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Table of Contents 
SHORT COMMUNICATION
Year : 2016  |  Volume : 61  |  Issue : 6  |  Page : 664-667
The relationship of psoriasis and melanocytic nevi


Department of Dermatology, Bezmialem Vakif University, Istanbul, Turkey

Date of Web Publication9-Nov-2016

Correspondence Address:
Fatma Pelin Cengiz
Department of Dermatology, Bezmialem Vakif University, 34710 Istanbul
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5154.193680

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   Abstract 

Background: There is limited data about the relationship between psoriasis and melanocytic lesions and melanoma. Immunologic pathways which were implicated in psoriasis induce a reduction in the number of melanocytic nevi. Aims and Objectives: To investigate the number of melanocytic nevi in psoriatic patients compared with controls and its relationship with disease severity and type of treatment. Methods: We performed a prospective study in 100 psoriatic patients and 100 controls. Clinical data were recorded for all participants. Results: As compared with controls, patients had overall fewer nevi congenital nevi. Among psoriatic patients, biologic agents and disease severity did not correlate with the number of nevi. Conclusions: Psoriatic patients have fewer nevi than controls. Frequency of nevi in psoriatic patients is not related to treatment and disease severity.


Keywords: Melanoma, nevi, psoriasis


How to cite this article:
Cengiz FP, Emiroglu N, Bahali AG, Ozkaya DB, Su O, Onsun N. The relationship of psoriasis and melanocytic nevi. Indian J Dermatol 2016;61:664-7

How to cite this URL:
Cengiz FP, Emiroglu N, Bahali AG, Ozkaya DB, Su O, Onsun N. The relationship of psoriasis and melanocytic nevi. Indian J Dermatol [serial online] 2016 [cited 2021 Mar 7];61:664-7. Available from: https://www.e-ijd.org/text.asp?2016/61/6/664/193680

What was known?
It has already been established that psoriatic patients have fewer nevi than normal population.



   Introduction Top


Psoriasis is a persistent, chronic inflammatory disease that affects up to 2% of the population. [1] Several researches demonstrated a relation between psoriasis and comorbidities, such as metabolic syndrome, cardiovascular diseases, inflammatory bowel diseases, depression/suicide, and risk of cancers. [2],[3],[4],[5],[6]

Although many studies show that the risk of melanoma and nonmelanoma skin cancer in patients with psoriasis is comparable with the general population, patients with psoriasis who have received more than 250 psoralen plus ultraviolet A (PUVA) treatments have a 14-fold higher risk of cutaneous squamous cell carcinoma than patients who have received fewer treatments. [7],[8],[9]

There are contradictory results about the relationship between melanoma and psoriasis in literature. Although there is evidence that Caucasians with extensive PUVA exposure have an increased risk of melanoma, other studies have found no significant association between psoriasis and melanoma. [10],[11] However, little is known about the association of melanocytic nevi with psoriasis. Previous studies on the influence of psoriasis vulgaris on the number of melanocytic nevi showed that patients affected with psoriasis vulgaris have fewer nevi compared with controls, and that the immunologic environment with regard to interleukin (IL-1α), IL-6, and tumor necrosis factor alpha (TNF-α) serum levels influences the number of nevi with an inverse correlation. [12],[13] The aims of this study were to investigate the number of melanocytic lesions in psoriatic patients and to assess whether there is an association between the severity of psoriasis, psoriasis therapies, and nevus count.


   Methods Top


We performed a prospective study on patients with psoriasis vulgaris, who were recruited from those consecutively attending the outpatient clinics of department of Dermatology at Bezmialem Vakif University, Istanbul, Turkey, from July through December 2015. One hundred psoriatic patients and 100 controls, with no family history of psoriasis, were enrolled in the study.

The study was approved by the local Ethics Committee. Informed consent was obtained from all participants, and the study was conducted according to the Declaration of Helsinki Principles.

Age at diagnosis of psoriasis, clinical characteristics; family history of psoriasis, Psoriasis Area and Severity Index score at enrollment, and previous and current therapies were registered. Treatments were classified as topical agents, phototherapy, cyclosporine, methotrexate, retinoids, and biologics.

For all the participants, melanocytic nevi ≥2 mm were counted on all body sites.

Statistical analysis

Continuous variables were compared using Student's t-test and Mann-Whitney U-test. Comparisons between categorical variables were performed with Chi-square test and Fisher corrections, when required. P < 0.05 was considered statistically significant.


   Results Top


A total of 200 participants, 100 psoriatic patients and 100 controls, were included in the study [Table 1]. In the psoriasis group, a family history of psoriasis was reported by 27 of the 100 (27%) patients, and none of the patients had a personal history of melanoma; the mean age of disease onset was 26.07 ± 17.39 (range: 0-71 years), and a diagnosis of psoriatic arthritis was made in 21 of the 100 (21%) patients.
Table 1: Demographic features of patients


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Mild psoriasis was diagnosed in 82 of the 100 (82%) patients, and moderate-to-severe psoriasis was diagnosed in 18 of the 100 (18%) patients. There are no statistically significant differences related to nevi count between mild psoriasis group and moderate-to-severe psoriasis group (P: 0.803). At enrollment, 38 of the 100 (38%) patients were treated with topical agents alone, 21 of the 100 (21%) with narrowband ultraviolet B, and 15 of the 100 (15%) with biologic agents. Overall, 75 of the 100 (75%) patients were treated at least once in their life with a conventional systemic treatment.

We found a wide variation in the total number of nevi both in psoriasis and control groups (from 0 to 100). Psoriatic patients had fewer nevi than controls, both in the overall nevus count (P: 0.002) [Table 2].
Table 2: Nevus count of patients


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Psoriatic patients were less likely to have congenital nevi (7 of 100; 7%) than controls (20 of 100; 20%) (P: 0.036). We did not find any association between therapies and nevi count (P: 0.213). Disease duration, presence of psoriatic arthritis, and previous exposure to phototherapy were not significantly associated with nevus count (P: 0.073) (P: 0.707) (P: 0.815).


   Discussion Top


Psoriasis is usually presented as erythematous, raised, scaly skin lesions. Histology of psoriasis is characterized by parakeratosis and psoriasiform hyperplasia. Abnormal expression of T-helper 1 (Th1), Th17 cells, and overproduction of pro-inflammatory cytokines, particularly TNF-α, interferon gamma (IFN-g), IL-2, and IL-12 has a major role on the pathogenesis of psoriasis. Therefore, the pathogenesis of psoriasis is considered to be an immunologically mediated process.

Secreted cytokines from activated cells induce epidermal acanthosis, hyperkeratosis, and parakeratosis, which characterize psoriasis plaques. Psoriasis is considered a Th1 condition, characterized by the production of IFN-g and TNF-α with the effect of IL-12. In the recent years, the importance of Th17 cells has been estimated in psoriasis. Th17 cells are stimulated by IL-23 (which shares the p40 subunit with IL-12) to produce IL-17 and also IL-22, which has recently been shown to be a major driver of acanthosis in psoriasis. The IL-23/Th17 axis may explain the hyperplasia of psoriatic keratinocytes by IL-22. [14]

One of the most common histopathological findings in psoriasis lesions is an increase in epidermal proliferation and parakeratosis. The scaling is caused by thickened stratum corneum with parakeratosis and epidermal thickening with acanthosis, papillomatosis, and absence of granular layer.

We found that psoriatic patients had significantly fewer nevi than controls. Twenty-three of the 100 patients versus 2 of the 100 healthy controls had no nevi and 65% of the (65 of 100) patients versus 20% (20 of 100) of the controls had 1-10 nevi. Two patients versus 28 of the healthy controls had more than 50 nevi.

Balato et al. showed that 22% of the patients had 0 nevi versus 1.1% of the controls, and that the global number of nevi ranged from 0 to 30 in psoriatic patients and from 0 to over 50 in controls. [12] Di Cesare et al. reported that controls had more congenital nevi compared with patients (44 of 189 [23.2%] and 20 of 189 [10.6%], respectively). In addition, they detected a very low percentage of clinical atypical nevi and no melanoma in both patients and controls. [13] Our results are consistent with Balato et al. and Di Cesare et al.

In line with Di Cesare et al., no relationship between the number of nevi and severity of disease, age at diagnosis, duration of psoriasis, metabolic comorbidities, obesity, phototherapy, and presence of psoriatic arthritis was found in our study.

Major cytokines in the pathogenesis of psoriasis are TNF-α, IL-1, IL-6, and transforming growth factor-β, which inhibit tyrosinase activity. [15] Immunosuppressive and immunomodulating agents which were used in the treatment of psoriasis vulgaris may lead to change in the cytokine profile. Patients with Crohn's disease had eruptive nevi during immunosuppressive therapies, including anti-TNF-α treatment. [16] Rapid development of melanoma has been recently reported in two patients treated with an anti-IL-6 agent, tocilizumab. [17],[18] In our study, patients treated with biologic agents did not have more nevi than patients treated otherwise. It may be the result of low sample size of biologic agents in our study. No cases of melanoma were detected in patients with psoriasis and their family.

Wang et al. reported the presence of Th17 cells in the skin lesions of vitiligo. [19] They showed that IL-17 by itself does not inhibit pigmentation signaling; however, IL-17 can increase the inhibitory effect of TNF on melanogenesis significantly. In addition, Kotobuki et al. reported that a combination of TNF, IL-1β, IL-6, and IL-17 could inhibit melanin production. [20] They showed that IL-17A dramatically induced IL-1β, IL-6, and TNF-α production in skin-resident cells such as keratinocytes and fibroblasts. This local environment results in local depigmentation in autoimmune vitiligo lesions.

It was also shown that TNF, IL-6, IL-1α, and TGF-β1 could independently modulate the expression of tyrosinase and related enzymes. [21] In addition, Yang et al. showed that IFN-g inhibits melanogenesis in primary cultured human melanocytes by altering melanogenic enzyme messenger RNA expression in addition to increased melanocyte apoptosis via direct affect of IFN-g. [22]


   Conclusions Top


Psoriatic patients have fewer melanocytic nevi than controls, suggesting a protective role of the cytokine profile of psoriasis and increased secretion of IL-17, TNF, IL-6, and IL-1β against the development of melanocytic lesions. The protective role of genetic background against melanoma and nonmelanoma skin cancers should be investigated in the relatives of psoriasis patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med 2009;361:496-509.  Back to cited text no. 1
    
2.
Gottlieb AB, Dann F, Menter A. Psoriasis and the metabolic syndrome. J Drugs Dermatol 2008;7:563-72.  Back to cited text no. 2
    
3.
Armstrong AW, Schupp C, Bebo B. Psoriasis comorbidities: Results from the National Psoriasis Foundation surveys 2003 to 2011. Dermatology 2012;225:121-6.  Back to cited text no. 3
    
4.
Kimball AB, Jacobson C, Weiss S, Vreeland MG, Wu Y. The psychosocial burden of psoriasis. Am J Clin Dermatol 2005;6:383-92.  Back to cited text no. 4
    
5.
Brauchli YB, Jick SS, Miret M, Meier CR. Psoriasis and risk of incident cancer: An inception cohort study with a nested case-control analysis. J Invest Dermatol 2009;129:2604-12.  Back to cited text no. 5
    
6.
Prizment AE, Alonso A, Folsom AR, Ahmed RL, Virnig BA, Warshaw EM, et al. Association between psoriasis and incident cancer: The Iowa's women's health study. Cancer Causes Control 2011;22:1003-10.  Back to cited text no. 6
    
7.
Boffetta P, Gridley G, Lindelöf B. Cancer risk in a population-based cohort of patients hospitalized for psoriasis in Sweden. J Invest Dermatol 2001;117:1531-7.  Back to cited text no. 7
    
8.
Stern RS, Lunder EJ. Risk of squamous cell carcinoma and methoxsalen (psoralen) and UV-A radiation (PUVA). A meta-analysis. Arch Dermatol 1998;134:1582-5.  Back to cited text no. 8
    
9.
Stern RS, Laird N. The carcinogenic risk of treatments for severe psoriasis. Photochemotherapy follow-up study. Cancer 1994;73:2759-64.  Back to cited text no. 9
    
10.
Stern RS; PUVA Follow up Study. The risk of melanoma in association with long-term exposure to PUVA. J Am Acad Dermatol 2001;44:755-61.  Back to cited text no. 10
    
11.
Ji J, Shu X, Sundquist K, Sundquist J, Hemminki K. Cancer risk in hospitalised psoriasis patients: A follow-up study in Sweden. Br J Cancer 2009;100:1499-502.  Back to cited text no. 11
    
12.
Balato N, Di Costanzo L, Balato A, Patruno C, Scalvenzi M, Ayala F. Psoriasis and melanocytic naevi: Does the first confer a protective role against melanocyte progression to naevi? Br J Dermatol 2011;164:1262-70.  Back to cited text no. 12
    
13.
Di Cesare A, Riitano A, Suppa M, Fidanza R, Zangrilli A, Esposito M, et al. Frequency of melanocytic nevi in psoriatic patients is related to treatment and not to disease severity. J Am Acad Dermatol 2013;69:947-53.  Back to cited text no. 13
    
14.
Di Cesare A, Di Meglio P, Nestle FO. The IL-23/Th17 axis in the immunopathogenesis of psoriasis. J Invest Dermatol 2009;129:1339-50.  Back to cited text no. 14
    
15.
Swope VB, Abdel-Malek Z, Kassem LM, Nordlund JJ. Interleukins 1 alpha and 6 and tumor necrosis factor-alpha are paracrine inhibitors of human melanocyte proliferation and melanogenesis. J Invest Dermatol 1991;96:180-5.  Back to cited text no. 15
    
16.
Bovenschen HJ, Tjioe M, Vermaat H, Witteman BM, Janssens RW, Stoof TJ, et al. Induction of eruptive benign melanocytic naevi by immune suppressive agents, including biologicals. Br J Dermatol 2006;154:880-4.  Back to cited text no. 16
    
17.
Finet A, Amini-Adle M, Balme B, Colson F, Thomas L. Nodular progression of lentigo malignant melanoma during a treatment with tocilizumab: Cause or coincidence? Clin Rheumatol 2013;32:277-80.  Back to cited text no. 17
    
18.
Bonny M, Buyse V, Suys E. Rapidly progressive malignant melanoma in a patient treated with tocilizumab. J Am Acad Dermatol 2012;67:e78-9.  Back to cited text no. 18
    
19.
Wang CQ, Cruz-Inigo AE, Fuentes-Duculan J, Moussai D, Gulati N, Sullivan-Whalen M, et al. Th17 cells and activated dendritic cells are increased in vitiligo lesions. PLoS One 2011;6:e18907.  Back to cited text no. 19
    
20.
Kotobuki Y, Tanemura A, Yang L, Itoi S, Wataya-Kaneda M, Murota H, et al. Dysregulation of melanocyte function by Th17-related cytokines: Significance of Th17 cell infiltration in autoimmune vitiligo vulgaris. Pigment Cell Melanoma Res 2012;25:219-30.  Back to cited text no. 20
    
21.
Martínez-Esparza M, Ferrer C, Castells MT, García-Borrón JC, Zuasti A. Transforming growth factor beta1 mediates hypopigmentation of B16 mouse melanoma cells by inhibition of melanin formation and melanosome maturation. Int J Biochem Cell Biol 2001;33:971-83.  Back to cited text no. 21
    
22.
Yang L, Wei Y, Sun Y, Shi W, Yang J, Zhu L, et al. Interferon-gamma inhibits melanogenesis and induces apoptosis in melanocytes: A pivotal role of CD8+cytotoxic T lymphocytes in vitiligo. Acta Derm Venereol 2015;95:664-70.  Back to cited text no. 22
    

What is new?
It was shown that treatment modality for psoriasis does not affect the number of nevi and patients who undergone biologic agents do not have more nevi than other psoriatic patients.



 
 
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  [Table 1], [Table 2]



 

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