Lichen Simplex Chronicus Medication

Updated: Aug 20, 2020
  • Author: Jason Schoenfeld, MD; Chief Editor: William D James, MD  more...
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Medication Summary

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



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


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.


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.


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.


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.