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Figure 1.
Adjusted odds ratios for solar keratosis by hair color comparing psoriatic patients and controls.

Adjusted odds ratios for solar keratosis by hair color comparing psoriatic patients and controls.

Figure 2.
Adjusted odds ratios for solarkeratosis by propensity to sunburn comparing psoriatic patients and controls.

Adjusted odds ratios for solarkeratosis by propensity to sunburn comparing psoriatic patients and controls.

Table 1. 
Prevalence of Actinic Keratoses Among Patients With Psoriasisand Controls by Sociodemographic Factors
Prevalence of Actinic Keratoses Among Patients With Psoriasisand Controls by Sociodemographic Factors
Table 2. 
Distribution of Actinic Keratoses Among Patients With Psoriasisand Controls
Distribution of Actinic Keratoses Among Patients With Psoriasisand Controls
Table 3. 
Prevalence of Any Solar Keratosis Among Patients With Psoriasisand Controls by Personal Characteristics and Sun Exposure
Prevalence of Any Solar Keratosis Among Patients With Psoriasisand Controls by Personal Characteristics and Sun Exposure
Table 4. 
Logistic Regression Analysis of the Relationship Between Solar Keratosis, Personal Characteristics, Psoriasis, and Interactions
Logistic Regression Analysis of the Relationship Between Solar Keratosis, Personal Characteristics, Psoriasis, and Interactions
1.
Armstrong  BKKricker  A The epidemiology of UV-induced skin cancer J Photochem Photobiol B. 2001;638- 18
PubMedArticle
2.
Vitasa  BCTaylor  HRStrickland  PT  et al.  Association of nonmelanoma skin cancer and actinic keratosis with cumulative solar ultraviolet exposure in Maryland watermen Cancer. 1990;652811- 2817
PubMedArticle
3.
Hogan  DJTo  TGran  LWong  DLane  PR Risk factors for basal cell carcinoma Int J Dermatol. 1989;28591- 594
PubMedArticle
4.
Christophers  E Psoriasis: epidemiology and clinical spectrum Clin Exp Dermatol. 2001;26314- 320
PubMedArticle
5.
Raychaudhuri  SPFarber  EM. The prevalence of psoriasis in the world J Eur Acad Dermatol Venereol. 2001;1520- 23
PubMedArticle
6.
Parks  BSYoun  JI Factors influencing psoriasis: an analysis based upon the extent of involvement and clinical type J Dermatol. 1998;2597- 102
PubMed
7.
Farber  EMBright  RDNall  ML Psoriasis: a questionnaire survey of 2,144 patients Arch Dermatol. 1968;98248- 259
PubMedArticle
8.
Mali-Gerrits  MGHGaasbeek  DBoezeman  JVan de Kerkhof  PCM Psoriasis therapy and the risk of skin cancers Clin Exp Dermatol. 1991;1685- 89
PubMedArticle
9.
Hannuksela-Svahn  APukkala  ELaara  EPoikolainen  KKarvonen  J Psoriasis, its treatment, and cancer in a cohort of Finnish patients J Invest Dermatol. 2000;114587- 590
PubMedArticle
10.
Eskelinen  AHalme  KLasus  AIdanpaan-Heikkila  J Risk of cutaneous carcinoma in psoriatic patients treated with PUVA Photodermatology. 1985;210- 14
PubMed
11.
Stern  RSLiebman  EJVakeva  L Oral psoralen and ultraviolet-A light (PUVA) treatment of psoriasisand persistent risk of nonmelanoma skin cancer: PUVA follow-up study J Natl Cancer Inst. 1998;901278- 1284
PubMedArticle
12.
Frentz  GOlsen  JHAvrach  WW Malignant tumours and psoriasis: climatotherapy at the Dead Sea Br J Dermatol. 1999;1411088- 1091
PubMedArticle
13.
Pasker-de Jong  PWielink  Gvan der Valk  Pvan der Wilt  GJ Treatment with UV-B for psoriasis and nonmelanoma skin cancer: a systematic review of the literature Arch Dermatol. 1999;135834- 840
PubMedArticle
14.
Chuang  TYHeinrich  LASchultz  MDReizner  GTKumm  RCCripps  DJ PUVA and skin cancer: a historical cohort study on 492 patients J Am Acad Dermatol. 1992;26173- 177
PubMedArticle
15.
Marks  RRennie  GSelwood  T The relationship of basal cell carcinomas and squamous cell carcinomas to solar keratoses Arch Dermatol. 1988;1241039- 1042
PubMedArticle
16.
Salasche  SJ Epidemiology of actinic keratoses and squamous cell carcinoma J Am Acad Dermatol. 2000;424- 7
PubMedArticle
17.
Kennedy  CBajdik  CDWillemze  RDe Gruijl  FRBouwes Bavinck  JNLeiden Skin Cancer Study, The influence of painful sunburns and lifetime sun exposure on the risk of actinic keratoses, seborrheic warts, melanocytic nevi, atypical nevi,and skin cancer J Invest Dermatol. 2003;1201087- 1093
PubMedArticle
18.
Kocsard  E Solar keratoses and their relationship to non-melanoma skin cancers Australas J Dermatol. 1997;38(suppl 1)S30
PubMedArticle
19.
Ackerman  BA Opposing views of 2 academies about the nature of solar keratosis Cutis. 2003;71391- 395
PubMed
20.
Fu  WCockerell  CJ The actinic (solar) keratosis: a 21st-century perspective Arch Dermatol. 2003;13966- 70
PubMedArticle
21.
Weinstock  MA Assessment of sun sensitivity by questionnaire: validity of items and formulation of a prediction rule J Clin Epidemiol. 1992;45547- 552
PubMedArticle
22.
Stern  RSMomtaz  K Skin typing for assessment of skin cancer risk and acute response to UV-B and oral methoxsalen photochemotherapy Arch Dermatol. 1984;120869- 873
PubMedArticle
23.
Stern  RSScotto  JFears  TR Psoriasis and susceptibility to nonmelanoma skin cancer J Am Acad Dermatol. 1985;1267- 73
PubMedArticle
24.
Stern  RZierler  SParrish  JA Psoriasis and the risk of cancer J Invest Dermatol. 1982;78147- 149
PubMedArticle
25.
Olsen  JHMoller  HFrentz  G Malignant tumors in patients with psoriasis J Am Acad Dermatol. 1992;27716- 722
PubMedArticle
26.
Margolis  DBilker  WHennessy  SVittorio  CSantanna  JStrom  BL The risk of malignancy associated with psoriasis Arch Dermatol. 2001;137778- 783
PubMed
27.
Henseler  TChristophers  E Disease concomitance in psoriasis J Am Acad Dermatol. 1995;32982- 986
PubMedArticle
28.
Kocsard  E The rarity of actinic keratoses in patients with psoriasis Z Hautkr. 1977;5255- 56
PubMed
29.
Henseler  T The genetics of psoriasis J Am Acad Dermatol. 1997;37S1- S11
PubMedArticle
30.
Zhao  PZhu  XLiu  YWang  BWang  CBurns  FJ Solar ultraviolet radiation and skin damage: an epidemiological study among a Chinese population Arch Environ Health. 1998;53405- 409
PubMedArticle
31.
Westphal  HJWurdel  CFlegel  H Actinic keratoses: sequelae of long-term PUVA therapy Dermatol Monatsschr. 1989;175623- 627
PubMed
32.
Carless  MALea  RACurran  JE  et al.  The GSTM1 null genotype confers an increased risk for solar keratosisdevelopment in an Australian caucasian population J Invest Dermatol. 2002;1191373- 1378
PubMedArticle
33.
Richter-Hintz  DTheir  RSteinwachs  S  et al.  Allelic variants of drug metabolizing enzymes as risk factors in psoriasis J Invest Dermatol. 2003;120765- 770
PubMedArticle
34.
Møller  PWallin  HDybdahl  MFrentz  GNexo  BA Psoriasis patients with basal cell carcinoma have more repair-mediated DNA strand-breaks after UVC damage in lymphocytes than psoriasis patientswithout basal cell carcinoma Cancer Lett. 2000;151187- 192
PubMedArticle
35.
Dybdahl  MFrentz  GVogel  UWallin  HNexo  BA Low DNA repair is a risk factor in skin carcinogenesis: a study of basal cell carcinoma in psoriasis patients Mutat Res. 1999;43315- 22
PubMedArticle
36.
Nickoloff  BJ Creation of psoriatic plaques: the ultimate tumor suppressor pathway J Cutan Pathol. 2001;2857- 64
PubMedArticle
Study
July 2004

Are Patients With Psoriasis Susceptible to the Classic Risk Factors for Actinic Keratoses?

Author Affiliations

From the School of Public Health (Dr Paltiel and Ms Adler) and the Department of Hematology (Dr Paltiel), Hadassah-Hebrew University MedicalCenter, Jerusalem, Israel; and the Departments of Dermatology, Hadassah-Hebrew University Medical Center (Dr Herschko), Rabin Medical Center, Petah Tikva,Israel (Drs Tsukrov and David), and Tel-Aviv University, Tel-Aviv, Israel (Drs Tsukrov and David). The authors have no relevant financial interest inthis article.

Arch Dermatol. 2004;140(7):805-810. doi:10.1001/archderm.140.7.805
Abstract

Background  An increased prevalence of benign solar damage (eg, facial wrinkles) but not neoplastic lesions was observed among patients with psoriasis whowere exposed to Dead Sea climatotherapy compared with controls.

Objectives  To compare the prevalence of actinic keratosis in psoriatic patients and controls and to assess whether known risk factors behave similarly inboth groups.

Design  Multicenter cross-sectional study.

Setting  Dermatology clinics in 4 participating Israeli hospitals and at a Dead Sea clinic.

Participants  Adult subjects (n = 460) with plaque-type psoriasis were recruited from the Israel Psoriasis Association (volunteer sample) and from dermatology clinics(convenience sample). The control group (n = 738) consisted of nonimmunosuppressed patients attending these clinics for benign conditions unrelated to sun exposure,such as atopic or contact dermatitis.

Main Outcome Measures  Prevalence and distribution of actinic keratoses and odds ratios associated with skin, hair, and eye color and propensity or history of sunburn adjustedfor age, ethnicity, and sun exposure .

Results  Actinic keratoses were observed in 200 controls (27%) and 51 subjects (11%) (P<.001). This increased prevalence occurred in bothsexes, participants aged 35 years or older, all ethnic groups, smokers, and nonsmokers. The anatomical distribution of lesions did not substantially differbetween subjects and controls. In multivariate analysis, psoriasis conferred a protective effect (odds ratio, <1), as did dark skin, dark eyes, anda history of severe sunburn in childhood. However, significant interactions were observed between psoriasis and hair color as well as psoriasis and propensityto sunburn, whereby a linear association was observed for controls but not for patients with psoriasis.

Conclusions  Psoriasis confers protection against actinic keratosis. Hair color and propensity to sunburn exert differential effects among psoriatic patientsand controls.

There is a consensus among the scientific community that the 3 major types of skin cancer—squamous cell carcinoma (SCC), basal cell carcinoma(BCC), and malignant melanoma—are caused by sun exposure.1,2 Furthermore, inherited characteristics, such as skin type and propensity to sunburn, mayhave a marked effect on the risk of skin cancer.3 It is not known whether the presence of other dermatologic conditions modifiesthe association between sun exposure, skin type, and actinic damage.

Psoriasis is a chronic skin condition that affects approximately 2%4 of the population, but with considerable ethnic and geographic variation.5 Manifestations of thedisease are often ameliorated by sun exposure.6,7 An increased incidence of nonmelanoma skin cancer (NMSC) (especially SCC) hasbeen reported in individuals with psoriasis who are exposed to high cumulative doses of psoralen–UV-A.811 Inone study, climatotherapy at the Dead Sea among Danish patients was found to be associated with an increased risk of NMSC.12 Thestudy results, however, were possibly confounded by the fact that patients selected for Dead Sea climatotherapy were those whose psoriasis was improvedby sun exposure. Treatment with UV-B may also be associated with a mild increase (2% per year) of NMSC.13 High-dose psoralen–UV-A therapy (1000 J/cm2) has also been reported to be associatedwith an increased risk of actinic keratosis.14

A cross-sectional study was previously performed in Israel that compared actinic damage among patients with psoriasis (87% of whom had undergone climatotherapyat the Dead Sea Solarium Clinic, Ein Bokek, Israel) and controls (individuals without psoriasis) (M.D., B. T., B. A., et al, unpublished data, 2000). Inthat study, the control subjects had higher self-reported rates of previous skin biopsies, removal of benign growth, or previous malignant neoplasms.There was an association between extent of exposure to the Dead Sea and benign photodamage, such as facial wrinkles, elastosis, solar lentigo, and poikiloderma.However, solar keratosis was more prevalent among controls than among patients with psoriasis and showed no association with days of exposure at the DeadSea. This surprising finding prompted a detailed analysis of factors associated with the presence of solar keratoses, with a comparison of persons with andwithout psoriasis.

METHODS
STUDY POPULATION

Subjects were patients with plaque-type psoriasis aged 20 to 70 years with a disease duration of at least 7 years. They were recruited from amongmembers of the Israel Psoriasis Association at a Dead Sea psoriasis clinic or attended dermatology clinics at 1 of the 4 participating hospitals. Controlswere patients aged 20 to 70 years who were attending dermatology clinics for benign skin conditions, eg, contact dermatitis and atopic dermatitis. Patientswith vitiligo, immunosuppression, autoimmunity, or suspected malignancy as the reason for the clinic visit were excluded as controls. We also excludedcontrols with skin types V or VI.

All participants provided signed informed consent, and the study protocol was approved by the institutional review boards of all participating hospitals.A questionnaire was administered to subjects and controls and included items concerning demographic characteristics, sun exposure, propensity to sunburn,and previously diagnosed benign and malignant neoplasms. A structured physical examination was performed by a qualified dermatologist who noted skin type,hair color, eye color, and the presence and location of suspected malignant skin lesions as well as solar keratosis and other signs of photodamage.

STATISTICAL ANALYSIS

We compared characteristics of subjects with psoriasis and controls using the χ2 test for categorical variables and the Mann-Whitneytest for comparing medians of continuous variables. Variables included in the analysis were group (patients with psoriasis or controls); skin type (I-IVreclassified into light or dark); eye color (black/brown or blue/green); hair color (black, brown, or blonde/red); propensity to sunburn (often/always,sometimes, or never), and history of severe sunburn in childhood (yes or no). We also constructed a summary variable of "fairness," which took into accounteye color, hair color, and complexion. We constructed logistic regression models for the presence of solar keratosis on examination, controlling forage (continuous variable), country of origin (Israel, Asia, North Africa, or other), yearly hours of sun exposure (recreational and occupational categorizedinto quartiles), and smoking history (current smoker: yes or no). To these models we added psoriasis/control status and individual measures of sun sensitivity,such as skin color, hair color, eye color, and propensity to sunburn. The models were slightly modified in terms of the covariates entered accordingto goodness-of-fit criteria (Hosmer-Lemeshow test).

We then tested whether there were significant interactions between psoriasis/control status and these variables. We also tested whether solar elastosis and solarkeratosis appeared together in the same anatomical locations and measured agreement using the κ statistic. All analyses were performed using SPSSsoftware (Version 10; SPSS Inc, Chicago, III). For all tests of significance, a 2-sided P value of .05 was considered statisticallysignificant.

RESULTS
UNIVARIATE ANALYSIS

The study population consisted of 460 subjects with psoriasis and 738 controls (N = 1198). Patients with psoriasis were more likely to be currentsmokers (34% vs 27%), male (57% vs 40%), and of European origin (31% vs 22%) than the controls. Of the patients with psoriasis, 49 (12%) had received psoralen–UV-Atherapy and 109 (26%) had been treated with UV-B. Very few malignant neoplasmswere noted on examination. Six cases of BCC and 3 of SCC were suspected amongthe patients with psoriasis, whereas among the controls the corresponding numbers were 11 and 3. Only 5 cases (2 SCCs [1 each among patients with psoriasisand controls] and 3 BCCs [1 among patients with psoriasis and 2 among controls]) were confirmed histologically. Solar keratoses were present among 200 controls(27%) and 51 patients with psoriasis (11%) (P = .001). In both psoriatic patients and controls, the prevalence of solar keratosisincreased with age. At all ages, in both sexes, and in all ethnic groups,the prevalence of solar keratosis was higher among controls than among psoriaticpatients (Table 1). Among the controls, European-American origin was more common in those with solar keratoses,but this pattern was not seen among the psoriatic patients.

Among those with solar keratosis, the number of lesions per subject varied from 1 to 105, with 26% of psoriatic patients and 38% of controls having6 or more lesions. Table 2 shows the comparison of the distribution of actinic keratosis in patients with psoriasisand controls. In both groups, lesions were most commonly seen in the head, neck, and face areas. Solar keratoses and solar elastosis were found simultaneouslyin the face region in 92 cases (κ = 0.34; P<001, indicating fair agreement).

Table 3 shows the associations between sun sensitivity and the presence of any solar keratosis in psoriaticpatients and controls. Of note, blue or green eye color was associated with a higher frequency of solar keratosis in both psoriatic patients and controls.Light skin was associated with this lesion in controls but not in psoriatic patients. With regard to hair color, no association was noted among the psoriaticpatients, whereas this characteristic was highly associated with the presenceof keratosis amongthe controls. The composite variable fairness, which combined hair, skin, and eye color into a single profile,was associated with the presence of solar keratosis in both psoriatic patientsand controls. Finally, a monotonic relationship was noted between propensityto sunburn and keratoses among the controls but not among the psoriatic patients.Similarly, a weak association between a history of severe sunburn in childhoodand solar keratosis was noted in the psoriatic patients, whereas the association was strong in the controls.

We assessed the prevalence of solar keratosis according to quartiles of sun exposure, and no association was noted among the psoriatic patients,whereas this lesion was associated with degree of sun exposure in the controls.Of note, the association was nonmonotonic, with a positive relationship notedacross the first, second, and third quartiles and a decrease observed for the fourth (heaviest exposure) quartile.

MULTIVARIATE ANALYSIS

The logistic regression analyses are shown in Table 4. In this multivariate analysis, we show the association between solar keratosis, patient characteristics (eg, skin color and eye color),group (patients with psoriasis or controls), and the interactions between them. The reported odds ratio are adjusted for covariates such as ethnic origin(ie, Asia-Africa, Europe-America, and Israel), sex, age, and degree of sunexposure. Smoking was removed because it did not contribute to the models.In these analyses, psoriasis exerted a protective effect (odds ratio, <1) on the presence of solar keratosis. Furthermore, dark skin, dark eyes, andblack hair were also protective against the presence of solar keratosis. Significant interactions were noted between black vs blonde hair color and psoriasis whenthe presence of solar keratosis was analyzed, and between propensity to sunburnand psoriasis, meaning that the relationship between these patient characteristicsand solar keratosis have differential effects in psoriatic patients and in nonpsoriatic patients (Figure 1 and Figure 2). This analysis shows a clear increasein the odds of solar keratosis with lighter hair color and with increased propensity for sunburn in the controls, whereas the relationship was flatamong the patients with psoriasis.

COMMENT

Traditional and well-established risk factors for NMSC and photodamage have included skin and hair characteristics as well as occupational and recreationalsun exposure.1 These factors,2,15,16 as well as a history of severe sunburn before the age of 20 years,17 arealso important in determining susceptibility to actinic keratoses. To our knowledge, there has not been a systematic comparison of the relative effectsof these risk factors in psoriatic and nonpsoriatic patients.

Solar or actinic keratoses are generally considered to be premalignant lesions,15,16,18 butsome authors19,20 consider them to be established SCCs. In the present cross-sectional study, their prevalencewas lower among psoriatic than nonpsoriatic patients attending dermatology clinics for problems unrelated to photodamage. Some of these differences maybe explained by differential distribution of age, ethnicity, and sun exposurebetween subjects and controls. However, on multivariate analysis, even afterthese factors and characteristics related to sun sensitivity, such as skincolor, eye color and hair color, were controlled for, the odds of solar keratosiswas strikingly lower for the patients with psoriasis than for the controls. Furthermore, in some instances (eg, hair color and propensity to sunburn),the classic risk factors appeared to have a differential effect in psoriatic patients compared with nonpsoriatic patients. This analysis provides preliminarydata that demonstrate a modifying effect of psoriasis on the classic factors that have been shown to affect susceptibility to neoplastic or preneoplasticphotodamage.

The first question that should be asked is whether our findings were the result of chance. Although the interactions we observed were statisticallysignificant, we did not perform the study with this hypothesis in mind. Selection bias may have played a role, as neither the psoriatic group nor the controlgroup was population based. However, given the high degree of sun exposureamong the patients with psoriasis, it would have been expected that they wouldbe at greater risk for the development of skin neoplasms and preneoplastic conditions than a population of patients with rashes and other dermatologiccomplaints. Since NMSC is not reported to the Israel Cancer Registry, we have no population-based estimate of actinic keratoses or NMSC in Israel; therefore,it is difficult for us to measure the degree of bias in the selection of the study population. Our analysis took into account confounders such as countryof origin, age, sex, and smoking. Indeed, the results were weakened when we adjusted for these factors, but some of the interactions remained. Unmeasuredconfounders may have played a role in these results.

Therefore, while these findings may be spurious, the observation that actinic keratosis is more prevalent among nonpsoriatic patients is consistentin all subgroups, and there is a suggestion that hair color and propensityto sunburn played a differential role in contributing to solar keratosis inthe 2 groups. Is there biological plausibility for this finding? A survey of psoriatic patients21 showed that skin type(based on ability to tan and susceptibility to sunburn) showed higher correlations with minimal erythema dose after UV irradiation than did hair or eye color.Interestingly, in 1984, Stern and Momtaz22 found that skin type (and not hair or eye color) predicted skin cancer risk in psoriaticpatients who were treated with psoralen–UV-A, providing additional evidence for a possible differential or inconsistent effect of the classic risk factorsfor NMSC among patients with psoriasis.

Apart from malignant changes ascribed to the treatment of psoriasis , little is known about actinic damage in this disease. Two studies performedin the 1980s suggested that persons with psoriasis have a similar risk of developing SCC compared with several other populations of patients.23,24 In a Danish cohort, the risk of NMSCamong patients with psoriasis was 2.5 times that of the general population.25 A more recent cohort study26 reported a 2- to 4-fold risk of NMSC developing among persons with psoriasis comparedwith hypertensive controls, with the risk varying with the severity of psoriasis. It is difficult to separate the risks associated with antipsoriatic treatmentfrom those inherently associated with the disease. Certain skin diseases, such as atopic dermatitis and urticaria, are substantially rarer among psoriaticpatients than among controls.27 In 1977, Kocsard28 reported that actinic keratoses are rare in patients with psoriasis compared with controls. His study, which was carried out amongAustralian military personnel, found relatively few cases of actinic keratosis, even among fair-skinned and blue-eyed persons with psoriasis, whereas 88%of the persons without psoriasis who were examined had evidence of these lesions.

The prevalence of psoriasis appears to vary by country and skin type,29 with a higher frequency noted in European populations compared with African or Asian populations and with specific HLA types.4 Furthermore, while actinic keratoses are thought tobe a "dose meter of chronic sun damage,"16 this does not seem to be the case in all populations.30 Toour knowledge, there is only 1 case report of multiple actinic keratoses that developed in sun-protected areas in a psoriatic patient who received a doseof 883 J/cm2 of UV-A,31 but little is known about the inherent (as opposed to treatment-related) risk of malignantand premalignant skin disorders in persons with psoriasis.

On a genetic level, the GSTM1 null phenotype32 has been shown to be a risk factor for solar keratosis in a white population, after skin type and ability to tan were controlledfor. On the other hand, a recent study33 has shown that GSTM1 variant alleles are associated withpsoriasis. Thus, alleles associated with an increased incidence of psoriasis may be associated with a decreased risk of actinic skin damage.

Furthermore, recent studies have shown that psoriatic patients with skin cancer (BCC) have evidence of increased DNA damage and defective DNArepair compared with those without BCC.34,35 Interestingly, Dybdahl et al35 reported that psoriatic patientswithout BCC had marginally higher repair than controls (although the results were not statistically significant), suggesting that skin cancers occur ina subgroup of psoriatic patients, while others may be protected. It is conceivable that in some patients with psoriasis, hyperproliferation of keratinocytesmay protect against the effects of sun damage when DNA repair mechanisms are intact, explaining the interactions we found in our study. Indeed, the occurrenceof SCC within psoriatic plaques is exceedingly rare.36 Our findings may serve as a foundation for future studies specifically designedto answer these questions. Notwithstanding the results of our study, it should be stressed that cutaneous neoplasia occurs in patients with psoriasis andthat efforts to prevent skin cancer in this population are still required.

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Article Information

Correspondence: Ora Paltiel, MDCM, MSc, School of Public Health, Hadassah-Hebrew University, POB 12000, Jerusalem, Israel 91120 (ora@vms.huji.ac.il).

Accepted for publication December 29, 2003.

This study was supported in part by the Dead Sea Medical Research and Development Center, Dead Sea, Israel.

Participating hospitals were Rabin Medical Center, Petah Tikva; Hadassah-Hebrew University Hospital, Ein-Karem, Jerusalem; Ha'emek Medical Center, Afula;Sheba-Tel-Hashomer Medical Center, Tel-Aviv; all in Israel.

References
1.
Armstrong  BKKricker  A The epidemiology of UV-induced skin cancer J Photochem Photobiol B. 2001;638- 18
PubMedArticle
2.
Vitasa  BCTaylor  HRStrickland  PT  et al.  Association of nonmelanoma skin cancer and actinic keratosis with cumulative solar ultraviolet exposure in Maryland watermen Cancer. 1990;652811- 2817
PubMedArticle
3.
Hogan  DJTo  TGran  LWong  DLane  PR Risk factors for basal cell carcinoma Int J Dermatol. 1989;28591- 594
PubMedArticle
4.
Christophers  E Psoriasis: epidemiology and clinical spectrum Clin Exp Dermatol. 2001;26314- 320
PubMedArticle
5.
Raychaudhuri  SPFarber  EM. The prevalence of psoriasis in the world J Eur Acad Dermatol Venereol. 2001;1520- 23
PubMedArticle
6.
Parks  BSYoun  JI Factors influencing psoriasis: an analysis based upon the extent of involvement and clinical type J Dermatol. 1998;2597- 102
PubMed
7.
Farber  EMBright  RDNall  ML Psoriasis: a questionnaire survey of 2,144 patients Arch Dermatol. 1968;98248- 259
PubMedArticle
8.
Mali-Gerrits  MGHGaasbeek  DBoezeman  JVan de Kerkhof  PCM Psoriasis therapy and the risk of skin cancers Clin Exp Dermatol. 1991;1685- 89
PubMedArticle
9.
Hannuksela-Svahn  APukkala  ELaara  EPoikolainen  KKarvonen  J Psoriasis, its treatment, and cancer in a cohort of Finnish patients J Invest Dermatol. 2000;114587- 590
PubMedArticle
10.
Eskelinen  AHalme  KLasus  AIdanpaan-Heikkila  J Risk of cutaneous carcinoma in psoriatic patients treated with PUVA Photodermatology. 1985;210- 14
PubMed
11.
Stern  RSLiebman  EJVakeva  L Oral psoralen and ultraviolet-A light (PUVA) treatment of psoriasisand persistent risk of nonmelanoma skin cancer: PUVA follow-up study J Natl Cancer Inst. 1998;901278- 1284
PubMedArticle
12.
Frentz  GOlsen  JHAvrach  WW Malignant tumours and psoriasis: climatotherapy at the Dead Sea Br J Dermatol. 1999;1411088- 1091
PubMedArticle
13.
Pasker-de Jong  PWielink  Gvan der Valk  Pvan der Wilt  GJ Treatment with UV-B for psoriasis and nonmelanoma skin cancer: a systematic review of the literature Arch Dermatol. 1999;135834- 840
PubMedArticle
14.
Chuang  TYHeinrich  LASchultz  MDReizner  GTKumm  RCCripps  DJ PUVA and skin cancer: a historical cohort study on 492 patients J Am Acad Dermatol. 1992;26173- 177
PubMedArticle
15.
Marks  RRennie  GSelwood  T The relationship of basal cell carcinomas and squamous cell carcinomas to solar keratoses Arch Dermatol. 1988;1241039- 1042
PubMedArticle
16.
Salasche  SJ Epidemiology of actinic keratoses and squamous cell carcinoma J Am Acad Dermatol. 2000;424- 7
PubMedArticle
17.
Kennedy  CBajdik  CDWillemze  RDe Gruijl  FRBouwes Bavinck  JNLeiden Skin Cancer Study, The influence of painful sunburns and lifetime sun exposure on the risk of actinic keratoses, seborrheic warts, melanocytic nevi, atypical nevi,and skin cancer J Invest Dermatol. 2003;1201087- 1093
PubMedArticle
18.
Kocsard  E Solar keratoses and their relationship to non-melanoma skin cancers Australas J Dermatol. 1997;38(suppl 1)S30
PubMedArticle
19.
Ackerman  BA Opposing views of 2 academies about the nature of solar keratosis Cutis. 2003;71391- 395
PubMed
20.
Fu  WCockerell  CJ The actinic (solar) keratosis: a 21st-century perspective Arch Dermatol. 2003;13966- 70
PubMedArticle
21.
Weinstock  MA Assessment of sun sensitivity by questionnaire: validity of items and formulation of a prediction rule J Clin Epidemiol. 1992;45547- 552
PubMedArticle
22.
Stern  RSMomtaz  K Skin typing for assessment of skin cancer risk and acute response to UV-B and oral methoxsalen photochemotherapy Arch Dermatol. 1984;120869- 873
PubMedArticle
23.
Stern  RSScotto  JFears  TR Psoriasis and susceptibility to nonmelanoma skin cancer J Am Acad Dermatol. 1985;1267- 73
PubMedArticle
24.
Stern  RZierler  SParrish  JA Psoriasis and the risk of cancer J Invest Dermatol. 1982;78147- 149
PubMedArticle
25.
Olsen  JHMoller  HFrentz  G Malignant tumors in patients with psoriasis J Am Acad Dermatol. 1992;27716- 722
PubMedArticle
26.
Margolis  DBilker  WHennessy  SVittorio  CSantanna  JStrom  BL The risk of malignancy associated with psoriasis Arch Dermatol. 2001;137778- 783
PubMed
27.
Henseler  TChristophers  E Disease concomitance in psoriasis J Am Acad Dermatol. 1995;32982- 986
PubMedArticle
28.
Kocsard  E The rarity of actinic keratoses in patients with psoriasis Z Hautkr. 1977;5255- 56
PubMed
29.
Henseler  T The genetics of psoriasis J Am Acad Dermatol. 1997;37S1- S11
PubMedArticle
30.
Zhao  PZhu  XLiu  YWang  BWang  CBurns  FJ Solar ultraviolet radiation and skin damage: an epidemiological study among a Chinese population Arch Environ Health. 1998;53405- 409
PubMedArticle
31.
Westphal  HJWurdel  CFlegel  H Actinic keratoses: sequelae of long-term PUVA therapy Dermatol Monatsschr. 1989;175623- 627
PubMed
32.
Carless  MALea  RACurran  JE  et al.  The GSTM1 null genotype confers an increased risk for solar keratosisdevelopment in an Australian caucasian population J Invest Dermatol. 2002;1191373- 1378
PubMedArticle
33.
Richter-Hintz  DTheir  RSteinwachs  S  et al.  Allelic variants of drug metabolizing enzymes as risk factors in psoriasis J Invest Dermatol. 2003;120765- 770
PubMedArticle
34.
Møller  PWallin  HDybdahl  MFrentz  GNexo  BA Psoriasis patients with basal cell carcinoma have more repair-mediated DNA strand-breaks after UVC damage in lymphocytes than psoriasis patientswithout basal cell carcinoma Cancer Lett. 2000;151187- 192
PubMedArticle
35.
Dybdahl  MFrentz  GVogel  UWallin  HNexo  BA Low DNA repair is a risk factor in skin carcinogenesis: a study of basal cell carcinoma in psoriasis patients Mutat Res. 1999;43315- 22
PubMedArticle
36.
Nickoloff  BJ Creation of psoriatic plaques: the ultimate tumor suppressor pathway J Cutan Pathol. 2001;2857- 64
PubMedArticle
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