- Email: [email protected]
Ultraviolet A sunbeds and vitamin D
LETTERS NOTES
& COMMENTS
Written action plans should be comprehensive and evidence-based To the Editor: I certainly applaud work towards the development of a written action plan (WAP) for atopic dermatitis as published by Chisolm et al1 in the Journal. However, the WAP presented by the authors has a number of limitations that suggests that this plan may be appropriate for patients only with mild disease and/or those with infrequent flares. Hydrocortisone, as recommended by the WAP authors for indefinite use, has been found in healthy skin to decrease collagen synthesis by more than 80% within 3 weeks.2 The clinical significance of this decrease in collagen synthesis is not known. Moreover, medium potency corticosteroids—also recommended for long-term use by the authors— decrease skin thickness by at least 6% within 4 weeks.3,4 Therefore, given no time or dosage limitations on the use of these agents, the WAP is a recipe for atrophy in our patients with more significant disease. If these corticosteroids were the only agents available that were ‘‘safe’’ and effective, we would accept the consequences. But when patients require long-term treatment, nonatrophogenic alternatives, such as tacrolimus and pimecrolimus, both of which have no atrophogenicity,3,4 should be part of any evidence-based WAP. The development of a WAP, as with asthma, should be a comprehensive and evidence-based approach. The authors and our patients could benefit from more thorough evaluation of the relative efficacies and toxicities of agents. Guidelines for care, such as those developed by the Primary Care Dermatology Society and the British Association of Dermatologists,5 may serve as excellent additional resources. Alan B. Fleischer, Jr, MD Department of Dermatology, Wake Forest University Health Sciences, Winston-Salem, North Carolina Funding sources: None. Dr Fleischer is a member of the advisory boards of Allergan, Amgen, Astellas, Galderma, GSK, and Stiefel; a consultant for Astellas, Asubio, Combe, Galderma, Gerson Lehrman, Intendis, Kikaku America International, Merz, Novartis, and Serentis; an investigator for 3M, Abbott, Amgen, J AM ACAD DERMATOL
Astellas, Asubio, Biogen, Dow, Centocor, Coria, Galderma, GSK, Genentech, Healthpoint, Intendis, Medicis, Novartis, Ortho-Neutrogena, Pfizer, and Stiefel; and is a member of the speakers bureaus for Amgen, Astellas, Galderma, Intendis, Medicis, Novartis, and Stiefel. Correspondence to: Alan B. Fleischer, Jr, MD, Wake Forest University Health Sciences, Medical Center Blvd, Winston-Salem, NC 27157 E-mail: [email protected] REFERENCES 1. Chisolm SS, Taylor SL, Balkrishnan R, Feldman SR. Written action plans: potential for improving outcomes in children with atopic dermatitis. J Am Acad Dermatol 2008;59: 677-83. 2. Nuutinen P, Riekki R, Parikka M, Salo T, Autio P, Risteli J, et al. Modulation of collagen synthesis and mRNA by continuous and intermittent use of topical hydrocortisone in human skin. Br J Dermatol 2003;148:39-45. 3. Reitamo S, Rissanen J, Remitz A, Granlund H, Erkko P, Elg P, et al. Tacrolimus ointment does not affect collagen synthesis: results of a single-center randomized trial. J Invest Dermatol 1998;111:396-8. 4. Queille-Roussel C, Paul C, Duteil L, Lefebvre MC, Rapatz G, Zagula M, et al. The new topical ascomycin derivative SDZ ASM 981 does not induce skin atrophy when applied to normal skin for 4 weeks: a randomized, double-blind controlled study. Br J Dermatol 2001;144:507-13. 5. Primary Care Dermatology Society website. Primary Care Dermatology & British Association of Dermatologists. Guidelines for the management of atopic eczema. Available at: http://www.pcds.org.uk/images/stories/pcdsbad-eczema.pdf. Accessed October 3, 2008. doi:10.1016/j.jaad.2008.10.015
Ultraviolet A sunbeds and vitamin D To the Editor: The current interest in vitamin D, implicating a low vitamin D status in a range of adverse health conditions, including some cancers and autoimmune diseases,1 has been exploited by the cosmetic tanning industry as a positive reason for using sunbeds. For example, the chairman of the Sunbed Association, a trade organization representing sunbed operators, manufacturers, and distributors of sunbeds in the United Kingdom, writes ‘‘A few minutes 2-3 times a week on a sunbed has long been known and recommended by international experts as a viable way of securing and maintaining adequate vitamin D levels.’’2 This claim is not without substance as peerreviewed studies have demonstrated that sunbeds NOVEMBER 2011 1059
J AM ACAD DERMATOL
1060 Letters
NOVEMBER 2011
designed for cosmetic tanning, which emit almost entirely ultraviolet (UV) A radiation, can be effective in raising serum 25-hydroxyvitamin D levels as a result of the small amount of UVB (typically around 1% of the UV emission) present in the lamp spectrum.3,4 So, should UVA sunbeds be condoned or supported as an effective means of addressing what may be perceived as vitamin D insufficiency? An analogy may be helpful in coming to a decision. Suppose a patient comes to you with an ailment and you offer two choices of treatment: a pill that is mildly effective but is associated with appreciable side effects, or another pill that is more effective with a much reduced risk of side effects. The choice that the doctor and/or patient would make is self-evident. Although UVA sunbeds may raise 25-hydroxyvitamin D status, their use is associated with a significantly increased risk of malignant melanoma, especially when use begins in adolescence or early adulthood.5-7 Addressing vitamin D status is a medical problem and patients deserve the best therapy combining high efficacy with minimal risk. Options include systemic medication, dietary supplementation or, when appropriate, phototherapy with UVB radiation, because it is radiation in this waveband, and not the UVA waveband, that is most effective in the cutaneous synthesis of vitamin D.8 UVA sunbeds, much like lipstick, are a cosmetic. They may make you look good but their health benefits are dubious and they should not be promoted to address a medical problem when more effective and safer options are available. Brian Diffey, PhD, DSc
Funding sources: None. Conflicts of interest: None declared. Correspondence to: Brian Diffey, PhD, DSc, Dermatological Sciences, University of Newcastle, Newcastle-upon-Tyne, NE2 4HH, United Kingdom E-mail: [email protected]
REFERENCES 1. Holick MF. Deficiency of sunlight and vitamin D. BMJ 2008;336:1318-9. 2. Chancellor should recommend sunbed sessions to reduce burden on health budgets. Available from: URL:http://www.sunbed association.org.uk/newsstories.php. Accessed September 2, 2011. 3. Thieden E, Jørgensen HL, Jørgensen NR, Philipsen PA, Wulf HC. Sunbed radiation provokes cutaneous vitamin D synthesis in humansea randomized controlled trial. Photochem Photobiol 2008;84:1487-92. 4. Moan J, Lagunova Z, Cicarma E, Aksnes L, Dahlback A, Grant B, et al. Sunbeds as vitamin D sources. Photochem Photobiol 2009;85:1474-9. 5. The International Agency for Research on Cancer Working Group on Artificial Ultraviolet (UV) Light and Skin Cancer. The association of use of sunbeds with cutaneous malignant melanoma and other skin cancers: a systematic review. Int J Cancer 2006;120:1116-22. 6. Lazovich D, Isaksson Vogel R, Berwick M, Weinstock MA, Anderson KE, Warshaw EM. Indoor tanning and risk of melanoma: a case-control study in a highly exposed population. Cancer Epidemiol Biomarkers Prev 2010;19:1557-68. 7. Hery C, Tryggvad ottir L, Sigurdsson T, Olafsd ottir E, Sigurgeirsson B, Jonasson JG, et al. A melanoma epidemic in Iceland: possible influence of sunbed use. Am J Epidemiol 2010; 172:762-7. 8. CIE technical report: action spectrum for the production of previtamin D3 in human skin. CIE 174:2006. Vienna: Commission Internationale de l’Eclairage; 2006.
Dermatological Sciences, University of Newcastle, United Kingdom
CASE Aggressive cutaneous infection with Mycobacterium marinum in two patients receiving antietumor necrosis factor-alfa agents To the Editor: Cutaneous infections with Mycobacterium marinum usually affect people in contact with water or fish, especially from tropical areas. We report two additional cases of unusually aggressive cutaneous infection with M marinum in fish tank owners receiving antietumor necrosis factor-alfa (TNFa) antibodies, underscoring the pitfalls of histologic diagnosis.
doi:10.1016/j.jaad.2011.06.044
LETTERS Case 1, a 41-year-old woman who had received methotrexate and infliximab for psoriatic arthritis over the previous 2 years, developed a rapidly progressive nodular lesion on her right index finger followed by the onset of inflammatory nodules on the right hand and forearm with a sporotrichoid pattern (Fig 1). Because she regularly cleaned a fish tank, infection with M marinum was first considered and confirmed by skin culture and molecular identification using polymerase chain reaction amplification of the 16S23S ribosomal DNA spacer followed by hybridization with specific probes (GenoType Mycobacterium;
& COMMENTS
Written action plans should be comprehensive and evidence-based To the Editor: I certainly applaud work towards the development of a written action plan (WAP) for atopic dermatitis as published by Chisolm et al1 in the Journal. However, the WAP presented by the authors has a number of limitations that suggests that this plan may be appropriate for patients only with mild disease and/or those with infrequent flares. Hydrocortisone, as recommended by the WAP authors for indefinite use, has been found in healthy skin to decrease collagen synthesis by more than 80% within 3 weeks.2 The clinical significance of this decrease in collagen synthesis is not known. Moreover, medium potency corticosteroids—also recommended for long-term use by the authors— decrease skin thickness by at least 6% within 4 weeks.3,4 Therefore, given no time or dosage limitations on the use of these agents, the WAP is a recipe for atrophy in our patients with more significant disease. If these corticosteroids were the only agents available that were ‘‘safe’’ and effective, we would accept the consequences. But when patients require long-term treatment, nonatrophogenic alternatives, such as tacrolimus and pimecrolimus, both of which have no atrophogenicity,3,4 should be part of any evidence-based WAP. The development of a WAP, as with asthma, should be a comprehensive and evidence-based approach. The authors and our patients could benefit from more thorough evaluation of the relative efficacies and toxicities of agents. Guidelines for care, such as those developed by the Primary Care Dermatology Society and the British Association of Dermatologists,5 may serve as excellent additional resources. Alan B. Fleischer, Jr, MD Department of Dermatology, Wake Forest University Health Sciences, Winston-Salem, North Carolina Funding sources: None. Dr Fleischer is a member of the advisory boards of Allergan, Amgen, Astellas, Galderma, GSK, and Stiefel; a consultant for Astellas, Asubio, Combe, Galderma, Gerson Lehrman, Intendis, Kikaku America International, Merz, Novartis, and Serentis; an investigator for 3M, Abbott, Amgen, J AM ACAD DERMATOL
Astellas, Asubio, Biogen, Dow, Centocor, Coria, Galderma, GSK, Genentech, Healthpoint, Intendis, Medicis, Novartis, Ortho-Neutrogena, Pfizer, and Stiefel; and is a member of the speakers bureaus for Amgen, Astellas, Galderma, Intendis, Medicis, Novartis, and Stiefel. Correspondence to: Alan B. Fleischer, Jr, MD, Wake Forest University Health Sciences, Medical Center Blvd, Winston-Salem, NC 27157 E-mail: [email protected] REFERENCES 1. Chisolm SS, Taylor SL, Balkrishnan R, Feldman SR. Written action plans: potential for improving outcomes in children with atopic dermatitis. J Am Acad Dermatol 2008;59: 677-83. 2. Nuutinen P, Riekki R, Parikka M, Salo T, Autio P, Risteli J, et al. Modulation of collagen synthesis and mRNA by continuous and intermittent use of topical hydrocortisone in human skin. Br J Dermatol 2003;148:39-45. 3. Reitamo S, Rissanen J, Remitz A, Granlund H, Erkko P, Elg P, et al. Tacrolimus ointment does not affect collagen synthesis: results of a single-center randomized trial. J Invest Dermatol 1998;111:396-8. 4. Queille-Roussel C, Paul C, Duteil L, Lefebvre MC, Rapatz G, Zagula M, et al. The new topical ascomycin derivative SDZ ASM 981 does not induce skin atrophy when applied to normal skin for 4 weeks: a randomized, double-blind controlled study. Br J Dermatol 2001;144:507-13. 5. Primary Care Dermatology Society website. Primary Care Dermatology & British Association of Dermatologists. Guidelines for the management of atopic eczema. Available at: http://www.pcds.org.uk/images/stories/pcdsbad-eczema.pdf. Accessed October 3, 2008. doi:10.1016/j.jaad.2008.10.015
Ultraviolet A sunbeds and vitamin D To the Editor: The current interest in vitamin D, implicating a low vitamin D status in a range of adverse health conditions, including some cancers and autoimmune diseases,1 has been exploited by the cosmetic tanning industry as a positive reason for using sunbeds. For example, the chairman of the Sunbed Association, a trade organization representing sunbed operators, manufacturers, and distributors of sunbeds in the United Kingdom, writes ‘‘A few minutes 2-3 times a week on a sunbed has long been known and recommended by international experts as a viable way of securing and maintaining adequate vitamin D levels.’’2 This claim is not without substance as peerreviewed studies have demonstrated that sunbeds NOVEMBER 2011 1059
J AM ACAD DERMATOL
1060 Letters
NOVEMBER 2011
designed for cosmetic tanning, which emit almost entirely ultraviolet (UV) A radiation, can be effective in raising serum 25-hydroxyvitamin D levels as a result of the small amount of UVB (typically around 1% of the UV emission) present in the lamp spectrum.3,4 So, should UVA sunbeds be condoned or supported as an effective means of addressing what may be perceived as vitamin D insufficiency? An analogy may be helpful in coming to a decision. Suppose a patient comes to you with an ailment and you offer two choices of treatment: a pill that is mildly effective but is associated with appreciable side effects, or another pill that is more effective with a much reduced risk of side effects. The choice that the doctor and/or patient would make is self-evident. Although UVA sunbeds may raise 25-hydroxyvitamin D status, their use is associated with a significantly increased risk of malignant melanoma, especially when use begins in adolescence or early adulthood.5-7 Addressing vitamin D status is a medical problem and patients deserve the best therapy combining high efficacy with minimal risk. Options include systemic medication, dietary supplementation or, when appropriate, phototherapy with UVB radiation, because it is radiation in this waveband, and not the UVA waveband, that is most effective in the cutaneous synthesis of vitamin D.8 UVA sunbeds, much like lipstick, are a cosmetic. They may make you look good but their health benefits are dubious and they should not be promoted to address a medical problem when more effective and safer options are available. Brian Diffey, PhD, DSc
Funding sources: None. Conflicts of interest: None declared. Correspondence to: Brian Diffey, PhD, DSc, Dermatological Sciences, University of Newcastle, Newcastle-upon-Tyne, NE2 4HH, United Kingdom E-mail: [email protected]
REFERENCES 1. Holick MF. Deficiency of sunlight and vitamin D. BMJ 2008;336:1318-9. 2. Chancellor should recommend sunbed sessions to reduce burden on health budgets. Available from: URL:http://www.sunbed association.org.uk/newsstories.php. Accessed September 2, 2011. 3. Thieden E, Jørgensen HL, Jørgensen NR, Philipsen PA, Wulf HC. Sunbed radiation provokes cutaneous vitamin D synthesis in humansea randomized controlled trial. Photochem Photobiol 2008;84:1487-92. 4. Moan J, Lagunova Z, Cicarma E, Aksnes L, Dahlback A, Grant B, et al. Sunbeds as vitamin D sources. Photochem Photobiol 2009;85:1474-9. 5. The International Agency for Research on Cancer Working Group on Artificial Ultraviolet (UV) Light and Skin Cancer. The association of use of sunbeds with cutaneous malignant melanoma and other skin cancers: a systematic review. Int J Cancer 2006;120:1116-22. 6. Lazovich D, Isaksson Vogel R, Berwick M, Weinstock MA, Anderson KE, Warshaw EM. Indoor tanning and risk of melanoma: a case-control study in a highly exposed population. Cancer Epidemiol Biomarkers Prev 2010;19:1557-68. 7. Hery C, Tryggvad ottir L, Sigurdsson T, Olafsd ottir E, Sigurgeirsson B, Jonasson JG, et al. A melanoma epidemic in Iceland: possible influence of sunbed use. Am J Epidemiol 2010; 172:762-7. 8. CIE technical report: action spectrum for the production of previtamin D3 in human skin. CIE 174:2006. Vienna: Commission Internationale de l’Eclairage; 2006.
Dermatological Sciences, University of Newcastle, United Kingdom
CASE Aggressive cutaneous infection with Mycobacterium marinum in two patients receiving antietumor necrosis factor-alfa agents To the Editor: Cutaneous infections with Mycobacterium marinum usually affect people in contact with water or fish, especially from tropical areas. We report two additional cases of unusually aggressive cutaneous infection with M marinum in fish tank owners receiving antietumor necrosis factor-alfa (TNFa) antibodies, underscoring the pitfalls of histologic diagnosis.
doi:10.1016/j.jaad.2011.06.044
LETTERS Case 1, a 41-year-old woman who had received methotrexate and infliximab for psoriatic arthritis over the previous 2 years, developed a rapidly progressive nodular lesion on her right index finger followed by the onset of inflammatory nodules on the right hand and forearm with a sporotrichoid pattern (Fig 1). Because she regularly cleaned a fish tank, infection with M marinum was first considered and confirmed by skin culture and molecular identification using polymerase chain reaction amplification of the 16S23S ribosomal DNA spacer followed by hybridization with specific probes (GenoType Mycobacterium;