% • Sorbitan sesquioleate (emulsifier) 5.0% Fragrance Mix II (14.0% in petrolatum) • Hydroxyisohexyl 3-cyclohexene carboxaldehyde (2.5%) • Citral 1.0% • Farnesol 2.5% • Coumarin 2.5% • Citronellol 0.5% • Hexyl cinnamal 5.0% Many of the specific fragrance ingredients are protected by the Fair Packaging and Labeling Act as they are considered trade secrets.19 It is important to keep in mind that many products labeled as “unscented”, “hypoallergenic”, or even “fragrance-free” do, in fact, contain masking fragrances.

Balsam of Peru Balsam of Peru (BOP) (myroxylon pereirae resin) is an aromatic fluid that comes from the bark of the tree Myroxylon balsamum, a tree native to El Salvador.19 It is a complex mixture of many ingredients, all of which have not yet been completely identified. Key ingredients including benzoyl cinnamate, benzoyl benzoate, benzoic acid, vanillin, and nerodilol can be found in the following three groups of products: fragrance in perfumes and toiletries, flavorings in foods and drinks, and medicaments. In the past, FMI and BOP were able to detect approximately 90% of fragrance allergies. However, with the increasing number of fragrances and botanicals in use today, their screening ability is now estimated to be around 60%.19 Thus, FMII and a number of botanical extracts are now part of the 2010 NACDG screening series that comprise 70 allergens. Often, additional cosmetic and botanical series are required to diagnose fragrance allergy. Patients with contact allergy to BOP may also react to a number of substances that are well known cross-reactants with BOP (Table 3). Thus, patients should be appropriately counseled to avoid these agents. Cross Reacting Agents Balsam of Tolu Benzoin Benzyl acetate Benzyl alcohol Cinnamic alcohol/cinnamic aldehyde Cinnamon oil Clove oil Essential oils of orange peel Eugenol Propolis Table 3: Cross-reactants with balsam of Peru Practical Considerations and Clinical Pearls 1. Choose allergens carefully: based on history, occupation, hobbies, and distribution of dermatitis. Patch testing may need to be expanded beyond the NACDG screening series to include, for example, a cosmetic/botanical supplemental series. This series may be indicated in patients using a variety of make-up products or for those who use “all natural” botanical products. Testing to personal care products may lead to identification of additional relevant allergens, as well as facilitate discovery of new and emerging allergens, as new compounds are being introduced at an escalating pace. 2. Have a good working knowledge of common allergens and their sources: this is critical for choosing the correct allergens to test as well as for counseling patients on allergen avoidance. 3. Have access to available resources: an excellent review of the main concepts of ACD is found in Contact Allergy: Alternatives for the 2007 NACDG Standard Screening Tray.19 Allergen information sheets are available to the members of the American Contact Dermatitis Society (ACDS) and can be found at www.contactderm.org. Identification of allergen-free products can be accomplished by generating a customized


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product list with the use of the Contact Allergen Management Program (CAMP) available to the members of the ACDS. Multiple allergens can be entered to generate a “shopping list” of products that are safe to use in a patient with allergic contact dermatitis to their cosmetics. Conclusion Allergic contact dermatitis to cosmetics is an important cause of ACD overall. The main causes of cosmetic allergy are fragrances and preservatives. It is rewarding for both the patient and the physician if the responsible agent can be identified and subsequently removed from the patent’s environment. Patient satisfaction and compliance will also improve if meaningful counseling is provided, including detailed information on safe to use personal care products. References 1. Environmental Working Group’s Skin Deep Cosmetic Safety Database. Available at: http://www.cosmeticsdatabase.com/research. Last accessed: March 1, 2011. 2. Eiermann HJ, Larsen W, Maibach HI, et al. Prospective study of cosmetic reactions: 1977-1980. North American Contact Dermatitis Group. J Am Acad Dermatol 6(5):909-17 (1982 May). 3. Adams RM, Maibach HI. A five-year study of cosmetic reactions. J Am Acad Dermatol 13(6):1062-9 (1985 Dec). 4. de Groot AC. Contact allergy to cosmetics: causative ingredients. Contact Dermatitis 17(1):26-34 (1987 Jul). 5. de Groot AC, Bruynzeel DP, Bos JD, et al. The allergens in cosmetics. Arch Dermatol 124(10):1525-9 (1988 Oct). 6. Wetter DA, Yiannias JA, Prakash AV, et al. Results of patch testing to personal care product allergens in a standard series and a supplemental cosmetic series: an analysis of 945 patients from the Mayo Clinic Contact Dermatitis Group, 20002007. J Am Acad Dermatol 63(5):789-98 (2010 Nov).

7. Romaguera C, Camarasa JM, Alomar A, et al. Patch tests with allergens related to cosmetics. Contact Dermatitis 9(2):167-8 (1983 Mar). 8. Adams RM, Maibach HI. A five-year study of cosmetic reactions. J Am Acad Dermatol 13(6):1062-9 (1985 Dec). 9. Kohl L, Blondeel A, Song M. Allergic contact dermatitis from cosmetics. Retrospective analysis of 819 patch-tested patients. Dermatology 204(4):334-7 (2002). 10. Biebl KA, Warshaw EM. Allergic contact dermatitis to cosmetics. Dermatol Clin 24(2):215-32 (2006 Apr). 11. Nielsen NH, Linneberg A, Menne T, et al. Allergic contact sensitization in an adult Danish population: two cross-sectional surveys eight years apart (the Copenhagen Allergy Study). Acta Derm Venereol 81(1):31-4 (2001 Jan-Feb). 12. Cohen DE, Rao S, Brancaccio RR. Use of the North American Contact Dermatitis Group Standard 65-allergen series alone in the evaluation of allergic contact dermatitis: a series of 794 patients. Dermatitis 19(3):137-41 (2008 May-Jun). 13. Uter W, Balzer C, Geier J, et al. Patch testing with patients’ own cosmetics and toiletries--results of the IVDK*, 1998-2002. Contact Dermatitis 53(4):226-33 (2005 Oct). 14. Wilkinson DS. Connubial photodermatitis. Contact Dermatitis 1:58 (1975). 15. Fisher AA. Consort contact dermatitis. Cutis 24(6):595-6, 668 (1979 Dec). 16. Morren MA, Rodrigues R, Dooms-Goossens A, et al. Connubial contact dermatitis: a review. Eur J Dermatol 2:219-23 (1992). 17. Warshaw EM, Buchholz HJ, Belsito DV, et al. Allergic patch test reactions associated with cosmetics: retrospective analysis of cross-sectional data from the North American Contact Dermatitis Group, 2001-2004. J Am Acad Dermatol 60(1):23-38 (2009 Jan). 18. Laguna C, de la Cuadra J, Martin-Gonzalez B, et al. [Allergic contact dermatitis to cosmetics]. Actas Dermosifiliogr 100(1):53-60 (2009 Jan-Feb). 19. Scheman A, Jacob S, Zirwas M, et al. Contact Allergy: alternatives for the 2007 North American contact dermatitis group (NACDG) Standard Screening Tray. Dis Mon 54(1-2):7-156 (2008 Jan-Feb). 20. Devos SA, Constandt L, Tupker RA, et al. Relevance of positive patch-test reactions to fragrance mix. Dermatitis 19(1):43-7 (2008 Jan-Feb).

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Alcohol and Skin Disorders: With a Focus on Psoriasis Natalia Kazakevich, MD,1 Megan N. Moody, MD, MPH,2 Jennifer M. Landau, BS,2 Leonard H. Goldberg, MD1,2,3 Weill Cornell Medical College, Methodist Hospital, Houston, TX, USA 2 DermSurgery Associates, Houston, TX, USA 3 Department of Dermatology, The University of Texas Medical School at Houston, Houston, TX USA 1

ABSTRACT Alcohol is a serious cause of morbidity and mortality in our society and is implicated in multiple health conditions, including hepatic failure, neurological damage, hematological disorders, and nutritional deficiencies, to name a few. Although alcohol induced cutaneous abnormalities can also cause significant morbidity, they tend to be overshadowed by the other disease states associated with alcohol use. In addition to the cutaneous stigmata linked to chronic alcoholic liver disease, alcohol can directly cause or exacerbate several skin conditions. In particular, alcohol misuse is implicated in the development of psoriasis and discoid eczema, as well as confers increased susceptibility to skin and systemic infections. Alcohol misuse might also exacerbate rosacea, porphyria cutanea tarda, and post adolescent acne. Herein, we review the evidence concerning the influences of alcohol in skin conditions with a focus on psoriasis. Key words: alcohol drinking, psoriasis, risk factors, skin disorders

Physiology of Alcohol Induced Toxicity Alcohol induces a wide range of physiological derangements in the human body. Alcohol is cytotoxic to the liver, leading to alcoholic steatosis, hepatitis and, at later stages, cirrhosis 1 with systemic sequelae. Alcohol is also toxic to the bone marrow, particularly the T cells, which in turn leads to attenuated immune function.2-4 The cardiovascular system may also be adversely affected by excess alcohol use. Specifically, high output cardiac failure, hypertension, and peripheral vasodilatation may be consequences of chronic and acute alcohol intake.2,5 Finally, alcohol misuse results in a myriad of nutritional deficiencies, including vitamin and trace element deficiencies2,5 secondary to interference with proper intestinal absorption and poor nutrition. All of these physiological conditions can contribute to the development of cutaneous manifestations associated with alcohol consumption. Alcohol and Skin Disorders Cutaneous abnormalities have been associated with alcoholism and are either caused indirectly through impaired functioning of other organ systems or directly from the toxic effects of alcohol on the skin.

testosterone production is also inhibited, further exacerbating the problem. Direct inhibition of testosterone production leads to gynecomastia, which presents as a disappearance and redistribution of body and pubic hair and female pattern fat redistribution.2 Caput medusae and hemorrhoids are the result of hepatofugal blood flow caused by portal hypertension from liver cirrhosis. Systemic and superficial skin infections, including bacterial and fungal infections, represent another health problem found to be more prevalent in alcoholics.2-4 The higher incidence of infections is likely attributable to multiple factors, including alcohol associated nutritional deficiencies in combination with immunodeficiency. Most notably, zinc and vitamin C deficiencies lead to poor wound healing, weakened mucosal barriers, and altered immune defenses with increased risk for infections. Group A streptococci, Corynebacterium, and Staphylococcus aureus are common bacterial culprits,2 as are fungal infections with various tinea and Candida species.2,3 Malabsorption associated with alcoholism is another mode by which alcohol can produce cutaneous abnormalities. Angular stomatitis, glossitis, perifollicular hemorrhages, pellagra, petechia, and ecchymosis are just a few such cutaneous manifestations.

Skin Changes Indirectly Caused by Alcohol The majority of cutaneous manifestations associated with excess alcohol use are indirectly mediated through the impairment of various organ systems. Hepatic dysfunction impairs estrogen and bile salt metabolism, resulting in characteristic findings of spider angiomata, palmar erythema, and pruritis.2,3,5 Male alcoholics are consequently hyperestrogenic. 2 In addition to high estrogen levels,

Skin Changes Directly Caused by Alcohol Porphyria Cutanea Tarda (PCT) is a metabolic disorder with cutaneous manifestations resulting from an aberration in hepatic heme biosynthesis. Whether acquired or inherited, PCT results from a deficiency in one of the hepatic enzymes involved in porphyrin metabolism, specifically uroporphyrinogen decarboxylase. 2,3,6 The resultant upstream accumulation of photoreactive porphyrin precursors renders the skin extremely


5

photosensitive. 2 Alcohol is a potent inducer of the hepatic enzymes and the heme metabolic pathway, leading to an accumulation of photoreactive porphyrin compounds proximal to the enzymatic defect and, thus, precipitating PCT flare-ups.3,6 The cutaneous characteristics of an acute PCT attack include skin blistering and erosions on sun exposed areas2,3 that resolve leaving residual scarring and milia. Alcohol impairs the vasomotor center of the brain, inducing peripheral vasodilatation.2,3 Hence, it has been suggested that this resultant cutaneous vasodilatation may exacerbate rosacea,2,3 contributing to the hallmark redness and flushing. Alcohol can also promote facial erythema in people without rosacea through a genetic deficiency involving an alcohol metabolism enzyme. This phenomenon is most commonly recognized in Asians, as studies have shown that 50% lack the ability to make aldehyde dehydrogenase, leading to an accumulation of acetaldehyde after alcohol consumption.2 The Role of Alcohol in the Pathogenesis of Psoriasis Psoriasis is a common chronic inflammatory autoimmune condition, affecting approximately 2% of the population in North America.3 It is characterized by epidermal hyperproliferation3,7 and a multifactorial etiology. A complex interplay between genetics and extrinsic factors, including the environment, trauma, infection, and social behaviors appear to be influential on the origin and clinical course of the disease.3,8-11 Extensive evidence demonstrates a link between excessive alcohol consumption and psoriasis. 3,4,11,12 The amount of alcohol consumed and the type of alcoholic beverage have both been shown to confer the most risk for development and/or exacerbation of plaque psoriasis.12 A recent prospective study following 82,869 women for 14 years showed that consumption of more then 2.3 alcoholic beverages per week was a significant risk factor for new onset psoriasis.12 Furthermore, the same study found that consuming non-light beer appears to be an independent risk factor for developing psoriasis in females.12 Similarly, in males, excess alcohol consumption (at levels higher then 100g/day) appears to be a risk factor for the development and increased activity of psoriasis.11,13 Moreover, the misuse of alcohol in patients with psoriasis has been shown to be associated with decreased response to treatment. 2,13,14 Interestingly, the cutaneous distribution of psoriasis in heavy drinkers tends to be predominantly acral, involving the dorsum of the hands and digits, resembling that seen in immunocompromised patients, such as those with human immunodeficiency virus (HIV) infection.2,4 This distribution highlights the potential role of alcohol induced immunosuppression in the development of psoriasis. The exact molecular mechanisms by which alcohol triggers or exacerbates psoriasis are yet to be fully elucidated. One theory is that alcohol misuse may induce immune dysfunction with resultant relative immunosuppression.2,3 Alcohol may also enhance the production of inflammatory cytokines and cell cycle activators, such as cyclin D1 and Keratinocyte Growth Factor, which could lead to epidermal hyperproliferation.2,7,15 Additionally, increased susceptibility to superficial infections commonly observed in alcoholics, such as those caused by 6

Streptococcus and trauma, has also been postulated to have implications in the development of psoriasis.7 Although the environment and genetics may not be amenable to prevention or alteration, social behaviors such as alcohol consumption can be modified with appropriate counseling and pharmacological interventions, and therefore, appears to be a promising adjunct to the medical therapy of psoriasis. Conclusion An overwhelming amount of evidence suggests a significant link between alcohol and psoriasis - a multifactorial autoimmune disorder. Not only may alcohol contribute, in the presence of appropriate genetic makeup, to the development of psoriasis, it also results in more extensive and treatment resistant disease. Ascertaining carefully the presence of this risk factor in all patients suffering from psoriasis and providing appropriate counseling and education may help the clinician to minimize the risks of disease exacerbation and achieve better therapeutic outcomes. References 1. Menon KV, Gores GJ, Shah VH. Pathogenesis, diagnosis, and treatment of alcoholic liver disease. Mayo Clin Proc 76(10):1021-9 (2001 Oct). 2. Smith KE, Fenske NA. Cutaneous manifestations of alcohol abuse. J Am Acad Dermatol 43(1 Pt 1):1-16 (2000 Jul). 3. Higgins EM, du Vivier AW. Cutaneous disease and alcohol misuse. Br Med Bull 50(1):85-98 (1994 Jan). 4. Higgins EM, du Vivier AW. Alcohol and the skin. Alcohol Alcohol 27(6):595-602 (1992 Nov). 5. Chou SP, Grant BF, Dawson DA. Medical consequences of alcohol consumption-United States, 1992. Alcohol Clin Exp Res 20(8):1423-9 (1996 Nov). 6. McColl KE, Moore MR, Thompson GG, et al. Abnormal haem biosynthesis in chronic alcoholics. Eur J Clin Invest 11(6):461-8 (1981 Dec). 7. Farkas A, Kemeny L, Szell M, et al. Ethanol and acetone stimulate the proliferation of HaCaT keratinocytes: the possible role of alcohol in exacerbating psoriasis. Arch Dermatol Res 295(2):56-62 (2003 Jun). 8. Liu SW, Lien MH, Fenske NA. The effects of alcohol and drug abuse on the skin. Clin Dermatol 28(4):391-9 (2010 Jul-Aug). 9. Shelling ML, Kirsner RS. Failure to counsel patients with psoriasis to decrease alcohol consumption (and smoking). Arch Dermatol 146(12):1370 (2010 Dec). 10. Higgins E. Alcohol, smoking and psoriasis. Clin Exp Dermatol 25(2):107-10 (2000 Mar). 11. Poikolainen K, Reunala T, Karvonen J, et al. Alcohol intake: a risk factor for psoriasis in young and middle aged men? BMJ 300(6727):780-3 (1990 Mar 24). 12. Qureshi AA, Dominguez PL, Choi HK, et al. Alcohol intake and risk of incident psoriasis in US women: a prospective study. Arch Dermatol 146(12):1364-9 (2010 Dec). 13. Gupta MA, Schork NJ, Gupta AK, et al. Alcohol intake and treatment responsiveness of psoriasis: a prospective study. J Am Acad Dermatol 28(5 Pt 1):730-2 (1993 May). 14. Higgins EA, du Vivier AWP. Alcohol abuse and treatment resistance in skin disease. J Am Acad Dermatol 30(6):1048 (1994 Jun). 15. Ockenfels HM, Keim-Maas C, Funk R, et al. Ethanol enhances the IFN-gamma, TGF-alpha and IL-6 secretion in psoriatic co-cultures. Br J Dermatol 135(5):746-51 (1996 Nov).


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7

Update on Drugs

EDITOR-IN-CHIEF Stuart Maddin, MD

University of British Columbia, Vancouver, Canada

ASSOCIATE EDITORS Hugo Degreef, MD, PhD

Catholic University, Leuven, Belgium

Jason Rivers, MD


EDITORIAL ADVISORY BOARD Murad Alam, MD

Name/Company

Gabapentin tablets GRALISE™ (DM-1796) Depomed, Inc. Abbott Products, Inc.

Northwestern University Medical School, Chicago, USA

Kenneth A. Arndt, MD

Beth Israel Hospital Harvard Medical School, Boston, USA

Wilma Fowler Bergfeld, MD Cleveland Clinic, Cleveland, USA

Jan D. Bos, MD

University of Amsterdam, Amsterdam, Holland

Alastair Carruthers, MD


Bryce Cowan, MD, PhD


Jeffrey S. Dover, MD

Yale University School of Medicine, New Haven, USA Dartmouth Medical School, Hanover, USA

Boni E. Elewski, MD

University of Alabama, Birmingham, USA

Barbara A. Gilchrest, MD

Boston University School of Medicine, Boston, USA

Christopher E.M. Griffiths, MD

University of Manchester, Manchester, UK

Aditya K. Gupta, MD, PhD, MBA/MCM University of Toronto, Toronto, Canada

Mark Lebwohl, MD

Mt. Sinai Medical Center, New York, USA

James J. Leydon, MD

University of Pennsylvania, Philadelphia, USA

Harvey Lui, MD


Howard I. Maibach, MD

University of California Hospital, San Francisco, USA

Jose Mascaro, MD, MS

University of Barcelona, Barcelona, Spain

Larry E. Millikan, MD

Tulane University Medical Center, New Orleans, USA

Jean Paul Ortonne, MD

Centre Hospitalier Universitaire de Nice, Nice, France

Ted Rosen, MD

Baylor College of Medicine, Houston, USA

Alan R. Shalita, MD

SUNY Health Sciences Center, Brooklyn, USA

Wolfram Sterry, MD

Humboldt University, Berlin, Germany

Richard Thomas, MD


Stephen K. Tyring, MD, PhD, MBA

University of Texas Health Science Center, Houston, USA

John Voorhees, MD

University of Michigan, Ann Arbor, USA

Guy Webster, MD

Jefferson Medical College, Philadelphia, USA

Klaus Wolff, MD University of Vienna, Vienna, Austria

Skin Therapy Letter © (ISSN 1201–5989) Copyright 2011 by SkinCareGuide.com Ltd. Skin Therapy Letter © is published 10 times annually by SkinCareGuide.com Ltd, 1004 – 750 West Pender, Vancouver, British Columbia, Canada, V6C 2T8. All rights reserved. Reproduction in whole or in part by any process is strictly forbidden without prior consent of the publisher in writing. While every effort is made to see that no inaccurate or misleading data, opinion, or statement appears in the Skin Therapy Letter ©, the Publishers and Editorial Board wish to make it clear that the data and opinions appearing in the articles herein are the responsibility of the contributor. Accordingly, the Publishers, the Editorial Committee and their respective employees, officers, and agents accept no liability whatsoever for the consequences of any such inaccurate or misleading data, opinion, or statement. While every effort is made to ensure that drug doses and other quantities are presented accurately, readers are advised that new methods and techniques involving drug usage, and described herein, should only be followed in conjunction with the drug manufacturer’s own published literature. Printed on acid-free paper effective with Volume 1, Issue 1, 1995. Subscription Information. Annual subscription: Canadian $94 individual; $171 institutional (plus GST); US $66 individual; $121 institutional. Outside North America: US$88 individual; $143 institutional. We sell reprints in bulk (100 copies or more of the same article). For individual reprints, we sell photocopies of the articles. The cost is $20 to fax and $15 to mail. Prepayment is required. Student rates available upon request. For inquiries: [email protected]

8

Approval Dates/Comments

The US FDA approved gabapentin extended release tablets in January 2011 for the once-daily treatment of post-herpetic neuralgia (PHN), the pain following herpes zoster infection (shingles). Treatment is to be titrated over a 2-week period to an 1800 mg oncedaily dose. The tablet swells in gastric fluid and gradually releases gabapentin. This formulation is not interchangeable with other gabapentin products because of differing pharmacokinetic profiles that affect the frequency of administration. Furthermore, the FDA has granted GRALISE™ Orphan Drug status.

Oxychlorine compound The US FDA approved a new skin care gel in February Epicyn™ HydroGel 2011 for the management of burning, itching, and pain Oculus Innovative Sciences, Inc. associated with various types of dermatoses, including atopic dermatitis and radiation dermatitis. The product is approved as a medical device and granted 510(k) clearance for marketing. This prescription product is intended for use under the supervision of a healthcare professional. In addition, the gel relieves the pain of first- and second-degree burns and maintains a moist wound and skin environment to help treat dry and waxy skin. The hydrogel is a shelfstable hypochlorous acid formulation based on the proprietary Microcyn® technology platform. Collagenase clostridium histolyticum XIAPEX® Pfizer Inc. Auxilium Pharmaceuticals, Inc.

The European Commission (European Medicines Agency) approved this novel injectable treatment in February 2011 for Dupuytren’s contracture in adults with a palpable cord. It was US FDA approved in 2010 under the trade name of XIAFLEX®.

Drug News A recently published study* in the New England Journal of Medicine reported that the human papilloma virus (HPV) quadrivalent (types 6, 11, 16 and 18) recombinant vaccine (Gardasil®) is as effective at preventing HPV infection and genital warts in men as it is in women. The study enrolled 4065 healthy boys and men (aged 16 to 26 years) from 18 countries in a randomized, placebo-controlled, double-blind trial and found that HPV vaccination was 90% effective in protecting against HPV and genital warts. Although the reduction in precancerous lesions may reduce the rates of penile and anal cancers in males, their incidences are significantly lower than cervical cancer. This investigation does not address the cancer risk in the specific age-gender group studied. Both of the HPV vaccines (Cervarix™ and Gardasil®) are recommended for females aged 9 through 26 for the prevention of cervical cancers caused by HPV types 16 and 18 (high risk types), which cause most cervical cancers. These vaccines are now on the US Centers for Disease Control and Prevention’s (CDC) routine childhood vaccination schedule for girls starting at age 9. Only one of the vaccines (Gardasil®) also protects against HPV types 6 and 11, which cause most genital warts in females and males. The quadrivalent vaccine is recommended for optional use in boys and men. Gardasil® was approved for use in males 9 through 26 years of age in 2009 by the US FDA, however, the CDC’s advisory panel voted against routine use of the vaccine in boys and men. More information on the CDC’s recommendations is available at: http://www.cdc.gov/ vaccines/vpd-vac/hpv/vac-faqs.htm *Giuliano AR, Palefsky JM, Goldstone S, et al. Efficacy of quadrivalent HPV vaccine against HPV infection and disease in males. N Engl J Med 364(5):401-11 (2011 Feb 3). • Editor: Dr. Stuart Maddin • Volume 16, Number 4 • April 2011