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What Is This Hair Change on the Scalp?

What Is This Hair Change on the Scalp?

 

 

A 64-year-old man presented for management of his chronic skin condition on the scalp (Figure). On physical examination, there were erythematous plaques with silvery scales on his elbows and knees (not shown) as well as on the scalp. Close examination of his scalp found that the plaques were confined to the right side of the scalp only. Abundant terminal hair growth was noted within these plaques. The left side of the scalp lacked the plaques, but demonstrated a diversity of hair shaft diameter and brown halos around hair shaft on dermatoscopy. The alopecic area was sharply delineated from the psoriatic area. 

What is Your Diagnosis?

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Diagnosis: Renbök Phenomenon in a Patient with Psoriasis and Androgenetic Alopecia 

The Renbök phenomenon is uncommon and describes how the presence of one dermatologic disorder inhibits the effect of another preexisting dermatologic pathology in the same patient. 

It was first described in 1991 by Happle and colleagues, in a case of new-onset psoriasis causing hair growth where there was previously none due to alopecia areata.1 

Since this initial case was presented, several case reports have also been published demonstrating the Renbök phenomenon in the setting of psoriasis and alopecia areata and alopecia universalis.1,2 There has also been a case reported of alopecia areata sparing a nevus flameneus.3 To our knowledge, this is the first reported case of a patient with psoriasis of the scalp and androgenetic alopecia, who retained terminal hair in the psoriatic plaques.

Clinical Presentation

The first documented occurrence of the Renbök phenomenon by Happle and colleagues described 4 patients with alopecia areata of the scalp and scalp psoriasis, who each demonstrated terminal hair growth within psoriatic plaques of the scalp, but no hair growth elsewhere on the scalp.1 This presentation stayed consistent in other documented cases in the setting of scalp psoriasis and alopecia areata or alopecia universalis.1,2 

In the documented case of alopecia universalis sparing a nevus flameneus, a patient had complete loss of terminal hair on the scalp, except in the location of a congenital melanocytic nevi, in which hair was retained.3 Although to our knowledge, the Renbök phenomenon has yet to be documented as occurring in the setting of psoriasis and androgenetic alopecia, there has been a documented case of thicker hair regrowth within psoriatic plaques compared to the rest of the scalp in a patient with androgenetic alopecia following shaving of the head.4 As this case still demonstrated hair loss in the characteristic distribution of androgenetic alopecia, including within psoriatic plaques, we believe our patient is the first documented case of psoriasis inhibiting the pathogenesis of androgenetic alopecia.

In our case, a 64-year-old man with psoriasis of the scalp and androgenetic alopecia presented for management of his psoriasis. Besides psoriatic plaques on his elbows and knees, the psoriatic plaques were found to be confined to the right side of the scalp (Figure). Abundant terminal hair growth was noted within these plaques. The left side of the scalp lacked psoriatic plaques, but demonstrated features of androgenetic alopecia. The alopecic area was sharply delineated from the psoriatic area. 

Mechanism And Pathogenesis

The Renbök phenomenon is uncommon and has mainly been described in the setting of psoriasis and alopecia areata. Androgenetic alopecia has a different pathophysiology than alopecia areata. Genetically predetermined increased activity of 5-α-reductase and a higher percentage of androgen receptors on the hair follicle define the effect of androgen on the growth of the hair follicle in androgenetic alopecia,5 while an autoimmune-driven inflammation is a key in alopecia areata. The Renbök phenomenon has not yet been documented to occur in a case of both psoriasis and androgenetic alopecia. The mechanism for this process is unclear but may involve insulin-like growth factor 1 (IGF-1), epidermal growth factor (EGF), and/or WNT/β-catenin signaling pathways, presenting new therapeutic targets for patients with androgenetic alopecia.

IGF-1 is an important peptide that stimulates both epidermal keratinocytes and hair follicle cells to undergo cell division and proliferation and is also believed to be important in regulating the hair cycle.6,7 IGF-1 injected into the murine skin caused proliferation of hair follicle cells in anagen, and a prolongation of anagen8; and this effect could be achieved in vitro.9 In androgenetic alopecia, the levels of IGF-1 were decreased in affected hair follicles,7 while in psoriasis, the levels of IGF-1 are higher than in nonpsoriatic skin.6 Thus, the decline in IGF-1 levels seen in androgenetic alopecia may be blunted or reversed by the increase in IGF-1 that occurs in psoriatic plaques, promoting a longer anagen phase in hair follicles and allowing retention of terminal hair in psoriatic plaques.  

Another factor that stimulates the anagen phase of the hair follicle is EGF.10 Continuous expression of EGF can prevent progression to the catagen phase, and use of EGF receptor inhibitors can inhibit hair growth.11 Psoriasis is associated with increased levels of EGF activity in affected keratinocytes.12 This link could indicate the possibility of promotion of the anagen phase of hair follicles in psoriatic plaques secondary to the effect of EGF. 

A significant role in the hair cycle belongs to WNT/β-catenin signaling pathway. β-catenin activity has been shown to be important in inducing certain stem cell lineages to differentiate into hair shaft cells and secondary hair follicle germ cells, among other cell types.13 The proliferation of these cells has been demonstrated to occur during the anagen phase of hair cycling, and to be decreased during telogen.13 β-catenin is responsible for initiation of anagen, and absence of β-catenin activity causes hair follicle regression.13 In androgenetic alopecia, the binding of androgens to the androgen receptor lead to a decrease of WNT/β-catenin signaling,14 while the increased expression of β-catenin was observed in the psoriatic keratinocytes.15 An increased nuclear β-catenin activity in hair follicles of psoriatic plaques can stimulate hair follicle growth and inhibit the effect of androgens to decrease β-catenin activity and promote androgenetic alopecia.

Our Patient

The psoriatic plaque on the scalp was treated with emulsion of fluocinolone acetonide in peanut oil and was well controlled after 3 weeks of treatment. The patient was not interested in addressing his androgenetic alopecia. 

Conclusion

The Renbök phenomenon is a rare occurrence, in which one dermatologic condition inhibits the effect of another dermatologic condition. It has previously been documented as occurring in cases of psoriasis and alopecia areata or alopecia universalis, as well as alopecia areata and a congenital nevi.1-3 We have presented what we believe is the first reported case of the Renbök phenomenon occurring in the presence of concomitant psoriasis and androgenetic alopecia. Possible mechanisms for this may include IGF-1, EGF, and WNT/β-catenin signaling pathways. Future investigation could elucidate the precise mechanism of abrogation of androgenetic alopecia in the setting of psoriasis, which could lead to a development of new treatments for the prevention of hair loss in the androgenetic alopecia.  

 

Mr Lemchak is a fourth-year osteopathic medical student at Lake Erie College of Osteopathic Medicine in Erie, PA.

Dr Akilov is assistant professor of dermatology and director of the cutaneous lymphoma program, both at the University of Pittsburgh Medical Center in Pittsburgh, PA.

 

Disclosure: The authors report no relevant financial relationships.  

 

References

1. Harris JE, Seykora JT, Lee RA. Renbok phenomenon and contact sensitization in a patient with alopecia universalis. Arch Dermatol. 2010;146(4):422-425.

2. Oiso N, Kawada A. Renbok phenomenon in a patient with alopecias areata universalis and psoriasis. J Dermatol. 2012;39(3):288-289.

3. Chen W. Alopecia areata universalis sparing nevus flammeus. Dermatology. 2005;210(3):227-228.

4. Sawan S, Descamps V. Scalp psoriasis: a paradigm of “switch-on” mechanism to anagen hair growth? Arch Dermatol. 2008;144(8):1064-1066.

5. Donovan JG, Goldstein BG, Goldenstein AO. Androgenic alopecia in men: pathogenesis, clinical features, and diagnosis. UpToDate. http://www.uptodate.com/contents/androgenetic-alopecia-in-men-pathogenesis-clinical-features-and-diagnosis. Updated March 9, 2016. Accessed April 25, 2016.

6. El-Komy M, Amin I, Zidan A, Kadry D, Zeid OA, Shaker O. Insulin-like growth factor-1 in psoriatic plaques treated with PUVA and methotrexate. J Eur Acad Dermatol Venereol. 2011;25(11):1288-1294.

7. Panchaprateep R, Asawanonda P. Insulin-like growth factor-1: roles in androgenetic alopecia. Exp Dermatol. 2014;23(3):216-218.

8. Li J, Yang Z, Li Z, Gu L, Wang Y, Sung C. Exogenous IGF-1 promotes hair growth by stimulating cell proliferation and down regulating TGF-ß1 in C57BL/6 mice in vivo. Growth Horm IGF Res. 2014;24(2-3):89-94.

9. Philpott MP, Sanders DA, Kealey T. Effects of insulin and insulin-like growth factors on cultured human hair follicles: IGF-I at physiologic concentrations is an important regulator of hair follicle growth in vitro. J Invest Dermatol.1994;102(6):857-861.

10. Hamada K, Randall VA. Inhibitory autocrine factors produced by the mesenchyme-derived hair follicle dermal papilla may be a key to male pattern baldness. Br J Dermatol. 2006;154(4):609-618.

11. Mak KK, Chan SY. Epidermal growth factor as a biologic switch in hair growth cycle. J Biol Chem. 2003;278(28):26120-26126.

12. Flisiak I, Szterling-Jaworowska M, Baran A, Rogalska-Taranta M. Effect of psoriasis activity on epidermal growth factor (EGF) and the concentration of soluble EGF receptor in serum and plaque scales. Clin Exp Dermatol. 2014;39(4):461-467.

13. Choi YS, Zhang Y, Xu M, et al. Distinct functions for Wnt/ß-catenin in hair follicle stem cell proliferation and survival and interfollicular epidermal homeostasis. Cell Stem Cell. 2013;13(6):720-733.

14. Kretzschmar K, Cottle DL, Schweiger PJ, Watt FM. The androgen receptor antagonizes wnt/ ß-catenin signaling in epidermal stem cells. J Invest Dermatol. 2015;135(11):2753-2763.

15. El-Wahed Gaber MA, El-Halim Kandil MA, El-Farargy SM, Galbet DA. Beta-catenin expression in psoriasis. Indian Dermatol Online J. 2015;6(1):13-16.

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