Lichen simplex chronicus

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karnik Raju Paila Bangaru, M.B.B.S.[2]

Synonyms and keywords: Neurodermatitis, neurodermatitides, circumscribed neurodermatitis, circumscribed neurodermatitides, localized neurodermatitis, localized neurodermatitides

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Overview

Lichen simplex chronicus (LSC) is a chronic skin condition associated with a persistent itch-scratch cycle, leading to a thick, leathery, dark (lichenified) skin. Similar to many other skin conditions, it may present with associated dryness, scaling or erythema. Commonly affected regions include neck, ankles, extremities, scalp and genital region. The incidence and prevalence of the condition are not well established, but this is observed to be more common in adult female patients. The pathophysiology remains unclear, but it's thought to arise from disturbances between central and peripheral neural tissue in the perception of itch, causing that persistent itch-scratch cycle. Several psychological disturbances like anxiety and depression have been associated with this dermatological condition.

Pathophysiology

  • LSC develops over the regions which are accessible to scratching.[1][2][3][4]
  • The pathogenesis of LSC is unclear, but clinical lesions are due to severe paroxysmal pruritus. The physical and emotional component of the cause are well known, compared to genetic, vascular and neurogenic component.
  • Skin with atopic dermatitis and atopic diathesis is most likely to develop lichenification.
  • There could be a potential relationship between central and peripheral neural tissue and inflammatory mediators in the perception of itch, leading to changes underlying LSC.
  • Emotional disturbances such as anxiety, depression and obsessive-compulsive disorder or other stressors contribute to itching in many cases. [5][6][7]
  • Some studies tried to find genetic support to pathology of LSC. Like, Serotonin transporter (5HTT) gene polymorphism and dysfunction association to LSC [8]. Transient receptor potential channel A1 ( TRPA1) which is seen in skin, sensory neuron and other tissues has been associated with decreased expression in the lesions of LSC. [9] Long interspersed element-1 (LINE-1) pattern changes in epidermis of LSC was found in a study. [10]
  • On microscopic histopathological analysis, LSC appears as a hyperkeratotic plaque, with parakeratosis, acanthosis, spongiosis, papillary dermal fibrosis with vertical streaking of collagen bundles, irregularly thickened rete edges, and pseudoepitheliomatous hyperplasia. Electron microscopy shows collagen fibers attached to and above lamina basalis.

Causes

The most common cause of LSC is emotional factors. Other causes of LSC include atopic dermatitis, eczema, mechanical trauma, extremes of temperature/humidity, scars, xerosis, psoriasis, insect bites, lithium [11], p-phenylenediamine (PPD) [12], and others.

Differentiating [disease name] from other Diseases

  • LSC must be differentiated from other diseases that cause thickened skin lesions such as:

Epidemiology and Demographics

  • LSC has been estimated to occur among 12% of the people around the world.

Age

  • LSC is more commonly observed among patients aged 30 to 50 years old.

Gender

  • LSC is more commonly affected to females than males.
  • The female to male ratio is approximately 2:1.

Race

  • Previous studies in past have shown LSC more common in African Americans and Asians.

Natural History, Complications and Prognosis

  • Prognosis is generally good with treatment, but some become persistent lesions.
  • Special association with erectile dysfunction is seen in some studies. [13]
  • Some cases of malignant transformation of the lesion into squamous cell carcinoma or verrucous carcinoma is seen.

Diagnosis

History and Symptoms

  • Diagnosis of LSC includes physical exams, history and dermoscopy. The most common symptom is Itching. LSC mostly occurs in easy to reach areas like head, neck, extensor sides of forearm, scalp, vulva, pubis, and scrotum. It can occur as a single or multiple lesions. Itching usually occurs in the night time, and its mostly absent when active.

Physical Examination

  • Lesions appear erythematous, scaly, well demarcated, rough plaques eventually turning into thickened and hyperpigmented due to chronic pruritus. These plaques can vary in size from 3 by 6 centimeters to 6 by 10 centimeters. The color of the lesion varies according to the stage of lesion.

Laboratory Findings

  • There are no specific laboratory findings associated with LSC. You can do few tests to identify the stressor behind the disease like serum IgE levels to support underlying atopy.

Other Diagnostic Studies

Treatment

Medical Therapy

  • The mainstay of therapy for LSC is to reduce pruritus and support the lesion and body to heal.
  • Topical anti-inflammatory therapy like corticosteroids, topical emollients, anti-histamines, and antibiotics if suspicion of secondary infection.
  • Corticosteroids decreases the inflammation, and also improve the lesion hyperkeratosis. Depending on the size, extent and location of lesion, choice of corticosteroid(mild or high potent topical preparations) is made. Intralesional steroid injections are used for refractory cases.[19][20]
  • Occlusion has been observed to improve the treatment effectiveness. Also, it prevents from scratching. [21]
  • Psychological treatment, such as psychotherapy, as well as drugs like anti-anxiety medications are found to be effective, because of the emotional factors of the disease.
  • Other treatments like Doxepin and capsaicin, aspirin/dichloromethane, immunomodulators like tacrolimus and pimecrolimus, and injections of botulinum toxins. [22]

Surgical/ Other therapy

Prevention

  • Effective measures for the primary prevention of LSC include helping patients to minimize scratching on individual basis. Treating the underlying mental disorder if its involved in the etiology of disease.

"Lichen Simplex Chronicus - StatPearls - NCBI Bookshelf". "Lichen Simplex Chronicus: Background, Pathophysiology, Etiology".

References

  1. Juarez, Michelle C.; Kwatra, Shawn G. (2020). "A systematic review of evidence based treatments for lichen simplex chronicus". Journal of Dermatological Treatment: 1–9. doi:10.1080/09546634.2019.1708856. ISSN 0954-6634.
  2. Boozalis, Emily; Tang, Olive; Patel, Shivani; Semenov, Yevgeniy R.; Pereira, Manuel P.; Stander, Sonja; Kang, Sewon; Kwatra, Shawn G. (2018). "Ethnic differences and comorbidities of 909 prurigo nodularis patients". Journal of the American Academy of Dermatology. 79 (4): 714–719.e3. doi:10.1016/j.jaad.2018.04.047. ISSN 0190-9622.
  3. Whang KA, Khanna R, Thomas J, Aguh C, Kwatra SG (2019). "Racial and Gender Differences in the Presentation of Pruritus". Medicines (Basel). 6 (4). doi:10.3390/medicines6040098. PMC 6963580 Check |pmc= value (help). PMID 31569651.
  4. Huang, Amy H.; Canner, Joseph K.; Khanna, Raveena; Kang, Sewon; Kwatra, Shawn G. (2020). "Real-World Prevalence of Prurigo Nodularis and Burden of Associated Diseases". Journal of Investigative Dermatology. 140 (2): 480–483.e4. doi:10.1016/j.jid.2019.07.697. ISSN 0022-202X.
  5. Lotti T, Buggiani G, Prignano F (2008). "Prurigo nodularis and lichen simplex chronicus". Dermatol Ther. 21 (1): 42–6. doi:10.1111/j.1529-8019.2008.00168.x. PMID 18318884.
  6. Tsintsadze N, Beridze L, Tsintsadze N, Krichun Y, Tsivadze N, Tsintsadze M (2015). "PSYCHOSOMATIC ASPECTS IN PATIENTS WITH DERMATOLOGIC DISEASES". Georgian Med News (243): 70–5. PMID 26087735.
  7. Liao YH, Lin CC, Tsai PP, Shen WC, Sung FC, Kao CH (2014). "Increased risk of lichen simplex chronicus in people with anxiety disorder: a nationwide population-based retrospective cohort study". Br J Dermatol. 170 (4): 890–4. doi:10.1111/bjd.12811. PMID 24372057.
  8. Kirtak N, Inaloz HS, Akçali C, Erdal E, Herken H, Yildirim M; et al. (2008). "Association of serotonin transporter gene-linked polymorphic region and variable number of tandem repeat polymorphism of the serotonin transporter gene in lichen simplex chronicus patients with psychiatric status". Int J Dermatol. 47 (10): 1069–72. doi:10.1111/j.1365-4632.2008.03821.x. PMID 18986359.
  9. Qiu Y, Tang N, Zhang W, Xiong JX, Hu L, Cai T (2020). "Down-regulated expression of transient receptor potential ankyrin 1 in lichen simplex chronicus". Ann Palliat Med. 9 (6): 3757–3765. doi:10.21037/apm-20-1712. PMID 33183050 Check |pmid= value (help).
  10. Yooyongsatit S, Ruchusatsawat K, Supiyaphun P, Noppakun N, Mutirangura A, Wongpiyabovorn J (2013). "Alterations in the LINE-1 methylation pattern in patients with lichen simplex chronicus". Asian Pac J Allergy Immunol. 31 (1): 51–7. PMID 23517394.
  11. Shukla S, Mukherjee S (1984). "Lichen simplex chronicus during lithium treatment". Am J Psychiatry. 141 (7): 909–10. doi:10.1176/ajp.141.7.909. PMID 6428244.
  12. Chey WY, Kim KL, Yoo TY, Lee AY (2004). "Allergic contact dermatitis from hair dye and development of lichen simplex chronicus". Contact Dermatitis. 51 (1): 5–8. doi:10.1111/j.0105-1873.2004.00252.x. PMID 15291824.
  13. Juan CK, Chen HJ, Shen JL, Kao CH (2015). "Lichen Simplex Chronicus Associated With Erectile Dysfunction: A Population-Based Retrospective Cohort Study". PLoS One. 10 (6): e0128869. doi:10.1371/journal.pone.0128869. PMC 4468076. PMID 26076496.
  14. Sand FL, Thomsen SF (2018). "Skin diseases of the vulva: eczematous diseases and contact urticaria". J Obstet Gynaecol. 38 (3): 295–300. doi:10.1080/01443615.2017.1329283. PMID 28780897.
  15. Chibnall R (2017). "Vulvar Pruritus and Lichen Simplex Chronicus". Obstet Gynecol Clin North Am. 44 (3): 379–388. doi:10.1016/j.ogc.2017.04.003. PMID 28778638.
  16. Muylaert BPB, Borges MT, Michalany AO, Scuotto CRC (2018). "Lichen simplex chronicus on the scalp: exuberant clinical, dermoscopic, and histopathological findings". An Bras Dermatol. 93 (1): 108–110. doi:10.1590/abd1806-4841.20186493. PMC 5871373. PMID 29641708.
  17. Voicu C, Tebeica T, Zanardelli M, Mangarov H, Lotti T, Wollina U; et al. (2017). "Lichen Simplex Chronicus as an Essential Part of the Dermatologic Masquerade". Open Access Maced J Med Sci. 5 (4): 556–557. doi:10.3889/oamjms.2017.133. PMC 5535688. PMID 28785363.
  18. Fruchter R, Melnick L, Pomeranz MK (2017). "Lichenoid vulvar disease: A review". Int J Womens Dermatol. 3 (1): 58–64. doi:10.1016/j.ijwd.2017.02.017. PMC 5419035. PMID 28492056.
  19. Brunner N, Yawalkar S (1991). "A double-blind, multicenter, parallel-group trial with 0.05% halobetasol propionate ointment versus 0.1% diflucortolone valerate ointment in patients with severe, chronic atopic dermatitis or lichen simplex chronicus". J Am Acad Dermatol. 25 (6 Pt 2): 1160–3. doi:10.1016/0190-9622(91)70317-u. PMID 1757609.
  20. Datz B, Yawalkar S (1991). "A double-blind, multicenter trial of 0.05% halobetasol propionate ointment and 0.05% clobetasol 17-propionate ointment in the treatment of patients with chronic, localized atopic dermatitis or lichen simplex chronicus". J Am Acad Dermatol. 25 (6 Pt 2): 1157–60. doi:10.1016/0190-9622(91)70316-t. PMID 1757608.
  21. Geraldez MC, Carreon-Gavino M, Hoppe G, Costales A (1989). "Diflucortolone valerate ointment with and without occlusion in lichen simplex chronicus". Int J Dermatol. 28 (9): 603–4. doi:10.1111/j.1365-4362.1989.tb02538.x. PMID 2583907.
  22. Day T, Bohl TG, Scurry J (2016). "Perianal lichen dermatoses: A review of 60 cases". Australas J Dermatol. 57 (3): 210–5. doi:10.1111/ajd.12308. PMID 25752318.
  23. Engin B, Tufekci O, Yazici A, Ozdemir M (2009). "The effect of transcutaneous electrical nerve stimulation in the treatment of lichen simplex: a prospective study". Clin Exp Dermatol. 34 (3): 324–8. doi:10.1111/j.1365-2230.2008.03086.x. PMID 19175614.

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