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Lichen Simplex Chronicus Medication

  • Author: Jason Schoenfeld, MD; Chief Editor: William D James, MD  more...
 
Updated: Mar 30, 2016
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.They decrease pruritus, thin lichenification, and reduce inflammation.

Clobetasol (Temovate)

 

Clobetasol is a class I superpotent topical steroid; it suppresses mitosis and increases the synthesis of proteins that decrease inflammation and cause vasoconstriction.

Betamethasone dipropionate cream 0.05% (Diprolene, Betatrex)

 

Betamethasone dipropionate cream 0.05% is for inflammatory dermatoses responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It affects the production of lymphokines and has an inhibitory effect on Langerhans cells.

Fluocinolone 0.01% or 0.025% cream (Synalar, Synalar HP, Fluonid)

 

Fluocinolone is a medium potency topical corticosteroid that inhibits cell proliferation; it also is immunosuppressive, antiproliferative, and anti-inflammatory. Flurandrenolide tape (4 mcg/cm2; Cordran tape) combines a topical steroid with the benefits of occlusion and is classified as a group I (potency) preparation.

Triamcinolone topical (Perrigo)

 

Triamcinolone topical is for inflammatory dermatoses responsive to steroids; it decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Hydrocortisone valerate cream 0.2% (Westcort)

 

Hydrocortisone valerate cream is an adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. It has mineralocorticoid and glucocorticoid effects, resulting in anti-inflammatory activity.

Fluocinonide

 

Fluocinonide is a high-potency topical corticosteroid that inhibits cell proliferation. It has immunosuppressive and anti-inflammatory properties.

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Antipruritic agents

Class Summary

Oral agents may control itching by blocking effects of endogenously released histamine. They may decrease the sense of pruritus, sedate/calm patients, and induce sleep. Topical agents stabilize neuronal membrane and prevent the initiation and transmission of nerve impulses, thereby producing local anesthetic action.

Diphenhydramine (Benadryl, Benylin, Diphen, AllerMax)

 

Diphenhydramine is for symptomatic relief of pruritus caused by the release of histamine.

Chlorpheniramine (Chlor-Trimeton)

 

Chlorpheniramine competes with histamine or H1-receptor sites on effector cells in blood vessels and the respiratory tract.

Hydroxyzine (Atarax, Vistaril)

 

Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the CNS.

Clonazepam (Klonopin)

 

Clonazepam is for anxiety associated with pruritus. It binds receptors at several sites within the CNS, including the limbic system and reticular formation. Its effects may be mediated through the GABA receptor system.

Pramoxine topical (Itch-X)

 

Pramoxine topical blocks nerve conduction and impulses by inhibiting the depolarization of neurons. It is a hypoallergenic topical anesthetic. It contains 0.5% menthol and 0.5% camphor, which are nonstaining agents that provide a subjective cooling effect to the skin and are much preferred to rubbing or scratching the skin.

Doxepin (Sinequan; Zonalon Cream)

 

Doxepin inhibits histamine and acetylcholine activity. Widespread topical use produces sedation, as does its use in areas of high percutaneous absorption (eg, genitals). Many individuals develop an allergy to topical doxepin. It is marketed orally as an antidepressant but is used for its antihistamine/antipruritic effects also.

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Immunosuppressant Agent

Tacrolimus ointment (Protopic)

 

Tacrolimus ointment's mechanism of action in LSC is unknown. It reduces itching and inflammation by suppressing the release of cytokines from T cells. It also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, it may inhibit the release of preformed mediators from skin mast cells and basophils and down-regulate the expression of FCeRI on Langerhans cells. It can be used in patients as young as 2 years. Drugs of this class are more expensive than topical corticosteroids. It is available as ointment in concentrations of 0.03 and 0.1%. It is indicated only after other treatment options have failed.

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Immune Modulator

Pimecrolimus (Elidel)

 

Pimecrolimus is derived from ascomycin, a natural substance produced by the fungus Streptomyces hygroscopicus var ascomyceticus. It selectively inhibits the production and release of inflammatory cytokines from activated T cells by binding to the cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids. It is indicated only after other treatment options have failed.

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Neuromuscular Blocker Agent, Toxin

OnabotulinumtoxinA (BOTOX®)

 

OnabotulinumtoxinA is one of several toxins produced by Clostridium botulinum. It blocks neuromuscular transmission through a 3-step process, as follows: (1) blockade of neuromuscular transmission; botulinum toxin type A (BTA) binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. (2) BTA is internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. (3) BTA blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter. The affected terminals are inhibited from stimulating muscle contraction. The toxin does not affect the synthesis or storage of acetylcholine or conduction of electrical signals along the nerve fiber. It prevents calcium-dependent release of acetylcholine and produces a state of denervation at the neuromuscular junction and postganglionic sympathetic cholinergic nerves in the sweat glands.

Typically, a 24- to 72-hour delay between administration of toxin and onset of clinical effects exists, which terminate in 2-6 months.

This purified neurotoxin complex is a vacuum-dried form of purified BTA, which contains 5 ng of neurotoxin complex protein per 100 U.

BTA has to be reconstituted with 2 mL of 0.9% sodium chloride diluent. With this solution, each 0.1 mL results in 5-U dose. The patient should receive 5-10 injections per visit.

OnabotulinumtoxinA must be reconstituted from vacuum-dried toxin into 0.9% sterile saline without preservative using the manufacturer's instructions to provide injection volume of 0.1 mL; it must be used within 4 hours of storage in the refrigerator at 2-8°C.

Preconstituted dry powder must be stored in the freezer at colder than 5°C.

Injections of BTA must be repeated at varying intervals to maintain long-term results.

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Contributor Information and Disclosures
Author

Jason Schoenfeld, MD Resident Physician, Department of Dermatology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences

Disclosure: Nothing to disclose.

Coauthor(s)

Thomas N Helm, MD Clinical Professor of Dermatology and Pathology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Director, Buffalo Medical Group Dermatopathology Laboratory

Thomas N Helm, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society of Dermatopathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Daniel J Hogan, MD Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Canadian Dermatology Association

Disclosure: Nothing to disclose.

James J Nordlund, MD Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Stephen H Mason, MD 

Stephen H Mason, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery, Women's Dermatologic Society, Skin Cancer Foundation

Disclosure: Nothing to disclose.

Siobahn M Hruby, MD Internal Medicine Physician, Boys Town National Research Hospital

Siobahn M Hruby, MD is a member of the following medical societies: American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.

References
  1. Weyers W, Weyers I, Bonczkowitz M, Diaz-Cascajo C, Schill WB. Lichen amyloidosus: a consequence of scratching. J Am Acad Dermatol. 1997 Dec. 37(6):923-8. [Medline].

  2. Weyers W. [Lichen amyloidosus--disease entity or the effect of scratching]. Hautarzt. 1995 Mar. 46(3):165-72. [Medline].

  3. Lotti T, Buggiani G, Prignano F. Prurigo nodularis and lichen simplex chronicus. Dermatol Ther. 2008 Jan-Feb. 21(1):42-6. [Medline].

  4. Tsintsadze N, Beridze L, Tsintsadze N, Krichun Y, Tsivadze N, Tsintsadze M. PSYCHOSOMATIC ASPECTS IN PATIENTS WITH DERMATOLOGIC DISEASES. Georgian Med News. 2015 Jun. 70-5. [Medline].

  5. Liao YH, Lin CC, Tsai PP, Shen WC, Sung FC, Kao CH. Increased risk of lichen simplex chronicus in people with anxiety disorder: a nationwide population-based retrospective cohort study. Br J Dermatol. 2014 Apr. 170 (4):890-4. [Medline].

  6. Juan CK, Chen HJ, Shen JL, Kao CH. Lichen Simplex Chronicus Associated With Erectile Dysfunction: A Population-Based Retrospective Cohort Study. PLoS One. 2015. 10 (6):e0128869. [Medline].

  7. Ball SB, Wojnarowska F. Vulvar dermatoses: lichen sclerosus, lichen planus, and vulval dermatitis/lichen simplex chronicus. Semin Cutan Med Surg. 1998 Sep. 17(3):182-8. [Medline].

  8. Pleimes M, Wiedemeyer K, Hartschuh W. [Lichen simplex chronicus of the anal region and its differential diagnoses : A case series.]. Hautarzt. 2009 Mar 7. [Medline].

  9. Juan CK, Chen HJ, Shen JL, Kao CH. Lichen Simplex Chronicus Associated With Erectile Dysfunction: A Population-Based Retrospective Cohort Study. PLoS One. 2015. 10 (6):e0128869. [Medline].

  10. Simonetta C, Burns EK, Guo MA. Vulvar Dermatoses: A Review and Update. Mo Med. 2015 Jul-Aug. 112 (4):301-7. [Medline].

  11. Guerrero A, Venkatesan A. Inflammatory Vulvar Dermatoses. Clin Obstet Gynecol. 2015 Sep. 58 (3):464-75. [Medline].

  12. Khaitan BK, Sood A, Singh MK. Lichen simplex chronicus with a cutaneous horn. Acta Derm Venereol. 1999 May. 79(3):243. [Medline].

  13. Gerritsen MJ, Gruintjes FW, Andreissen MA, van der Valk PG, van de Kerkhof PC. Lichen simplex chronicus as a complication of herpes zoster. Br J Dermatol. 1998 May. 138(5):921-2. [Medline].

  14. Burkhart CG, Burkhart CN. Acne keloidalis is lichen simplex chronicus with fibrotic keloidal scarring. J Am Acad Dermatol. 1998 Oct. 39(4 Pt 1):661. [Medline].

  15. Woodruff PW, Higgins EM, du Vivier AW, Wessely S. Psychiatric illness in patients referred to a dermatology-psychiatry clinic. Gen Hosp Psychiatry. 1997 Jan. 19(1):29-35. [Medline].

  16. Shukla S, Mukherjee S. Lichen simplex chronicus during lithium treatment. Am J Psychiatry. 1984 Jul. 141(7):909-10. [Medline].

  17. Chey WY, Kim KL, Yoo TY, Lee AY. Allergic contact dermatitis from hair dye and development of lichen simplex chronicus. Contact Dermatitis. 2004 Jul. 51(1):5-8. [Medline].

  18. Ising H, Lange-Asschenfeldt H, Lieber GF, Weinhold H, Eilts M. [Effects of long-term exposure to street traffic exhaust on the development of skin and respiratory tract diseases in children]. Schriftenr Ver Wasser Boden Lufthyg. 2003. 81-99. [Medline].

  19. Thaipisuttikul Y. Pruritic skin diseases in the elderly. J Dermatol. 1998 Mar. 25(3):153-7. [Medline].

  20. Brunner N, Yawalkar S. 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. 1991 Dec. 25(6 Pt 2):1160-3. [Medline].

  21. Datz B, Yawalkar S. 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. 1991 Dec. 25(6 Pt 2):1157-60. [Medline].

  22. Geraldez MC, Carreon-Gavino M, Hoppe G, Costales A. Diflucortolone valerate ointment with and without occlusion in lichen simplex chronicus. Int J Dermatol. 1989 Nov. 28(9):603-4. [Medline].

  23. Drake LA, Millikan LE. The antipruritic effect of 5% doxepin cream in patients with eczematous dermatitis. Doxepin Study Group. Arch Dermatol. 1995 Dec. 131(12):1403-8. [Medline].

  24. Kantor GR, Resnik KS. Treatment of lichen simplex chronicus with topical capsaicin cream. Acta Derm Venereol. 1996 Mar. 76(2):161. [Medline].

  25. Yosipovitch G, Sugeng MW, Chan YH, Goon A, Ngim S, Goh CL. The effect of topically applied aspirin on localized circumscribed neurodermatitis. J Am Acad Dermatol. 2001 Dec. 45(6):910-3. [Medline].

  26. Kelekci HK, Uncu HG, Yilmaz B, Ozdemir O, Sut N, Kelekci S. Pimecrolimus 1% cream for pruritus in postmenopausal diabetic women with vulvar lichen simplex chronicus: A prospective non-controlled case series. J Dermatolog Treat. 2008 Apr 11. 1-5. [Medline].

  27. Heckmann M, Heyer G, Brunner B, Plewig G. Botulinum toxin type A injection in the treatment of lichen simplex: an open pilot study. J Am Acad Dermatol. 2002 Apr. 46(4):617-9. [Medline].

  28. Messikh R, Atallah L, Aubin F, Humbert P. [Botulinum toxin in disabling dermatological diseases]. Ann Dermatol Venereol. 2009 May. 136 Suppl 4:S129-36. [Medline].

  29. Engin B, Tufekci O, Yazici A, Ozdemir M. The effect of transcutaneous electrical nerve stimulation in the treatment of lichen simplex: a prospective study. Clin Exp Dermatol. 2009 Apr. 34(3):324-8. [Medline].

 
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Plaque of lichen simplex chronicus demonstrating accentuated skin markings. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.
Area of lichen simplex chronicus originally believed to be chronic contact dermatitis. The true nature was revealed when the patient admitted to rubbing this area while watching television. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.
Plaques of lichen simplex chronicus on the hand.
Lichen simplex chronicus of the dorsal hand and wrist demonstrating increased skin thickness and accentuation of skin markings.
Plaque of lichen simplex chronicus of the leg with accentuated skin markings and excoriations.
H and E biopsy of lichen simplex chronicus from forearm skin viewed at 40x magnification. Note the characteristic hyperkeratosis, hypergranulosis, pseudoepitheliomatous hyperplasia, and papillary dermal fibrosis.
H and E biopsy of lichen simplex chronicus from forearm skin viewed at 100x magnification. Note the characteristic hyperkeratosis, hypergranulosis, pseudoepitheliomatous hyperplasia, and papillary dermal fibrosis.
 
 
 
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