eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses

Lichen Simplex Chronicus: Treatment & Medication

Author: Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), NOVA Southeastern University; Investigator, Hill Top Research, Florida Research Center
Coauthor(s): Stephen H Mason, MD, Assistant Professor of Dermatology, Medical College of Georgia; Siobahn M Bower, MD, Internal Medicine Resident, Creighton University
Contributor Information and Disclosures

Updated: Oct 15, 2009

Treatment

Medical Care

Treatment is aimed at reducing pruritus and minimizing existing lesions because rubbing and scratching cause lichen simplex chronicus.

• Topical steroids are the current treatment of choice because they decrease inflammation and itch while concurrently softening the hyperkeratosis.^13,14,15 Because lesions are by nature chronic, treatment most likely is lifelong. On larger and more active lesions, a midpotency steroid may be used to treat acute inflammation. Occasionally, occlusion is used to increase potency and enhance delivery of the agent. Occlusion also provides a physical barrier to the scratching. Midpotency topical steroids are not recommended for thin skin (eg, vulva, scrotum, axilla, face). Direct long-term therapy more at daily use of low-potency nontrophogenic topical corticosteroids. High-potency topical corticosteroids may be used for 3-week courses on thicker-skinned areas.
• Oral antianxiety medications and sedation may be considered in certain patients. According to individual need, treatment can be scheduled throughout the day, at bedtime, or both. Antihistamines such as diphenhydramine (Benadryl) and hydroxyzine (Atarax) are common. Doxepin (Sinequan) and clonazepam (Klonopin) may be considered in appropriate cases.
• For infected lesions, a topical or oral antibiotic can be considered.
• Other topical medications reported to decrease pruritus include doxepin cream¹⁶ and capsaicin cream.¹⁷
• One study suggests that topical aspirin/dichloromethane is effective in patients with lichen simplex chronicus who have not responded to topical corticosteroids.¹⁸
• For topical corticosteroid unresponsive patients or those with lesions on thin skin, a few case reports and small studies have shown efficacy of topical immunomodulators tacrolimus and pimecrolimus.¹⁹
• A more investigational treatment for patients who fail conventional therapy is local botulinum toxin injections.^20,21
• A clinical guideline summary from the American College of Obstetricians and Gynecologists, Diagnosis and management of vulvar skin disorders, may be helpful.²²

Consultations

• Consultation with a dermatologist may be considered for severe cases requiring more than topical treatments or to facilitate patch testing.
• Consultation with an allergist may be considered in individuals with multisystemic atopic symptoms.
• Consultation with a psychiatrist may be necessary for patients with severe stress or compulsive scratching.

Medication

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

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli. Decrease pruritus, thin lichenification, and reduce inflammation.

Clobetasol (Temovate)

Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Betamethasone dipropionate cream 0.05%(Diprolene, Betatrex)

For inflammatory dermatoses responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.

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

Medium potency topical corticosteroid that inhibits cell proliferation; also is immunosuppressive, antiproliferative, and anti-inflammatory. Flurandrenolide tape (4 mcg/cm²; Cordran tape) combines this potent topical steroid with the benefits of occlusion.

Triamcinolone 0.025%, 0.1%, 0.5% cream or ointment (Perrigo)

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Hydrocortisone valerate cream 0.2% (Westcort)

An adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects, resulting in anti-inflammatory activity.

Fluocinonide cream 0.1% or 0.05% (Lidex)

High-potency topical corticosteroid that inhibits cell proliferation. Has immunosuppressive and anti-inflammatory properties.

Antipruritic agents

Oral agents may control itching by blocking effects of endogenously released histamine. Decrease 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)

For symptomatic relief of pruritus caused by release of histamine.

Chlorpheniramine (Chlor-Trimeton)

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

Hydroxyzine (Atarax, Vistaril)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.

Clonazepam (Klonopin)

For anxiety associated with pruritus. Binds receptors at several sites within the CNS, including the limbic system and reticular formation. Effects may be mediated through GABA receptor system.

Pramoxine (Itch-X)

Blocks nerve conduction and impulses by inhibiting depolarization of neurons. Hypoallergenic topical anesthetic. 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)

Inhibits histamine and acetylcholine activity. Widespread use produces sedation, as does its use in areas of high percutaneous absorption (eg, genitals). Many individuals develop allergy to topical doxepin.

Immunosuppressant Agent

Tacrolimus (Protopic)

Mechanism of action in LSC unknown. Reduces itching and inflammation by suppressing release of cytokines from T cells. 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, may inhibit release of preformed mediators from skin mast cells and basophils and down-regulate expression of FCeRI on Langerhans cells. Can be used in patients as young as 2 y. Drugs of this class are more expensive than topical corticosteroids. Available as ointment in concentrations of 0.03 and 0.1%. Indicated only after other treatment options have failed.

Immune Modulator

Pimecrolimus (Elidel)

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

Neuromuscular Blocker Agent, Toxin

Botulinum toxin type A (BOTOX ®)

One of several toxins produced by Clostridium botulinum. 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. Toxin does not affect synthesis or storage of acetylcholine or conduction of electrical signals along the nerve fiber. 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 24-72 h delay between administration of toxin and onset of clinical effects exists, which terminate in 2-6 mo.
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. Patient should receive 5-10 injections per visit.
Must be reconstituted from vacuum-dried toxin into 0.9% sterile saline without preservative using manufacturer's instructions to provide injection volume of 0.1 mL; must be used within 4 h of storage in refrigerator at 2-8°C.
Preconstituted dry powder must be stored in freezer at <5°C.
Injections of BTA must be repeated at varying intervals to maintain long-term results.

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