Both of these common ‘bumpy skin’ conditions will frequently be seen by community pharmacists, who are well-placed to help, says Rod Tucker

Two common skin conditions for which patients may seek advice are keratosis pilaris and milia and pharmacists are ideally placed to offer advice on these conditions.

Keratosis pilaris

Keratosis pilaris (KP) is an extremely common skin condition that normally occurs within the first decade of life. It peaks at puberty, affecting 50-80% of adolescents and continues in up to 40% of adults, with a slightly higher prevalence in women.

KP is more prevalent in those who are overweight, diabetic (particularly type 1 patients) and can worsen during pregnancy and after childbirth. It is often associated with other dry skin conditions including atopic eczema and ichthyosis as well as hay fever and asthma.

The name arises from keratosis, which refers to a localised overgrowth of the skin protein, keratin and pilaris, derived from the Latin for hair (pilus). It is described as an autosomal dominant condition.

Hence, it can develop if a single parent carries the abnormal gene and, in fact, a family history is observed in nearly 40% of cases. Many patients find that KP improves during the summer months but worsens over the winter period. For most, the condition is self-limiting and tends to improve with age.

Clinically, KP presents as 10 to 100 white or red keratotic papules 1-2 mm in diameter with varying degrees of perifollicular (ie surrounding the follicle) inflammation. The affected skin has a rough, dry and bumpy texture that resembles gooseflesh hence it is often colloquially referred to as ‘chicken skin’.

Although KP can occur on any area of the body where hair growth occurs, in up to 90% of cases, it presents on the outer and upper arms, thighs and buttocks. In a small number of cases, KP is seen on the chest, face and eyebrows.

The majority of patients are asymptomatic although some may experience mild pruritis. It is often perceived more as a cosmetic nuisance than a specific medical problem.


Under normal circumstances, keratinous material within follicles is exfoliated (ie shed) but in KP there is follicular hyperkeratosis, (ie an excessive production of keratin within the hair follicles).

This keratinous material accumulates and ultimately blocks the follicular orifice leading to the observed papules. The underlying reason for the hyperkeratosis remains unclear and at least three different theories have been proposed to account for the overproduction of keratin.

Some evidence suggests that KP is associated with a mutation in the FLG gene profilaggrin, which codes for the protein. This protein has several important roles one of which is the development of an effective skin barrier.

While the resultant defective skin barrier provides an explanation for the increased dryness seen in KP lesional skin, not all patients have FLG gene mutations, indicating the importance of other pathological factors.

An alternative hypothesis is based on the observation that hairs that can be extracted from a keratotic lesion have an unusual coiled shape. This second theory proposes that the coiled hair shaft ruptures the cells lining the follicle and that destruction of these epithelial cells is the primary driver for the subsequent defective keratinization and inflammation.

A third and final theory relates to the fact that blocked follicles lack functional sebaceous glands. It is believed that the non-functional sebaceous glands are a trigger for the hair shaft and skin barrier abnormalities.

Keratosis pilaris can also be induced after treatment with drugs, including ciclosporin in transplant patients and chemotherapy agents such as vemurafenib, Dabrafenib and Nilotinib. Rarely, KP has been linked to environmental exposure to cutting oil used by machinists.


The genetic nature of KP means that the condition cannot be cured but is controllable –although no treatments have been found to be universally effective and all require continued use. It is worth reassuring patients that KP doesn’t generally require treatment and that it often resolves over time.

Milder cases can be easily managed using emollients containing keratolytic agents such as lactic acid or salicylic acid, both of which have been shown to effective. An emollient containing either of these keratolytics serves a dual purpose, namely, removal of the follicular plugs and increased skin hydration.

Lactic acid modulates keratinization whereas salicylic acid leads to reduced cohesion between keratinocytes though in studies, lactic acid appears to be more effective. The humectant urea, which has keratolytic properties is also effective, particularly in combination with salicylic acid.

Topical steroids are partially effective and can be used where there is significant perifollicular inflammation though this is an unlicensed over-the-counter use.

Several commercial washes containing exfoliating agents may be of value, but gently rubbing the affected areas during showering with an exfoliating pad or pumice stone is likely to be equally effective for unclogging the blocked follicles.

Patients for whom the above measures have not been effective or in those with more extensive disease should be referred to their GP.

Topical retinoids such as tazarotene and tretinoin have antiproliferative properties which alter keratinocyte differentiation and some studies have shown these agents to be effective.

Other therapies not available on the NHS include laser treatment and microdermabrasion, both of which are effective but the condition relapses over time.


Milia (singular milium) have been defined as benign, superficial keratinous (keratin-filled) cysts. The term arises from the Latin (milium) because the lesions closely resemble millet seeds. Milia can be classified as primary, when lesions arise spontaneously, or secondary in which case lesions occur as a result of either skin trauma or disease.

Two rare forms of primary milia have been reported: milia en plaque characterised by multiple groups of milia on an erythematous plaque, seen more commonly in women between the fourth and seventh decade and multiple eruptive milia, which can present on the face and neck, shoulders, upper back and axillae and which may occur through autosomal dominant transfer. All forms of milia are asymptomatic or occasionally mildly pruritic.

Primary milia affect between 40 and 50% of newborns presenting as uniform, white domed-shaped lesions, 1-2 mm in diameter, typically on the face, especially around the eyelids, cheeks and nose but can also occur inside the mouth and in the genital area. Milia in newborns spontaneously resolves in a few weeks, though primary milia that develop in children and adults, typically around the eyes, tend to persist and are unlikely to resolve unless treated.


Primary milia form due to the trapping of dead skin cells beneath the epidermis that are subsequently covered to form a small cyst.

As with KP, the precise cause is unknown, and lesions are thought to arise from vellus hairs (i.e. very fine hairs) at the lower part of the infundibulum (ie the area of the hair follicle above the entry of the sebaceous gland duct).

Primary milia are a feature of several genodermatoses (ie genetic skin diseases) including Rombo syndrome and basal cell naevus syndrome. It has also been suggested that milia can arise from sebaceous glands which are not fully developed, and this might explain the high prevalence in newborns.

Secondary milia are clinically identical to the primary form and are usually derived from eccrine sweat glands and less commonly from hair follicles. Secondary lesions can be induced by skin trauma such as burns including excessive exposure to sunlight, radiotherapy, following a tattoo, use of chemical peels, skin grafts and laser therapy.

Secondary milia are commonly associated with blistering diseases such as bullous pemphigoid, herpes zoster, contact dermatitis and lichen sclerosis and less frequently from the use of certain medicines, including prolonged use of topical steroids at the site of use, non-steroidal anti-inflammatory drugs, ciclosporin, fluorouracil cream, penicillamine and acitretin.


Milia are harmless and patients should be informed that the lesions can spontaneously resolve over time. Suggested self-care includes exfoliating washes, gently rubbed over the affected areas, although the effectiveness of this approach is unclear.

However, if milia en plaque or eruptive milia are suspected then referral to the GP is warranted. In addition, patients who wish to have lesions removed for cosmetic reasons should also be referred.

Removal should only be performed under medical supervision and can be achieved, without anaesthetic, by breaking the surface of the lesion with a sterile needle or point of a blade and squeezing out the contents. Other methods of treatment include cryotherapy, laser therapy, chemical peels and dermabrasion. Isolated reports in the literature indicate that milia en plaque can be successfully treated with topical retinoids and oral minocycline though these are unlicensed indications.

Rod Tucker is a community pharmacist