J AM ACAD DERMATOL
586 Letters
MARCH 2014
Funding sources: None. Disclosures: Dr Kishi has received honoraria for participation in advisory boards for Pharma International Inc and for being a speaker for Chugai, Mitsubishi Tanabe Pharma, and Sato. Dr Hayashi has been a consultant for Eisai, Galderma, and Maruho, and a speaker for Candela, Daiichi-Sankyo, Dainihon-Sumitomo, Galderma, GlaxoSmithKline. JMEC, Maruho, Pola Pharmacy, Sato, Shionogi, Tokiwa, and Torii, and has received research grants from Daiichi-Sankyo, Galderma, Maruho, Shionogi, and Mitsubishi-Tanabe Pharma. Mr Aoki and Mr Yamada have been employees of Mitsubishi Tanabe Pharma. Dr Kumada has been a speaker for MSD, Mitsubishi Tanabe Pharma. Correspondence to: Akiko Kishi, MD, Department of Dermatology, Toranomon Hospital, 2-2-2 Toranomon, Minato-ku, Tokyo 105-8470, Japan E-mail: [email protected] REFERENCES 1. Jacobson IM, McHutchison JG, Dusheiko G, Di Bisceglie AM, Reddy KR, Bzowej NH, et al. Telaprevir for previously untreated chronic hepatitis C virus infection. N Engl J Med 2011;364: 2405-16. 2. Kumada H, Toyota J, Okanoue T, Chayama K, Tsubouchi H, Hayashi N. Telaprevir with peginterferon and ribavirin for treatment-naive patients chronically infected with HCV of genotype 1 in Japan. J Hepatol 2012;56:78-84. 3. Torii H, Sueki H, Kumada H, Sakurai Y, Aoki K, Yamada I, et al. Dermatological side-effects of telaprevir-based triple therapy for chronic hepatitis C in phase III trials in Japan. J Dermatol 2013;40:587-95. 4. Montaudie H, Passeron T, Cardot-Leccia N, Sebbag N, Lacour JP. Drug rash with eosinophilia and systemic symptoms due to telaprevir. Dermatology 2010;221:303-5. http://dx.doi.org/10.1016/j.jaad.2013.11.003
The diagnostic challenge of vulvar squamous cell carcinoma: Clinical manifestations and unusual human papillomavirus types To the Editor: Treatment for early stage vulvar cancer lesions is readily available with limited morbidity; advanced stages of the disease, however, require interventions with serious morbidity. We sought to characterize clinical presentation of vulvar carcinoma to better understand reasons for delayed diagnosis and to determine which human papillomavirus (HPV) subtypes are causative. Twenty-three cases of invasive vulvar squamous cell carcinoma (SCC) were identified using the pathology databases at the University of Pennsylvania. DNA was extracted from formalin-fixed paraffin embedded samples. HPV-PCR products were
Table I. Demographic and lesion characteristics Age at diagnosis (median, IQR) Smoking status (n, %) Never smoker Past smoker Current smoker Smoking status unknown Medical history (n, %) History of HIV infection History of genital warts History of diabetes History of inflammatory bowel disease History of organ transplant History of other cancer History of autoimmune disease History of eczema History of prior systemic treatments (n, %) Yes None/unknown History of topical treatments to vulvar area (n, %) Yes None/unknown History of abnormal Paps (n, %) Yes None/unknown History of concurrent or previous vulvar dermatoses diagnosed clinically (n, %) Yes None/unknown Previous vulvar symptoms (n, %) Yes None/unknown Lesion size in cm (median, IQR)* Type of provider who first evaluated patient (N) Ob/gyn Other Time from initial presentation in medical system to biopsy in months (Median, IQR)y
61
(43-76)
8 6 7 2
35% 26% 31% 9%
3 6 5 0
21% 27% 22% 0%
2 4 0 1
9% 17% 0% 4%
3 20
14% 86%
8 15
35% 65%
8 15
35% 65%
4 19
83% 17%
17 6
74% 26%
18 5 1
78% 22% (0-2)
IQR, Interquartile range. *Data available for 15 of 23 specimens. y One day to 1 month rounded up to 1 month.
detected with PGMY-GP1-primer system. HPV-PCR products were then cloned and sequenced. NCBI-BLAST analysis revealed the presence of different HPV types.1 Clinical data were extracted from the medical record (Table I). Studies have shown that vulvar cancer patients often have lengthy medical contact and treatment for vulvar symptoms prior to diagnosis.2,3 Most patients in our study (74%) were aware of vulvar symptoms
J AM ACAD DERMATOL
Letters 587
VOLUME 70, NUMBER 3
Table II. Associations with HPV type HPV type Positive Negative Demographic characteristic
Age at diagnosis (median)* Past or current smoker History of genital warts History of immunosuppressiony History of prior systemic treatments History of topical treatments to vulvar area History of abnormal Pap smear History of concurrent or previous vulvar dermatoses diagnosed clinically Previous vulvar symptoms Lesion size in cm (median)* Time from initial presentation in medical system to biopsy in months (median)*
N = 13
N=4
P-value
59 10 4 6 2
67 1 0 2 1
1 1
5
1
1
4 3
1 1
1 1
10 1.5 1
2 1.65 2
.428 .099 .529
.538 .831 .64
P-values for Fisher exact test unless otherwise noted. *Kruskal-Wallis equality of populations rank test. DNA quality assessment by beta-globin reference gene PCR of the DNAs extracted from the sections. Six samples were negative and were excluded from the HPV testing, leaving 17 total cases reported. y Patients with a known history of diabetes mellitus, organ transplant, or HIV.
(itching, bleeding, discharge), lesions, or both. Documented exam descriptors used for the vulvar cancers included ‘‘exophytic,’’ ‘‘plaque,’’ ‘‘fungating,’’ ‘‘white,’’ ‘‘raised,’’ ‘‘thickened,’’ and ‘‘erythematous.’’ With these variable presentations, vulvar cancer can mimic conditions including lichen sclerosus, contact dermatitis, warts, and other inflammatory or benign neoplastic conditions. The mean time from initial presentation to biopsy revealing invasive SCC was 3.6 months. Prior studies show delays from 6 months to 5 years between first reported symptoms and diagnosis.2 Our findings highlight the need for providers to maintain a low threshold for biopsy to rule out malignant disease in any long-standing vulvar lesion or ‘‘rash.’’ Clinicians should also be aware of the 2 pathways for development of vulvar SCC. The first is HPV-induced, ‘‘usual type’’ vulvar SCC, which occurs in younger women. Two thirds (68.8%) of invasive vulvar cancers diagnosed are usual-type caused by HPV.3 The second pathway occurs predominantly in older patients, independent of HPV infection, often in association with chronic inflammation of the vulva (including lichen sclerosus).4 Usual type vulvar SCC is caused by high-risk HPV types such as 16, 18, and 33. In our study,
75% of cases were HPV positive. We noted a greater likelihood of HPV positivity among past and current smokers (P \ .10) (Table II). The most common subtype was HPV 16 (8 samples). HPV 18, 45, and 53 were each detected in one sample. Two samples tested positive for HPV 120, a recently characterized novel -PV related most closely to HPV-23.5 The finding of HPV 120 in 3 vulvar cancer specimens is intriguing as it is a relatively newly described HPV genotype. HPV 120 has been described to have multiple anatomic niches, including oral, vulvar, penile, and anal mucosa. However, the pathologic consequences of HPV 120 infection remain unclear.5 Vulvar SCC can have varied clinical presentations leading to significant diagnostic delay. Providers should include carcinoma in their differential of vulvar dermatoses and maintain a low threshold for conducting biopsy. In our study, 76% of samples were positive for high-risk HPV, some with unusual subtypes (eg, HPV 120), suggesting that currently available vaccines may not entirely eliminate the risk for vulvar cancers. Aditi Sagdeo, MD,a Rachel H. Gormley, MD,b Katrina Abuabara, MD, MA,b Stephen K. Tyring, MD, PhD,d Peter Rady, MD, PhD,d David E. Elder, MBchB,c and Carrie L. Kovarik, MDb Perelman School of Medicine at the University of Pennsylvania,a Department of Dermatologyb and Department of Pathology and Laboratory Medicine,c University of Pennsylvania, Philadelphia; Department of Dermatology,d The University of Texas Medical School at Houston, Houston, Texas Funding sources: None. Conflicts of interest: None declared. Correspondence to: Carrie L. Kovarik, MD, Department of Dermatology, 2 Maloney, Hospital of the University of Pennsylvania, Philadelphia, PA 19104 E-mail: [email protected] REFERENCES 1. Fuessel Haws AL, He Q, Rady PL, Zhang L, Grady J, Hughes TK, et al. Nested PCR with the PGMY09/11 and GP5(1)/6(1) primer sets improves detection of HPV DNA in cervical samples. J Virol Methods 2004;122:87-93. 2. Jones RW, Joura EA. Analyzing prior clinical events at presentation in 102 women with vulvar carcinoma. Evidence of diagnostic delays. J Reprod Med 1999;44:766-8. 3. Gargano JW, Wilkinson EJ, Unger ER, Steinau M, Watson M, Huang Y, et al. Prevalence of human papillomavirus types in invasive vulvar cancers and vulvar intraepithelial neoplasia 3 in
J AM ACAD DERMATOL
588 Letters
MARCH 2014
the United States before vaccine introduction. J Low Genit Tract Dis 2012;16:471-9. 4. van der Avoort IA, Shirango H, Hoevenaars BM, Grefte JM, de Hullu JA, de Wilde PC, et al. Vulvar squamous cell carcinoma is a multifactorial disease following two separate and independent pathways. Int J Gynecol Pathol 2006;25:22-9. 5. Bottalico D, Chen Z, Kocjan BJ, Seme K, Poljak M, Burk RD. Characterization of human papillomavirus type 120: a novel betapapillomavirus with tropism for multiple anatomical niches. J Gen Virol 2012;93:1774-9.
We chose the S-RAPI given the similarities between problematic tanning and other addictions,1,2 and the strong psychometric properties of the S-RAPI among university students.4 The Tanning Problems Index (TPI) included 11 items characterizing potential problems associated with past-year tanning (Table I includes items, scale anchors, and response distributions). We removed 5 of the S-RAPI’s 16 items because they were irrelevant to tanning (see Table I footnote). Following Institutional Review Board approval, 414 students from a large Midwestern university who reported indoor/outdoor tanning were administered online questionnaires (Table II). The TPI showed good internal consistency ( ¼ .86). Overall, we found that 9% to 29% of students across items (Table I) reported a problem at least once in the past year. In support of construct validity, those screening positive for tanning dependence on the Tanning-DSM (M ¼ 5.6, SD ¼ 5.6) had significantly higher TPI scores than those screening negative (M ¼ 1.4, SD ¼ 2.9), t(412) ¼ 9.92, P \ .001. In support of criterion validity, higher TPI scores were associated with more frequent past-month tanning, r(412) ¼ .36, P \.001, more money spent on tanning r(409) ¼ .41, P \ .001, greater perceived difficulty to stop tanning, r(410) ¼ .55, P \.001, and less frequent use of sunscreen, r(410) ¼ .15, P ¼ .003. In a linear regression analysis with past-month tanning
http://dx.doi.org/10.1016/j.jaad.2013.11.027
Development of a brief scale to assess frequency of symptoms and problems associated with tanning See related articles on pages 473 and 562 To the Editor: Some university students are at risk to display tanning behaviors analogous to drug use behaviors (eg, continuing to tan despite negative consequences, tanning beyond what is necessary to achieve their desired appearance).1,2 Screeners1,2 and structured interviews3 help identify those who may be dependent on tanning. Additionally, researchers and clinicians may find useful a measure that assesses frequency of symptoms and psychosocial consequences of tanning. We assessed the psychometric properties of a tanning adaptation of the Short-Rutgers Alcohol Problem Index (S-RAPI).4
Table I. N (%) by response option to items in the Tanning Problems Index Response options reflecting past-year frequency of problems (N = 414) Items
1. Not able to do your homework or study for a test 2. Got into fights with other people (friends, relatives, strangers) 3. Neglected your responsibilities 4. Felt that you needed to tan more than you used to in order to get the same effect 5. Tried to control your tanning (tried to tan less often) 6. Had withdrawal symptoms, i.e., felt sick because you stopped or cut down on tanning 7. Felt that you had a problem with tanning 8. Missed a day or part of a day of school or work 9. Wanted to stop tanning but couldn’t 10. Felt physically or psychologically dependent on tanning 11. Was told by a friend, neighbor, or relative to stop or cut down tanning
0 times
1-2 times
3-5 times
6-9 times
101 times
333 (80%) 352 (85%)
55 (13%) 47 (11%)
17 (4%) 9 (2%)
5 (1%) 4 (1%)
4 (1%) 2 (1%)
288 (70%) 295 (71%)
96 (23%) 72 (17%)
23 (6%) 37 (9%)
3 (1%) 5 (1%)
4 (1%) 5 (1%)
313 (76%) 376 (91%)
67 (16%) 27 (7%)
22 (5%) 7 (2%)
9 (2%) 1 (\1%)
3 (1%) 3 (1%)
362 357 374 357
31 34 29 33
14 16 8 18
7 5 2 3
0 2 1 3
(87%) (86%) (90%) (86%)
322 (78%)
(8%) (8%) (7%) (8%)
54 (13%)
(3%) (4%) (2%) (4%)
32 (8%)
(2%) (2%) (1%) (1%)
4 (1%)
(0%) (1%) (\1%) (1%)
2 (1%)
Values may not add to 100% due to rounding. The following items were removed from the Short-Rutgers Alcohol Problems Index: ‘‘Caused shame or embarrassment to someone,’’ ‘‘Relatives avoided you,’’ ‘‘Suddenly found yourself in a place that you could not remember getting to,’’ ‘‘Felt like you were going crazy,’’ ‘‘Had a bad time.’’ Directions used in our examination of the Tanning Problems Index: ‘‘How many times did the following things happen to you while you were tanning or because of your tanning during the last year?’’
586 Letters
MARCH 2014
Funding sources: None. Disclosures: Dr Kishi has received honoraria for participation in advisory boards for Pharma International Inc and for being a speaker for Chugai, Mitsubishi Tanabe Pharma, and Sato. Dr Hayashi has been a consultant for Eisai, Galderma, and Maruho, and a speaker for Candela, Daiichi-Sankyo, Dainihon-Sumitomo, Galderma, GlaxoSmithKline. JMEC, Maruho, Pola Pharmacy, Sato, Shionogi, Tokiwa, and Torii, and has received research grants from Daiichi-Sankyo, Galderma, Maruho, Shionogi, and Mitsubishi-Tanabe Pharma. Mr Aoki and Mr Yamada have been employees of Mitsubishi Tanabe Pharma. Dr Kumada has been a speaker for MSD, Mitsubishi Tanabe Pharma. Correspondence to: Akiko Kishi, MD, Department of Dermatology, Toranomon Hospital, 2-2-2 Toranomon, Minato-ku, Tokyo 105-8470, Japan E-mail: [email protected] REFERENCES 1. Jacobson IM, McHutchison JG, Dusheiko G, Di Bisceglie AM, Reddy KR, Bzowej NH, et al. Telaprevir for previously untreated chronic hepatitis C virus infection. N Engl J Med 2011;364: 2405-16. 2. Kumada H, Toyota J, Okanoue T, Chayama K, Tsubouchi H, Hayashi N. Telaprevir with peginterferon and ribavirin for treatment-naive patients chronically infected with HCV of genotype 1 in Japan. J Hepatol 2012;56:78-84. 3. Torii H, Sueki H, Kumada H, Sakurai Y, Aoki K, Yamada I, et al. Dermatological side-effects of telaprevir-based triple therapy for chronic hepatitis C in phase III trials in Japan. J Dermatol 2013;40:587-95. 4. Montaudie H, Passeron T, Cardot-Leccia N, Sebbag N, Lacour JP. Drug rash with eosinophilia and systemic symptoms due to telaprevir. Dermatology 2010;221:303-5. http://dx.doi.org/10.1016/j.jaad.2013.11.003
The diagnostic challenge of vulvar squamous cell carcinoma: Clinical manifestations and unusual human papillomavirus types To the Editor: Treatment for early stage vulvar cancer lesions is readily available with limited morbidity; advanced stages of the disease, however, require interventions with serious morbidity. We sought to characterize clinical presentation of vulvar carcinoma to better understand reasons for delayed diagnosis and to determine which human papillomavirus (HPV) subtypes are causative. Twenty-three cases of invasive vulvar squamous cell carcinoma (SCC) were identified using the pathology databases at the University of Pennsylvania. DNA was extracted from formalin-fixed paraffin embedded samples. HPV-PCR products were
Table I. Demographic and lesion characteristics Age at diagnosis (median, IQR) Smoking status (n, %) Never smoker Past smoker Current smoker Smoking status unknown Medical history (n, %) History of HIV infection History of genital warts History of diabetes History of inflammatory bowel disease History of organ transplant History of other cancer History of autoimmune disease History of eczema History of prior systemic treatments (n, %) Yes None/unknown History of topical treatments to vulvar area (n, %) Yes None/unknown History of abnormal Paps (n, %) Yes None/unknown History of concurrent or previous vulvar dermatoses diagnosed clinically (n, %) Yes None/unknown Previous vulvar symptoms (n, %) Yes None/unknown Lesion size in cm (median, IQR)* Type of provider who first evaluated patient (N) Ob/gyn Other Time from initial presentation in medical system to biopsy in months (Median, IQR)y
61
(43-76)
8 6 7 2
35% 26% 31% 9%
3 6 5 0
21% 27% 22% 0%
2 4 0 1
9% 17% 0% 4%
3 20
14% 86%
8 15
35% 65%
8 15
35% 65%
4 19
83% 17%
17 6
74% 26%
18 5 1
78% 22% (0-2)
IQR, Interquartile range. *Data available for 15 of 23 specimens. y One day to 1 month rounded up to 1 month.
detected with PGMY-GP1-primer system. HPV-PCR products were then cloned and sequenced. NCBI-BLAST analysis revealed the presence of different HPV types.1 Clinical data were extracted from the medical record (Table I). Studies have shown that vulvar cancer patients often have lengthy medical contact and treatment for vulvar symptoms prior to diagnosis.2,3 Most patients in our study (74%) were aware of vulvar symptoms
J AM ACAD DERMATOL
Letters 587
VOLUME 70, NUMBER 3
Table II. Associations with HPV type HPV type Positive Negative Demographic characteristic
Age at diagnosis (median)* Past or current smoker History of genital warts History of immunosuppressiony History of prior systemic treatments History of topical treatments to vulvar area History of abnormal Pap smear History of concurrent or previous vulvar dermatoses diagnosed clinically Previous vulvar symptoms Lesion size in cm (median)* Time from initial presentation in medical system to biopsy in months (median)*
N = 13
N=4
P-value
59 10 4 6 2
67 1 0 2 1
1 1
5
1
1
4 3
1 1
1 1
10 1.5 1
2 1.65 2
.428 .099 .529
.538 .831 .64
P-values for Fisher exact test unless otherwise noted. *Kruskal-Wallis equality of populations rank test. DNA quality assessment by beta-globin reference gene PCR of the DNAs extracted from the sections. Six samples were negative and were excluded from the HPV testing, leaving 17 total cases reported. y Patients with a known history of diabetes mellitus, organ transplant, or HIV.
(itching, bleeding, discharge), lesions, or both. Documented exam descriptors used for the vulvar cancers included ‘‘exophytic,’’ ‘‘plaque,’’ ‘‘fungating,’’ ‘‘white,’’ ‘‘raised,’’ ‘‘thickened,’’ and ‘‘erythematous.’’ With these variable presentations, vulvar cancer can mimic conditions including lichen sclerosus, contact dermatitis, warts, and other inflammatory or benign neoplastic conditions. The mean time from initial presentation to biopsy revealing invasive SCC was 3.6 months. Prior studies show delays from 6 months to 5 years between first reported symptoms and diagnosis.2 Our findings highlight the need for providers to maintain a low threshold for biopsy to rule out malignant disease in any long-standing vulvar lesion or ‘‘rash.’’ Clinicians should also be aware of the 2 pathways for development of vulvar SCC. The first is HPV-induced, ‘‘usual type’’ vulvar SCC, which occurs in younger women. Two thirds (68.8%) of invasive vulvar cancers diagnosed are usual-type caused by HPV.3 The second pathway occurs predominantly in older patients, independent of HPV infection, often in association with chronic inflammation of the vulva (including lichen sclerosus).4 Usual type vulvar SCC is caused by high-risk HPV types such as 16, 18, and 33. In our study,
75% of cases were HPV positive. We noted a greater likelihood of HPV positivity among past and current smokers (P \ .10) (Table II). The most common subtype was HPV 16 (8 samples). HPV 18, 45, and 53 were each detected in one sample. Two samples tested positive for HPV 120, a recently characterized novel -PV related most closely to HPV-23.5 The finding of HPV 120 in 3 vulvar cancer specimens is intriguing as it is a relatively newly described HPV genotype. HPV 120 has been described to have multiple anatomic niches, including oral, vulvar, penile, and anal mucosa. However, the pathologic consequences of HPV 120 infection remain unclear.5 Vulvar SCC can have varied clinical presentations leading to significant diagnostic delay. Providers should include carcinoma in their differential of vulvar dermatoses and maintain a low threshold for conducting biopsy. In our study, 76% of samples were positive for high-risk HPV, some with unusual subtypes (eg, HPV 120), suggesting that currently available vaccines may not entirely eliminate the risk for vulvar cancers. Aditi Sagdeo, MD,a Rachel H. Gormley, MD,b Katrina Abuabara, MD, MA,b Stephen K. Tyring, MD, PhD,d Peter Rady, MD, PhD,d David E. Elder, MBchB,c and Carrie L. Kovarik, MDb Perelman School of Medicine at the University of Pennsylvania,a Department of Dermatologyb and Department of Pathology and Laboratory Medicine,c University of Pennsylvania, Philadelphia; Department of Dermatology,d The University of Texas Medical School at Houston, Houston, Texas Funding sources: None. Conflicts of interest: None declared. Correspondence to: Carrie L. Kovarik, MD, Department of Dermatology, 2 Maloney, Hospital of the University of Pennsylvania, Philadelphia, PA 19104 E-mail: [email protected] REFERENCES 1. Fuessel Haws AL, He Q, Rady PL, Zhang L, Grady J, Hughes TK, et al. Nested PCR with the PGMY09/11 and GP5(1)/6(1) primer sets improves detection of HPV DNA in cervical samples. J Virol Methods 2004;122:87-93. 2. Jones RW, Joura EA. Analyzing prior clinical events at presentation in 102 women with vulvar carcinoma. Evidence of diagnostic delays. J Reprod Med 1999;44:766-8. 3. Gargano JW, Wilkinson EJ, Unger ER, Steinau M, Watson M, Huang Y, et al. Prevalence of human papillomavirus types in invasive vulvar cancers and vulvar intraepithelial neoplasia 3 in
J AM ACAD DERMATOL
588 Letters
MARCH 2014
the United States before vaccine introduction. J Low Genit Tract Dis 2012;16:471-9. 4. van der Avoort IA, Shirango H, Hoevenaars BM, Grefte JM, de Hullu JA, de Wilde PC, et al. Vulvar squamous cell carcinoma is a multifactorial disease following two separate and independent pathways. Int J Gynecol Pathol 2006;25:22-9. 5. Bottalico D, Chen Z, Kocjan BJ, Seme K, Poljak M, Burk RD. Characterization of human papillomavirus type 120: a novel betapapillomavirus with tropism for multiple anatomical niches. J Gen Virol 2012;93:1774-9.
We chose the S-RAPI given the similarities between problematic tanning and other addictions,1,2 and the strong psychometric properties of the S-RAPI among university students.4 The Tanning Problems Index (TPI) included 11 items characterizing potential problems associated with past-year tanning (Table I includes items, scale anchors, and response distributions). We removed 5 of the S-RAPI’s 16 items because they were irrelevant to tanning (see Table I footnote). Following Institutional Review Board approval, 414 students from a large Midwestern university who reported indoor/outdoor tanning were administered online questionnaires (Table II). The TPI showed good internal consistency ( ¼ .86). Overall, we found that 9% to 29% of students across items (Table I) reported a problem at least once in the past year. In support of construct validity, those screening positive for tanning dependence on the Tanning-DSM (M ¼ 5.6, SD ¼ 5.6) had significantly higher TPI scores than those screening negative (M ¼ 1.4, SD ¼ 2.9), t(412) ¼ 9.92, P \ .001. In support of criterion validity, higher TPI scores were associated with more frequent past-month tanning, r(412) ¼ .36, P \.001, more money spent on tanning r(409) ¼ .41, P \ .001, greater perceived difficulty to stop tanning, r(410) ¼ .55, P \.001, and less frequent use of sunscreen, r(410) ¼ .15, P ¼ .003. In a linear regression analysis with past-month tanning
http://dx.doi.org/10.1016/j.jaad.2013.11.027
Development of a brief scale to assess frequency of symptoms and problems associated with tanning See related articles on pages 473 and 562 To the Editor: Some university students are at risk to display tanning behaviors analogous to drug use behaviors (eg, continuing to tan despite negative consequences, tanning beyond what is necessary to achieve their desired appearance).1,2 Screeners1,2 and structured interviews3 help identify those who may be dependent on tanning. Additionally, researchers and clinicians may find useful a measure that assesses frequency of symptoms and psychosocial consequences of tanning. We assessed the psychometric properties of a tanning adaptation of the Short-Rutgers Alcohol Problem Index (S-RAPI).4
Table I. N (%) by response option to items in the Tanning Problems Index Response options reflecting past-year frequency of problems (N = 414) Items
1. Not able to do your homework or study for a test 2. Got into fights with other people (friends, relatives, strangers) 3. Neglected your responsibilities 4. Felt that you needed to tan more than you used to in order to get the same effect 5. Tried to control your tanning (tried to tan less often) 6. Had withdrawal symptoms, i.e., felt sick because you stopped or cut down on tanning 7. Felt that you had a problem with tanning 8. Missed a day or part of a day of school or work 9. Wanted to stop tanning but couldn’t 10. Felt physically or psychologically dependent on tanning 11. Was told by a friend, neighbor, or relative to stop or cut down tanning
0 times
1-2 times
3-5 times
6-9 times
101 times
333 (80%) 352 (85%)
55 (13%) 47 (11%)
17 (4%) 9 (2%)
5 (1%) 4 (1%)
4 (1%) 2 (1%)
288 (70%) 295 (71%)
96 (23%) 72 (17%)
23 (6%) 37 (9%)
3 (1%) 5 (1%)
4 (1%) 5 (1%)
313 (76%) 376 (91%)
67 (16%) 27 (7%)
22 (5%) 7 (2%)
9 (2%) 1 (\1%)
3 (1%) 3 (1%)
362 357 374 357
31 34 29 33
14 16 8 18
7 5 2 3
0 2 1 3
(87%) (86%) (90%) (86%)
322 (78%)
(8%) (8%) (7%) (8%)
54 (13%)
(3%) (4%) (2%) (4%)
32 (8%)
(2%) (2%) (1%) (1%)
4 (1%)
(0%) (1%) (\1%) (1%)
2 (1%)
Values may not add to 100% due to rounding. The following items were removed from the Short-Rutgers Alcohol Problems Index: ‘‘Caused shame or embarrassment to someone,’’ ‘‘Relatives avoided you,’’ ‘‘Suddenly found yourself in a place that you could not remember getting to,’’ ‘‘Felt like you were going crazy,’’ ‘‘Had a bad time.’’ Directions used in our examination of the Tanning Problems Index: ‘‘How many times did the following things happen to you while you were tanning or because of your tanning during the last year?’’
