Keratosis Pilaris Treatment

Keratosis pilaris is a very common genetic follicular disorder manifested by the appearance of rough bumps on the skin and hence colloqually referred to as "chicken skin" or "goose bumps".

Primarily, it appears on the back and outer sides of the upper arms, but can also occur on thighs and buttocks or any body part except glabrous skin (like the palms or soles of feet). Worldwide, keratosis pilaris affects an estimated 40 to 50% of the adult population and approximately 50 to 80% of all adolescents. Varying in degree, keratoisi pilaris can range from minimal to severe.

Keratosis pilaris tends to occur as excess keratin, a natural fibrous protein in the skin found normally in human hair, nails and callus, accumulates around hair follicles (process known as hyperkeratinization).

Keratosis pilaris is more than anything else unattractive, and it most often appears as a proliferation of tiny hard bumps that are seldom sore or itchy. Though people with keratosis pilaris experience this condition year round, it’s during the colder months when moisture levels in the air are lower that the problem can become exacerbated and the “goose bumps” are apt to look and feel more pronounced in color and texture.

There are several different types of keratosis pilaris, including keratosis pilaris rubra (red, inflamed bumps), alba (rough, bumpy skin with no irritation), rubra faceii (reddish rash on the cheeks) and related disorders.

Keratosis pilaris alba is the more common variant and is characterized by small gray-white papules with a negligible inflammatory component.

Keratosis pilaris rubra has a significant inflammatory component, and thus patients present with small red papules. This variation is most conspicuous during the winter months.

Observe for small, horny, follicular papules with (ie, rubra) or without (ie, alba) surrounding redness.

Most commonly, lesions occur on the back of thel upper arms and anterior thighs. Less commonly, lesions involve the face, buttocks, and trunk.

In involved areas, lesions are extensive, monomorphic, and very evenly spaced.

A fine hair may pierce the papules, or hair may be found coiled up within the keratin plug.

The keratin plug cannot be eliminated with pressure.

Cells that contain keratin are constantly being shed and replaced by new ones. The condition known as dandruff results when the scalp sheds such cells. Hormonal influence may occur because a high prevalence and intensity of keratosis pilaris is noted during puberty and in women with hyperandrogenism. In severe cases, the pores can become clogged and cause acne. The clogged pores resemble comedones of keratinized plugs surrounding the hair follicle.

Treatment of Keratosis Pilaris

Many people find keratosis pilaris lesions cosmetically unappealing and therefore seek treatment. Occasionally, they may become secondarily infected because of scratchy tight-fitting clothing or abrasive self-therapy, in which case treatment of the infection is necessary. A significant inflammatory component may be present and may be relieved with topical steroid therapy. Treatment of the noninflamed horny papules can be difficult because they have proven resistant to most modes of therapy.

Treatment options for keratosis pilaris focus on exfoliating or softening the dermis to reduce clogged pores. Treatment initially begins with adherence to nonpharmacologic measures and compliance with daily living functions that will not worsen the condition. An important first step is to use a mild cleansing agent with abrasive properties, often termed scrub, but one that is not drying (for sensitive skin). The goal is to clean and open the pores of the dermis. Other measures to prevent excessive dryness include taking tepid, brief showers and using a humidifier, especially during the winter months when low humidity dries out the skin.

BIO SKIN CARE™ cream softens rough and dry skin, removes excessive keratin and thus unclogs pores. It is also anti-inflammatory, regulates the production of keratin and while it helps to attract moisture when first applied it also restores the skin's capacity to hold in moisture by accelerating the production of collagen, elastin and glycosaminoglycans from within the deep layers of the skin. BIO SKIN CARE™ should be applied to the affected area twice a day.

Other keratin-softening agents such as AHAs exfoliate the dermis. In concentrations of 2% to 20%, the AHAs are reported to not peel the skin, whereas concentrations greater than 20% will produce peeling. Examples are glycolic acid, lactic acid, malic acid, citric acid, and tartaric acid. These agents act as keratolytics, resulting in a smoother, nonscaly dermis. AHAs should be applied to dried skin and should initially be used in a low concentration and, if tolerated, increased to a higher concentration. Many patients require application every other day for a period of one to two weeks and then can be instructed on daily use of the product. Keratolytics commonly cause redness or irritation due to peeling. Patients should also be warned that keratolytics can increase photosensitivity; thus, sunscreen protection is advised.

Drug treatment for keratosis pilaris with Over the Counter agents consists of moisturizers, including the emollients and humectants, hydrocortisone, and keratin-softening agents (alpha-hydroxy acids [AHAs] and urea). The emollients help retain water that is already present in the dermis. Examples of emollients include mineral oil, petrolatum, and refined lanolin. Humectants help draw water into the skin to hydrate the dermis. Examples include glycerin, sorbitol, and propylene glycol. In almost all circumstances, it is vital that multiple agents are used in the treatment regimen, and the importance of compliance should be stressed. Application of the agents to damp hydrated skin, e.g., immediately following swimming, a bath, or a shower, is generally recommended. The use of products such as loofah sponges or bath brushes may also be beneficial in assisting the removal of keratin plugs. Additionally, a bedtime application should always be part of the treatment regimen.

Lesions with significant inflammation may improve with the use of medium-potency emollient-based topical steroid preparations. Inflammation is usually reduced markedly by 7 days, at which point the steroid should be discontinued.

Hydrocortisone for self-care at concentrations of 0.5% and 1% should be applied as a thin layer two to four times a day for approximately seven days to reduce any inflammation at the site. Once inflammation is controlled, therapy designed to soften the lesion itself should be initiated. Cuation is necessary when applying hydrocortisone to the face because the skin is thinner than on other body areas. Hydrocortisone use in children ages 2 to 6 years should be limited due to the risk of systemic absorption and skin atrophy.

Prescription Treatment Options

Prescription treatment options to treat KP are topical corticosteroids, urea, retinoids, and topical immunomodulators. Topical prescription corticosteroids, e.g., triamcinolone 1% or desonide 0.05%, may be useful if OTC products are found to be ineffective against inflammation. Prescription topical agents should be applied two to four times a day as a thin layer to the affected areas. Like milder concentrations of hydrocortisone, caution should be used with the prescription agents. Additionally, prescription-strength hydrocortisone can inhibit collagen formation and thereby lead to skin striate.

Concentrations of urea greater than 30% may be used to alleviate rough surfaces of the dermis. However, the urea concentration contained in the legend products is usually sensitizing and not a popular choice.

Topical retinoids used in the treatment of keratosis pilaris include adapalene, tazarotene, and tretinoin. Their mechanism of action may be to increase turnover of follicular epithelial cells. These agents should be applied as a thin layer to dry skin at bedtime to no more than 20% of the body surface. The adverse effects of redness, extreme dryness, and peeling are in some instances rate-limiting effects for most people. However, some topical retinoids are available in reduced concentrations or in an emollient cream base when compared to the original products. If possible, therapy should be started in the more humid months of summer; intitiation of therapy should be avoided in the dry winter months. If a moisturizer is needed, it should be applied and completely allowed to dry before the retinoid is applied. Contact of the retinoid with the eyes and mouth should be avoided. Also avoid exposure to ultraviolet light. Like the AHAs, topical retinoids initially should be used every other day with a low-concentration product and increased to higher concentrations as tolerated. Burning and pruritus are commonly seen in the first four weeks and usually lessen with time. Topical retinoids are teratogenic and should not be used by women of childbearing age. One product's package insert suggests female patients should begin therapy during a normal menstrual period. Prescribing information also states that children under the age of 12 should not use topical retinoids.

Topical immunomodulators, pimecrolimus, and tacrolimus may also be of benefit if other therapies have been ineffective. However, a public health advisory has been issued by the FDA about a potential risk of skin cancer with the use of topical immunomodulators for the treatment of eczema. Topical immunomodulators act to inhibit inflammation primarily by inhibiting T cells. These products should be applied twice daily to the affected areas. If a moisturizer is also being used, the patient should be instructed to apply the moisturizer after pimecrolimus. Patients should be cautioned to avoid excessive exposure to sunlight. Patients may initially complain of a feeling of warmth or burning and skin irritation, especially during the first few days of use. Most of these reactions will usually subside after five to seven days of treatment. An advantage of the topical immunomodulators is that their use is indicated for children 2 years of age and older. Another advantage is that these agents do not inhibit collagen production and will not cause skin thinning. Occlusive dressings should be avoided with these agents. These agents should not be used in patients with a compromised immune system or during pregnancy since there are no adequate and well-controlled studies of topically applied agents in pregnancy.