Prurigo Nodularis Medication

The goal of pharmacotherapy for prurigo nodularis is to break the itch-scratch-itch cycle by reducing pruritus, rubbing, picking, and scratching. One should always consider and rule out treatable endogenous and exogenous causes of pruritus.

Class Summary

These agents may control itching by blocking the transmission of nerve impulse.

Pramoxine topical (Itch-X)

Blocks nerve conduction and impulses by inhibiting depolarization of neurons.

Capsaicin topical

Derived from plants of Solanaceae family. May render skin and joints insensitive to pain by depleting substance P in peripheral sensory neurons.

Class Summary

These agents regulate skin cell production and development.

Calcipotriene (Dovonex)

Synthetic vitamin D-3 analog. Used in the treatment of moderate plaque psoriasis.

Class Summary

These agents may be beneficial for patients with severe pruritus.

Methoxsalen (8-MOP, Oxsoralen)

Inhibits mitosis by binding covalently to pyrimidine bases in DNA when photoactivated by UV-A.

Trioxsalen (Trisoralen)

Inhibits mitosis by covalently binding, in presence of UV-A radiation, to pyrimidine bases in DNA.

Class Summary

These agents may control itching by blocking effects of endogenously released histamine but probably best used as a sedative to control pruritus, especially at night.

Diphenhydramine (Benadryl, Belix Oral)

First-line treatment. For symptomatic relief of pruritus caused by release of histamine.

Chlorpheniramine (Chlor-Trimeton)

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

Hydroxyzine (Anxanil, Atarax, Atozine, Durrax, Vistaril)

First-line treatment. Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS and can be used as an anxiolytic.

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. These agents also modify the body's immune response to diverse stimuli.

Triamcinolone (Kenalog)

First-line treatment if few lesions (for intralesional use).

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

Intramuscular injection may be used for widespread skin disorder, or intralesional injections may be used for localized skin disorder. Consider limiting total monthly dose to 20 mg to ensure HPA axis will not be suppressed.

Clobetasol (Temovate)

First-line treatment (for topical use). Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Ointment may be more efficacious than cream secondary to the former's occlusive properties.

Flurandrenolide (Cordran Tape)

First-line treatment (for topical use). Also helps protect nodule from continued trauma if tape is left in place.

Class Summary

These agents have immunomodulatory effects.

Thalidomide (Thalomid)

May suppress excessive production of tumor necrosis factor alpha (TNF-alpha), and may down-regulate selected cell-surface adhesion molecules involved in leukocyte migration.

If < 50 kg (110 lb), start at low end of dose regimen.

Can cause severe, life-threatening birth defects and is contraindicated in pregnant women. Also contraindicated in women of childbearing potential unless using 2 forms of reliable contraception and complying with serial pregnancy testing while on therapy.

Also contraindicated in sexually active men not using latex condom as barrier contraception. Drug available only under special restricted distribution program called STEPS (System for Thalidomide Education and Prescribing Safety) Program; only prescribers and pharmacists registered with this program may prescribe and dispense thalidomide. For more information, contact the Celgene Corporation at 1-888-423-5436.

Tacrolimus ointment (Protopic)

Mechanism of action in prurigo nodularis not known. 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 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.

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. 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. Indicated only after other treatment options have failed.

OnabotulinumtoxinA (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 botulinum toxin must be repeated at varying intervals to maintain long-term results.