Overview of treatment of vulvar skin disorders and pruritus


Treatment of most sexually transmitted infections is not considered in this section. Throughout this website, we refer you to the CDC website for the most updated information on sexually transmitted infections.

Successful management of epithelial disorders of the vulva is dependent upon more than a prescription topical. Elements of the treatment plan include:

  • Elimination of irritants (Annotation J: lifestyle issues)
  • Comfort measures and general skin therapy
  • Understanding proper use of steroids
  • Selection of the appropriate vehicle for treatment
  • Correct application of the treatment
  • Anti-bacterial, anti-viral, and anti-fungal therapy
  • Approaches to pruritus


Without this important step, therapeutics will be sabotaged by ongoing adverse conditions. Annotation J discusses in detail irritants that women frequently encounter from life style. These include anything that chafes or occludes the skin: tight clothing including jeans, thongs, lycra or spandex that does not breathe, panty hose, daily or frequent panty liner use, use of liners that absorb urine, feminine hygiene products, including some pads, douches, topical treatments, even if “natural,” tight underwear to bed, etc. Some sports activities such as bicycle riding, horseback riding, and sedentary behaviors such as sitting all day at computers or immobility due to health problems, may also exacerbate a vulvovaginal problem. Common medications may cause vulvar skin reactions, as may common household products such as soaps, bleaches, and detergents. Women may be over cleansing or scrubbing with rough cloths, or using hair dryers on their skin, etc. The impact of possible exposure to irritants cannot be underestimated when considering possible etiologies of a patient’s complaints.

In addition to hygiene and life style, external factors can intensify pruritus and pain. Overheated rooms, insulating clothing and the warmth of a bed at night are well known to alter comfort levels. Internal factors such as hot spices, alcohol, hot beverages, and a number of medications such as beta blockers and allopurinol intensify the perception of itch. Psychogenic factors such as tension and stress also play a role.

We instruct patients to look carefully at their lifestyle issues, to make note of “triggers” for increased discomfort, and to alter them significantly. A useful patient handout is Ten Suggestions for Keeping the Vulva and Vagina Healthy.


A useful patient handout is General Vulvar Care.

Soak and seal: Soaks are a mainstay of dermatologic treatment. Brief soaks in comfortable water serve several purposes.1 The water brings symptomatic relief from pruritus and pain. The soak also gently removes crusting, lessening the chance of bacterial or yeast overgrowth. Third, hydration temporarily restores the physiologic, moist environment that enhances healing and promotes comfort. Dry skin is an important factor in itching.2 Finally, soaks may be suggested at any point, to any patient without an examination.

Plain, comfortably warm water is all that is required: in the tub, in a sitz bath or with a hand held shower. If none of these is possible, compresses with wash cloths applied as the patient lies on a waterproof sheet will suffice. Five to ten minutes of soaking is adequate, repeated 3-4 times through the day, if necessary, depending on the severity of the condition. The patient pats dry gently, then seals in the moisture with a thin film of plain petrolatum (Vaseline®). We have come to call this “soak and seal” to make the concept easy for patients. (Warm soaks and patting dry are also recommended prior to application of medications for improved absorption.)

Petrolatum occludes the stratum corneum, but it neither forms nor acts like an epicutaneous impermeable membrane; instead, it also permeates throughout the stratum corneum interstices, allowing normal barrier recovery despite its occlusive properties.3 Despite many misconceptions to the contrary, petrolatum does not “block pores” and is noncomedogenic.4 Ever since its initial inclusion in the U.S. Pharmacopoeia in 1880, petrolatum’s beneficial properties for skin care and treatment have been extensively reported.5 Crisco®, mineral oil, or cooking oil are often used but have not been studied. The soak and seal process can be omitted after control of the condition is achieved.

Occasionally, a woman experiences loss of the epithelial barrier and sufficient pathology that even plain water burns. For these, a soak in physiological saline, one level teaspoon of salt per four cups of water is helpful. One cup of baking soda added to a tub of warm water may also be tolerated.

Women often find it difficult to believe that plain water and Vaseline® can help complex conditions for which they have been long seeking effective treatment. They need reassurance that these simple tools are the keys to success.

Other comfort measures

Cool gel packs, crushed ice, or frozen peas or corn in a protective bag applied to the irritated skin may be very soothing.


While many women can benefit from the commercially available medications that we will review below, it is important to be aware that some will react to the base in which the medication is formulated. Recommendations for treatment will depend upon the patient’s history. If many appropriate, commercially available drugs have been tried, compounding of medications with neutral bases may be advised.

Selection of the appropriate medication vehicle for vulvovaginal treatment

Numerous vehicles exist for skin treatment but gels, lotions, powders, and solutions are seldom used for vulvovaginal conditions. Ointments are preferred because of their freedom from the irritation caused by other vehicles, including creams. 6

Women often come for evaluation with a history of experiencing irritation and burning from all topical treatment agents. A common additive, propylene glycol (PG), accounts for much of this. PG is toxic when used as a solvent for administering other medications.7 Research has suggested that individuals who cannot tolerate propylene glycol probably experience a special form of irritation, but that they only rarely develop allergic contact dermatitis. Other investigators believe that the incidence of allergic contact dermatitis to propylene glycol may be greater than 2% in patients with eczema.8 The sensitizing potential of PG is well documented, but the true incidence of its role in allergic reaction is unknown. 9

Some molecules simply burn some people, e.g. lidocaine and estradiol.

When traditional prescriptions are not tolerated, compounding offers excellent control of the vehicle as well as the strength of the medication. In addition, medications can be combined, e.g. hydrocortisone with clotrimazole, or cleocin, estradiol and hydrocortisone. A compounding pharmacist can also minimize the burning sensation of difficult molecules such as lidocaine by pH-balancing the formulation: weakly acidic for the vagina, more neutral for the vulva.

Bases for compounding

Compounding pharmacies provide the selection of a number of bases, available to any compounding pharmacist. The two simplest and best-tolerated bases are:

  • Petrolatum Base: white petrolatum is approved as an active ingredient in over-the-counter (OTC) skin-protectant drug products as well as in ophthalmic10 and anorectal drug products.11 Petrolatum temporarily protects injured or exposed skin from harmful or annoying stimuli and may provide relief to such skin. It also slows the loss of water from the skin by forming a barrier on the skin’s surface. Petrolatum enhances the appearance and feel of hair, by increasing hair body, suppleness, or sheen, or by improving the texture of hair that has been damaged physically or by chemical treatment.
  • Methylcellulose: methylcellulose is also considered a non-irritating base.

Other well-tolerated bases that have a creamy texture to them include:

  • Neutral Base: stearyl alcohol, cetyl alcohol, polysorbate 80, Span 80 (sorbitan , monooleate), poloxamer 188, glycerine USP (Natural), Bace C (Polyglycol 300MW, NF Liquid), benzyl alcohol, distilled water
  • Vanishing Base: stearic acid, stearyl alcohol, cetyl alcohol, polyoxyl 40 stearate, isopropyl myristate
  • Stearyl Lanolin Base: stearyl, stewaric acid, lanolin, bees wax, white petrolatum, cottonseed oil, cetyl alcohol, mineral oil, gylcerine USP (Natural), Trolamine (triethanolamine), preserved water, sodium hydroxide

Multiple other bases are available but we avoid them because of their possibly sensitizing ingredients such as aloe and Vitamin E.

There are two bases for compounded suppositories:

  • MBK- hydrogenated vegetable oil, palm kernel oil, cottonseed oil, soybean oil, polythylene glycol 400 (solvent), distearate (emulsifier)
  • A/B suppository base- Base A polyglycol 1450 (carbowax), Base B polyglycol 3350 (miralax used for capsule coating). The A/B suppostiory does not melt as easily as MBK; compounders suggest that the suppository be moistened in water prior to insertion to facilitate melting.

Testing the vehicle

Providing a patient a base sample for testing prior to compounding the medication in it provides reassurance. The woman first applies the plain base to the forearm for 24 hours. If this is tolerated without erythema, itching or burning, she tries it on the vulva for a day or two. Lack of reaction in both areas indicates safety in using the compounded medication. If there is a reaction to this, one knows that the problem is the medication, not the base.

Irritation from compounds

When irritation occurs despite careful selection and testing of base, a first step is to dilute the compound by having the woman apply plain petrolatum prior to application. With this dilution, she may be able to work up to tolerating the compound.

If not, she may be intolerant of the medication placed in the base. If it is a steroid, substitution of another member of the steroid class prescribed, e.g., halobetasol for clobetasol, may prove successful. When no alternative exists, e.g., estradiol, weakening the strength from, e.g., 0.01% to 0.005% may be more effective than dilution with petrolatum.

It is possible that the irritation attributed to the topical is actually provoked vulvar pain from rubbing or manipulating the tissue to apply the topical.

If a woman continues to be intolerant of topical treatments despite all efforts, patch testing for allergies by a dermatologist who does North American Series patch testing may prove valuable. This testing is entirely different from prick tests done by allergists and from other patch testing that does not include as many substances as the North American Series.

Adequate instruction in application of topical treatment

The vulva is a mysterious area for many women who need help learning where to apply a topical and how much to apply. This instruction is best achieved by showing her with a large mirror, naming the anatomical parts and showing her where the ointment goes, then demonstrating with an office lubricant the exact amount to be used. Verbal explanation, even with a diagram, is not the same, especially since many patients do not look like the diagram.

Understanding proper use of steroids

Topical steroids

Corticosteroid medications, usually applied topically, but sometimes used intralesionally or intramuscularly, are the mainstay of treatment for many vulvar skin conditions. Oral prednisone is rarely used.

Steroids are confusing. Eight classes (I-VIII, ranked by their ability to vasoconstrict) represent their various potencies. The longer a steroid vasoconstricts, the more potent it is. In addition to reducing inflammation through constriction of cutaneous capillaries, directly decreasing erythema, steroids decrease the mitotic rate of rapidly proliferating epidermis and decrease fibroblast proliferation. 12

There is no such thing as the best steroid. As with estrogens or antibiotics, the choice always depends on the condition being treated, the patient’s age and reliability, other medical conditions, length of treatment, and potential side effects.

The best advice is to learn to use a few topical steroids well. Then use the lowest steroid potency that will manage the problem. Steroids are not a cure; chronic skin diseases require long-term therapy. Steroid-responsive vulvar dermatoses include thick scaly lesions (lichen sclerosus, psoriasis, lichen simplex chronicus), and blisters and erosions (lichen planus, dermatitis/eczema, bullous diseases).

Complexity can be eliminated by becoming familiar with four standard topical steroids.

A low potency steroid hydrocortisone is available as an OTC formulation of 1% or as prescription strength 2.5%. It is often used for mild eczema and for management of dermatitis in delicate areas of the groin and anus.

A mid-potency steroid is triamcinolone. Of several strengths, 0.1% is the most useful. It is given for treatment of adult eczema and may be used as maintenance for conditions initially controlled with stronger steroids.

A high potency steroid is fluocinonide in the 0.05% strength, used for severe eczema and lichen simplex chronicus.

A super potent steroid is clobetasol 0.05% needed for treatment of lichen sclerosus, lichen simplex chronicus, psoriasis, lichen planus, and erosive diseases.

Dose and application of topical steroid

Describing the amount to apply of a topical medication is always a challenge, and it is natural for women to want to apply a thick layer of ointment several times a day. Dosage terms used vary from the size of a pea, the size of a lead pencil eraser tip, a scant quarter inch from the tube to be spread in a thin film over the affected area. The amount really depends on the size of the affected tissue. We usually tell patients to use the smallest amount of ointment that will spread and we demonstrate with office lubricant exactly how far a small amount of ointment will spread.

An ounce or thirty grams is a standard dispensing quantity. One refill will be adequate to cover needs for a year. Patients with dermatoses need to be seen at least annually, so that unlimited refills or refills by phone are not advised. Topical steroids are often started at twice-daily intervals for two to four weeks. The patient is then seen and then tapered to once or twice-weekly maintenance if she is comfortable. If not, the daily intervals are continued for another two to four weeks. A reduction in potency can be tried and continued as maintenance if symptoms are controlled. (See the Treatment Plan tables for individual diseases for more precise directions in how steroids can be used in vulvovaginal care.)

Lack of improvement with topical steroid

If symptoms are not coming into control, the clinician needs to consider a variety of possibilities:

  • time (more than a few days, sometimes several weeks) is needed for steroid medications to relieve symptoms
  • irritants have not been eliminated Annotation J
  • the patient continues to scratch at night and needs sedation Approach to pruritus
  • there is superimposed bacterial or fungal infection  antibacterial therapy and antifungal therapy
  • the lesions are too thick for the steroid to penetrate intralesional steroids
  • there is a problem in compliance or proper use of the topical. Non-adherence is frequent if the woman is concerned that the steroid will damage the skin.
Side effects of steroids

Concern about side effects from steroids often prevents clinicians from prescribing them in adequate strength and duration of treatment, resulting in on-going discomfort for many women. All clinicians have been taught that potent corticosteroids should be avoided on genital skin and that use there would result in atrophy, steroid dermatitis, and steroid rosacea. The British taught us, however, that the ultra-potent steroids can be used safely and effectively for lichen sclerosus.13 The modified mucous membranes of the vulva are relatively resistant to the side effects of topical corticosteroids.14 In addition, the steroids mentioned above are all reasonably safe from systemic side effects, even for long-term use.15 Patients should be informed that the suppression of the hypo-thalamic-pituitary-adrenal axis, aseptic necrosis of the femoral head, irreversible striae formation, glaucoma, and cataracts are associated with long-term oral prednisone use, not with proper use of topical therapy. It would take 2 g of clobetasol (size of a sample tube) per day to suppress the adrenal axis.16

Patients need to understand that when topical steroids are used, depressed local immunity makes emergence of HSV or HPV, as well as Candida albicans, possible. Women should be evaluated to discern whether these conditions, versus symptoms from the dermatosis, are the basis of a flare. Potent steroids need to be avoided on relatively thin epithelium of the crural creases and the perianal skin. 17

Intralesional steroid therapy

Intralesional steroid injections are invaluable for recalcitrant hyperkeratosis of lichen sclerosus, lichen planus and lichen simplex chronicus, as well as for painful inflammatory nodules of hidradenitis suppurativa. These problems arise when topical steroids are inadequate to penetrate hyperkeratotic epithelium or when intolerance or non-compliance are problems.

Triamcinolone (Kenalog®) is the preparation used for these injections. This is a suspension that must be shaken thoroughly prior to withdrawal from the vial, and prior to injection. A 27 gauge needle is necessary for both processes. To minimize the possibility of atrophy, 10 mg/ml is diluted with 1 ml normal saline or 1% lidocaine. 0.1 ml will cover approximately one square cm of hyperkeratotic epithelium. For a nodule of hidradenitis, 0.5 ml injected into the center of the painful nodule will bring relief.

The injections, even with lidocaine, are painful, but bring excellent response within 24 hours.

Systemic steroid therapy: oral and intramuscular

Anogenital lesions are usually responsive to topical therapy but some conditions–erosive lichen planus, severe lichen simplex chronicus, Crohn disease, Behçet disease, severe aphthosis, and hidradenitis suppurativa–may require systemic management. This is usually achieved with oral Prednisone 40-60 mg daily for 7-10 days. If longer therapy is required, a taper to 20 mg for five days, and 10 mg for five days is necessary to prevent rebound and to allow for recovery of the hypothalamic-pituitary-adrenal axis.

Prednisone causes a number of short-term side effects. It is given in the morning to prevent insomnia. Caution is used for patients with bipolar disease or history of depression, and any patient may note a slight increase (agitation) or decrease (depression) in mood. Blood sugar will be elevated transiently, but in a diabetic may necessitate use of insulin or an increase in insulin doses. Elevated blood pressure may also occur. Transient adrenal suppression may occur and patients need instructions to tell any clinician involved in care that she is taking oral steroids. The long-term adverse effects of osteoporosis, cataract formation, aseptic necrosis are not seen if therapy is limited to less than a month.

Intramuscular triamcinolone (Kenalog®) represents a unique form of systemic steroid therapy. A dose of 60-80 mg is injected into the buttock or thigh as a depot covering approximately 21 days. The injection can be repeated monthly for a series of four injections for recalcitrant dermatoses. The same side effects are possible, but with resolution of the depot in 21 days, adrenal suppression is less of a concern. The same shaking of the suspension in the vial and in the syringe are necessary. In addition, a 1.5 inch needle to should be used to place the depot deep enough for effective sustained absorption and lessened risk of atrophy.

Calcineurin Inhibitors

Calcineurin inhibitors, pimecrolimus (Elidel®) and tacrolimus (Protopic®) possess anti-itch properties, as well as the ability to reduce skin inflammation, but are not associated with the side effects of steroids. They work by preventing T-cell activation, inhibiting cytokine release, and by down-regulating high affinity immunoglobulin E receptor expression on Langerhans cells.18 Their disadvantages include significant burning on application and the FDA’s public health advisory warning about the possibility of lymphoma and skin cancers in patients treated with these drugs. It has not been clearly established that the cancers reported are associated with the direct use of the calcineurin inhibitors. 19 Most dermatologists believe that any relationship between their use and the development of malignancy is coincidental rather than causal,20 but caution is advised with use for dermatoses that have an increased risk for squamous cell carcinoma, lichen sclerosus, and lichen planus.

Pimecrolimus comes in a single 1% strength; it is applied once or twice daily to bring the condition in control, then changed to a low dose steroid (hydrocortisone) for maintenance.

Tacrolimus comes in two strengths 0.03% and 0.1%. Because of the tendency to burn, it is best started in the 0.03% strength with petrolatum underneath once a day. If there is still burning, it can be used on top of a steroid every other day, with the goal of working up to once, then twice daily. When the condition is controlled, switching to moderate or potent steroid maintenance twice a week is desirable, although not always possible.

Steroid-sparing drugs

If steroid (or calcineurin inhibitor) use is causing side effects or is ineffective, there are a number of medications that are used by experienced vulvar dermatologists which may be useful in treating recalcitrant dermatoses. These are used rarely, if at all, in the generalist vulvovaginal specialty practice and should only be used in consultation with a dermatologist.

They usually work as adjunctive medications, together with steroids, helping to arrest the abnormal immune system response that is causing the disease, thereby allowing reduction in the dose of steroid. They include the following drugs: Azathioprine (Imuran), Cyclophosphamide (Cytoxan, Endoxana), Mycophenolate mofetil (CellCept), Cyclosporin (Neoral), Griseofulvin, Hydroxychloroquine, Methotrexate, and others.

Antifungal therapy

Cutaneous Candida may be present at initial evaluation of the patient, or may arise as a result of local immune suppression from steroid use. Any of the topical azoles– particularly propylene glycol-free clotrimazole–may be applied once or twice daily for control. Use of oral fluconazole 150 mg once or twice weekly is convenient and by-passes the possibility of skin irritation. It is safe, with few adverse effects; its inhibition of cytochrome P450 enzymes makes numerous drug-drug interactions possible.21 These may increase the level of medications, e.g., fluconazole can prolong the effect of zolpidem (Ambien®). Clinicians need to be familiar with all of these to caution women of the possible interactions.

Antiviral therapy

Herpes simplex may be a primary complaint, a second condition complicating a dermatosis, or also may arise because of local immune suppression from steroid therapy. The suppressive anti-viral drugs acyclovir (Zovirax®), 800 mg daily, valacyclovir (Valtrex®), 1 gm daily, and famcyclovir (Famvir®) 1 gm daily, are all equally safe and equally effective in the inhibition of DNA polymerase.22 23 Occasionally the dose will need to be increased because of incomplete suppression.

Imiquimod (Aldara 5%®) may be effective for other genital viral infections such as molluscum and HPV-related condylomata,24 and for HPV warts,25 for which specific anti-viral drugs do not exist. It is commonly applied every other day three times a week until the condition resolves, or up to 16 weeks. Aldara’s inflammatory sides effects make adherence to this treatment challenging for patients.

Antibacterial therapy

Dermatoses, especially those with fissures are subject to bacterial superinfection, commonly with Staphylocccus aureus and Streptococcus pyogenes. Culturing the genital skin as part of an initial evaluation, especially when pronounced erythema or skin breakdown is present, is suggested. In the non-penicillin allergic patient, staphylococcus and streptococcus can be treated with dicloxacillin 250-500 mg four times daily for seven days, penicillin V potassium 250-500 mg four times daily for seven days or amoxicillin plus clavulanate (Augmentin®) 500 mg two or three times daily for seven days. Of comparable efficacy is the cephalosporin, cephalexin (Keflex ®) 250-500 mg three times daily for seven days.

If there is involvement with methicillin-resistant S. aureus (MRSA), antibiotic choices include trimethoprim-sulfa one or two double strength tablets twice a day for two weeks, doxycycline 100 mg twice a day for two weeks, minocycline 100 mg twice daily for two weeks, or rifampin 600 mg daily for two weeks. Linezolid (Zyvox®) 600 mg twice daily for two weeks is another expensive alternative.

The familiar nonprescription topical antibiotics neomycin and bacitracin are well-known causes of allergic contact dermatitis and therefore avoided. A prescription topical mupirocin (Bactroban®) 2% is as effective as neomycin or bacitracin. Although it is more expensive, it is a rare cause of contact dermatitis. 26

Approach to pruritus

Pruritus is a complex process classified in four different categories:27 1) pruriceptive pruritus involving stimulation of the free nerve endings of a subset of nociceptive C-fibers in the skin. The sensation is transmitted to the dorsal horn of the spinal cord, then up the spinothalamic tract to the cerebral cortex for processing; 2) neuropathic pruritus, caused by damage of the itch-transmitting afferents of the peripheral nerves or the spinal cord, e.g., post-herpetic pruritus; 3) neurogenic pruritus, arising because of disease of central structures of the CNS such as brain tumors or abscesses; 4) Psychogenic pruritus based on metabolic disorders in the CNS. Type 1 is the type involved in inflamed skin.

In the skin, many factors contribute to the induction, exacerbation, or suppression of pruritus. Physical stimuli such as heat and cold modulate the perception of itch; painful heat and cold can significantly diminish it, whereas moderate cold intensifies itching. 28 Mechanical factors such as rubbing or scratching can briefly suppress itch by activating nerve fibers that selectively activate and de-activate brain centers.29 The most important factors, however, are mediators that directly induce itch by binding to pruriceptors, or indirectly, by releasing products that induce other cells to release pruritogenic substances: e.g., histamine from mast cells, interleukin-31 from T cells, nerve growth factor from eosinophils and keratinocytes, 30

In the skin, pruritus is mediated by free nerve endings of non-myelinated nerve fibers located at the dermo-epidermal junction and within the epidermis. After induction of itch in the skin, specialized nerve fibers transmit the sensation to the central nervous system. Both the peripheral and central nervous systems play an important role in the perpetuation of itching. A number of inflammatory mediators directly activate pruritus: mediating nerve fibers, and some of these mediators can also produce long-term changes in the skin. For example, significantly elevated levels of Nerve Growth Factor and Substance P cause increase in cutaneous itch fibers, adding to the intensity and chronicity of the pruritus.31

A common approach to treatment of pruritus utilizes causative vs symptomatic treatment. Causative treatment involves finding the underlying disorder and then correcting it, thereby eliminating the itch sensation. Symptomatic treatment, often used in addition to treating the underlying disease, involves substituting another sensation for the itch – cold, heat, counter-irritation.32 The complexity of pruritus often requires a combination of systemic and topical therapies in addition to education and general care.

Treatment of pruritus

Yeast infection needs to be considered in every case of vulvovaginal itching. Even if yeast does not appear on wet prep, yeast culture should be done to rule it out in the process of treatment. As has been pointed out, itching can be caused by many conditions and only correct diagnosis can lead to treatments that work.


Local therapy for inflammatory skin conditions

Topical steroid therapy represents the mainstay of anti-inflammatory therapy.33 Details of appropriate steroid use are covered above.

Calcineurin Inhibitors are second-line topical treatments for dermatoses, as above, and possess anti-itch properties, as well.

Local Anesthetics

Topical anesthetics work by directly interfering with the transmission of impulses along the sensory nerve fibers or by depressing cutaneous sensory receptors. Benzocaine (based on the PABA molecule and chemically unrelated to lidocaine) is highly sensitizing and not recommended. Lidocaine 5% ointment is helpful to many. It may be applied in 1/8 tsp amounts (the size of a lead pencil eraser) four to five times daily.34 Lidocaine is absorbed from skin and mucous membranes, so that no more than 15 g should be applied in the course of a day. Lidocaine burns after application; the discomfort may be reduced by compounding lidocaine 5% in petrolatum, pH balanced.

Pramoxine is another topical anesthetic helpful for mild pruritus of histamine-induced itch.35 Capsaicin is not well tolerated on the vulva because of burning.

Alternative therapies

Several alternatives to the traditional treatment of pruritus include menthol, camphor, and phenol, but these are often not well tolerated on the vulva. Oatmeal baths are comforting. Herbs with high mucilage content–flax, fenugreek, English plantain, hearts ease, marshmallow, mulberry, mullein and slippery elm–36 are suggested, but evidence for vulvar use is lacking. Tannins from wet tea bags are soothing, but another tannin-containing herb witch hazel is an irritant. People with known allergy to garlic, onions, tulips, or other plants of the Liliaceae family may have allergic reactions to aloe. Individuals using aloe gel for prolonged times have developed allergic reactions including hives and eczema-like rash.37

Systemic therapies

Steroids are discussed above.

Since histamine-release causes or exacerbates pruritus, antihistamines or H1 antagonists are widely used for this problem, although some experts consider them rarely effective for itch.38 The main anti-pruritic effect is the blockade of H1 receptors in C-afferent fiber terminals.39 These medications take approximately 15-30 minutes to take effect. They can be short or long-acting.40

Doxepin, a dibenzoxepin tricyclic compound is an active antihistamine, and also acts by depressing cutaneous sensory receptors.41 25-50 mgs are taken orally at bedtime, since the drug is sedating. Doxepin 5% cream is also helpful applied up to four times daily, but may cause drowsiness.

Hydroxyzine hydrochloride (Atarax®) in a pediatric dose of 10 mg at bedtime is helpful to promote nighttime sleep in a patient with pruritus. This may be increased to 20 or 30 mg, but for some, even 10 mg leaves morning sedation. Diphenhydramine (Benadryl®) 25 mg orally may be of help. The newer non-sedating athihistamines, loratidine (Claritin®), fexofenadine (Allegra®), and Zyrtec have had limited success in the treatment of pruritus.42

The modern antihistamine in higher dosages may be able to prevent degranulation of mast cells,43 also preventing the release of other pruritogenic mediators in addition to histamine. 44


Anticonvulsant medications are FDA-approved for neuropathic pain; in addition, they are helpful in the treatment of pruritus. Both gabapentin (Neurontin®) 300 mg daily, titrating up to 1800 mg daily and pregabalin (Lyrica®) 50 mg daily, titrating up to 300 mg daily are used. Their mechanism of action for pruritus is probably similar to that of pain management but is not yet clarified. They are thought to reduce the stimulated release of transmitters by binding at specific calcium channels.45 A new theory of importance in the management of pruritus suggests that pregabalin and gabapentin may enhance analgesia by reducing the affective and aversive aspects of pain. 46


Serotonin reuptake inhibitors (SSRI) such as paroxetine 20 mg daily and sertraline 75-100 mg daily have been documented as helpful for the pruritus of various systemic disorders, not dermatologic. 47 Central nervous effects of serotonin may have a regulatory action on itch-related transmission. 48

Mirtazepine, a tetracyclic antidepressant with H1 antihistaminic and serotonergice effects has shown an antipruritic effect in idiopathic pruritus as well as cholestatic, uremic and neoplasm-induced pruritus.49 Dosage is 15-45 mg daily. The tricyclic doxepin is mentioned under topical treatments. (LINK above to doxepin)


Naltrexone, an opiate receptor anatagonist, produces a long-lasting selective blockade of µ-opiate receptors, and has now been shown helpful for pruritus associated with dermatological diseases. 50 A dose of 50 mg daily can lessen itching. Side effects of dizziness, nausea, vomiting, headache, drowsiness, dry mouth, and cramps were limited, not requiring treatment.51


  1. Lynch, P. Principles of genital diagnosis and therapy. In: Edwards L, Lynch PJ, eds. Genital Dermatology Atlas. 2nd edition. Philadelphia,Wolters Kluwer, 2011,14.
  2. Metz M, Stander S. Chronic pruritus- pathogenesis, clinical aspects and treatment. JEADV 2010:24:1249-1260.
  3. Ghadially R, Halkier-Sorensen L, Elias PM. Effects of petrolatum on stratum corneum structure and function. J Am Acad Dermatol. 1992 Mar; 26(3 Pt 2):387-96.
  4. Fulton JE Jr, Pay SR, Fulton JE III. Comedogenicity of current therapeutic products, cosmetics, and ingredients in the rabbit ear. J Am Acad Dermatol. 1984 Jan;10(1):96-105.
  5. Morrison DS. Petrolatum: a useful classic. Cosm & Toil 1996; 11:59-69.
  6. McPherson T, Cooper S. Vulval lichen sclerosus and lichen planus. Dermatol Ther 2010; 23:523-32.
  7. Wilson KC, Reardon C, Theodore A, Farber H. Propylene Glycol Toxicity: A Severe Iatrogenic Illness in ICU Patients Receiving IV Benzodiazepines. Chest 2005; 128(3):1674-81.
  8. American Medical Association, Council on Drugs (1994). AMA Drug Evaluations Annual 1994 (Chicago, Illinois: American Medical Association): 1224.
  9. www.skintherapyletter.com/2011/16.5/2.html
  10. http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=347.10&SearchTerm=petrolatum
  11. http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=346.50&SearchTerm=petrolatum
  12. McKay M. Topical therapy of gynecologic skin disorders. In:Black M, McKay M, eds. Obstetric and Gynecololgic Dermatology, 2nd ed. London, Mosby, 2002, 209.
  13. Dalziel KL, Wojnarowska F. Long-term control of vulval lichen sclerosus after treatment with a potent topical steroid cream. J Reprod Med 1993; 38:25.
  14. Moyal -Barracco M, Edwards L. Diagnosis and therapy of anogenital lichen planus. Dermatol Ther 2004; 17:38-46.
  15. Lynch, 2011.
  16. Ohman EM, Rogers S, Meenan FO, et al. Adrenal suppression following low dose topical clobetasol propionate. J R Soc Med 1987;80:422-423.
  17. Edwards, L. Dermatologic therapy of chronic genital disease. Dermatol Ther 2004; 17:1-7.
  18. Hanifin JM, Pallor AS, Eichenfield L, et al.Efficacy and safety of tacrolimus ointment treatment of up to 4 years in patients with atopic dermatitis. J Am Acad Dermatol 2005; 53(2 Suppl 2):S186-94.
  19. FDA Public Health Advisory: Elidel (pimecrolimus) cream and Protopic (tacrolimus) ointment.
  20. Lynch 2011.
  21. Lynch 2011.
  22. Perry CM, Wagstaff AJ. Famciclovir. A review of its pharmacological properties and therapeutic efficacy in herpesvirus infections. Drugs 1995; 50:396.
  23. Perry CM, Faulds D. Valaciclovir. A review of its antiviral activity, pharmacokinetic properties and therapeutic efficacy in herpesvirus infections. Drugs 1996; 52:754.
  24. Skinner RB Jr. Treatment of molluscum contagiosum with imiquimod 5% cream. J Am Acad Dermatol 2002; 47:S221.
  25. Gunter J. Genital and perianal warts: new treatment opportunities for human papillomavirus infection. Am J Obstet Gynecol 2003; 189:S3.
  26. http://www.drugs.com/pro/bactroban-ointment.html
  27. Twycross R, Greaves MW, Handwerker H, et al. Itch: scratching more than the surface. QJM 2003; 96:7-26.
  28. Pfab F, Valet M, Sprenger T, et al. Temperature modulated histamine-itchin lesional and nonlesional skin in atopic eczema- a combined psycholphysical and neuroimaging study. Allergy 2010; 65:84-94.
  29. Yosipovitch G, Ishiuji Y, Patael RS, et al. The brain processing of scratching. J Invest Dermatol 2008; 128:10806-11811.
  30. Metz, 2010.
  31. Ikoma A, Steinhoff M, Stander S, et al. The neurobiology of itch. Nat Rev Neurosci 2006;7:535-47.
  32. Lovell P, Vender RB. Management and treatment of pruritus. In: Madden S, ed. Skin Ther Letter, 2007; 12(1):1-6.
  33. Lynch, 2011.
  34. Lynch, 2011.
  35. Yosipovitch G, Maibach HI. Effect of topical pramoxine on experimentaly induced pruritus in humans. J Am Acad Dermatol 1997; 37 (2PT 1);278-80.
  36. Millikan LE. Alternative therapy in pruritus. Dermatol Ther 2003; 16(2):175-80.
  37. http://www.mayoclinic.com/health/aloe-vera/NS_patient-Aloe
  38. Lynde CB, Kraft JN, Lynde CW. Novel agents for intractable itch. http://skintherapyletter.com/2008/13.1/2.html
  39. Thurmond RL, Gelfand EW, Dunford PJ. The role of histamine H1 and H4 receptors in allergic inflammation: the search for new antihistamines. Nat Rev Drug Discov 2008; 7:41-53.
  40. DermNet NZ, Pruritus (itch). URL: http://www.dermnetnz.org/systemic/itch.html
  41. Hercogova J. Topical anti-itch therapy. Dermatol ther 2005; 18(4):341-3.
  42. Hercogova 2005.
  43. Weller K, mauurer M. Desloratidine inhibits human skin mast cell activation and histamine release. J Invest Dermatol 2009; 129:2723-26.
  44. Vadiadi M. Kalogeromitros D, Kempuraj D, et al. Rupatadine inhibits proinflammatory mediator secretion from human mast cells triggered by different stimulit. Int Arch Allergy Immunol 2010; 151:38-45.
  45. Taylor CP. Mechanisms of analgesia by gabapentin and pergabalin-calcium channel alpha2-delta [Cavalpha2-delta] ligands. Pain 2009; 142:13-16.
  46. Taylor 2009.
  47. Zylicz Z, Krajnik M, Sorge AA et al. Paroxetine in the treatment of severe non-dermatological pruritus: a randomized controlled trial. J Pain Symptom Manage 2003; 26:1105-12.
  48. Zylick 2003.
  49. Davis, MP, Frandsen JL, Walsh D, et al. Mirtazepine for pruritus. J Pain Symptom Manage 2003; 23:288-291.
  50. Phan NQ, Bernhard JD, Luger TA, Ständer S. Antipruritic treatment with systemic μ-opioid receptor antagonists: a review. J Am Acad Dermatol. 2010 Oct;63(4):680-8.
  51. Terg R, coronel e, Sorda J, Munoz AE, Finder J. Efficacy and safety of oral naltrexone treatment for pruritus of cholestasis: a crossover, double-blind, placebo-controlled study. J Hepatol 2002; 37(6):717-22.