Pharmacists often give patients advice for treating acne. So why not turn this expertise into a clinical service, suggests Rod Tucker
Acne is a very common skin problem, affecting 80% of teenagers (from 13 to 18 years old) at some point,1 and each year accounts for some 3.5 million GP appointments.2 Although predominately a teenage problem, acne persists into adult life affecting roughly 12% of women and 5% of men at 40 years old or over.3,4
Although considered by many as a trivial disease that teenagers will simply ‘grow out’ of, research suggests that the impairment in the quality of life experienced by those with acne is comparable with the impact of other chronic diseases such as asthma, epilepsy and arthritis.5
Given the large number of patients with acne, pharmacists are likely to encounter patients with prescription products as well as those seeking advice and treatment. Consequently, there is the potential for pharmacies to develop services directed towards medicine optimisation for both groups of patients.
Acne is a disease of the pilosebaceous follicle and, though the precise cause of acne remains unclear, there are at least four factors implicated in the pathophysiology: release of inflammatory agents in the skin, abnormal keratinocyte proliferation and differentiation (comedogenesis), proliferation of the anaerobic organism Cutibacterium acnes (C acnes) – which is present within functionally blocked follicles – and an increased production of altered sebum.
It is currently believed that the initial event is an inflammatory response and that this precedes the abnormal keratinocyte proliferation. C acnes is able to activate toll-like receptors on the surface of monocytes and neutrophils and this leads to the production of pro-inflammatory cytokines, such as interleukin 12 and 8 and tumour necrosis factor. In addition, C acnes stimulates inflammation through the production of pro-inflammatory mediators, which diffuse through the follicular wall.
During the development of acne, proliferation of the epithelial keratinocyte increases but this is accompanied by a reduction in desquamation (shedding) of these cells, leading to blockage of the pilosebaceous follicle. This blocked follicle is termed a microcomedone and is the initial acne lesion from which all other types develop.
During adolescence, there is an increase in the production of sex hormones (mainly androgens) that cause sebaceous gland hyperplasia with a corresponding increase in the output of sebum. This gives the skin
a greasy appearance, which is the first sign in the development of acne. It is known that in addition to androgens, numerous other mediators have an affect on sebaceous gland cells (sebocytes).
It has been recently discovered that leptin, a hormone related to regulation of bodyweight, also effects sebocytes by inducing the production of pro-inflammatory interleukins and an alteration in the lipid profile of sebum.
This observation suggests a potential mechanism through which diet could be linked with the development of inflammatory acne.6 Furthermore, sebaceous glands are influenced by corticotrophin-releasing hormone that may also help to explain the link between worsening acne and stress.
Typically, a patient with acne presents with the following lesions:
•Open comedones (blackheads)
•Closed comedones (whiteheads)
Severe acne will be more widespread with lots of inflammatory lesions, as well as:
There is no universally-accepted grading system for acne but in primary care, acne is considered to be mild, moderate or severe.
It is vital to examine the skin to determine the type and extent of the lesions present.
The treatment for the different levels of acne severity are summarised in Table 1.
Mainly, acne is limited to the face with a smaller subset of patients having lesions on the chest and back. Nevertheless, if acne affects the chest and back, unless it is mild, a referral to the GP is advisable since treating these areas with topical agents becomes more difficult.
Topical agents should be applied to all acne-prone areas of the skin rather the individual lesions, as most drugs target emerging rather than existing lesions.
The most effective pharmacy product for acne benzoyl peroxide (BP) and its clinical efficacy has been demonstrated in many studies.8
Benzoyl peroxide has both comedolytic (breaking down blackheads and whiteheads) and bactericidal actions. In fact, twice daily application of 5% BP gel can reduce the population of C acnes by more than 95% after five days – a feat that no antibiotic can match.9
There is currently no known resistance to BP, and this is due to its mode of action. Once in the skin, BP degrades to benzoic acid and hydrogen peroxide, generating free radicals that destroy C acnes.
The most common problems with BP are a powerful bleaching effect that will discolour material, such as clothes, pillows and bedding, and skin irritation.
One way to reduce the irritancy is to initially apply BP products for limited periods of time (say 15 minutes) before washing them off and to gradually increase the contact time.
Other treatments available through pharmacies include nicotinamide gel and salicylic acid. Nicotinamide has an anti-inflammatory action, though there is a lack of evidence for its effectiveness. Salicylic acid has mild comedolytic affects and could be used for patients with very mild acne.
Acne products are available in gels and creams and there is little evidence that any particular vehicle is more effective. While some authorities argue that patients with greasy skin benefit from using a gel (due to the drying effect) and a cream for those with dry skin, there is little evidence to support this. It is more important that the patient finds a topical formulation which they are happy to use.
1. Chu T. Acne and other facial eruptions. Medicine 1997; 25:30–25.
2. Dawson AL. Acne vulgaris. British Medical Journal 2014; 346:2634.
3. Shen Y, Wang T, Zhou C, Wang X, Ding X, Tian S et al. Prevalence of acne vulgaris in Chinese adolescents and adults: a community-based study of 17,345 subjects in six cities. Acta Derm Venereol 2012; 92(1): 40-44.
4.Perkins AC, Cheung CE, Hillebrand GG, Miyamoto K, Kimball AB. Comparison of the epidemiology of acne vulgaris among Caucasian, Asian, Continental Indian and African American women. J Eur Acad Dermatol Venereol 2011; 25(9): 1054-60.
5.Mallon E, Newton JN, Klassen A, Stewart-Brown SL, Ryan TJ, Finlay AY. The quality of life in acne: a comparison with general medical conditions using generic questionnaires. Br J Dermatol 1999; 140(4): 672 – 76.
6.Torocsik D, Kovacs D, Camera E et al. Leptin promotes a proinflammatory lipid profile and induces inflammatory pathways in huma SZ95 sebocytes. Br J Dermatol 2014; 171: 1326-1335.
7.Zaenglein AL, Pathy AL, Schlosser BJ et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol 2016; 74(5): 945-73
8.Tucker R, Walton S. The role of benzoyl peroxide in the management of acne vulgaris Pharm J. 2007; 279: 48 – 53.
9.Jeremy AHT, Holland DB, Roberts
SG, Thomson KF, Cunliffe WJ (2003) Inflammatory events are involved in acne lesion initiation. J Invest Dermatol 121(1): 20–27
10.Acne.org. Comedogenic (pore-clogging) ingredients. Available on-line at: www.acne.org/comedogenic-list.html [Accessed April 2018]
11. British Skin Foundation Acne Survey of 2,299 acne suffers (2014 – 15). Available online at: www.britishskinfoundation.org.uk/LinkClick.aspx?fileticket=i2bE2n4c8m0=&tabid=172 [Accessed April 2018]
– Nguyen QG, Markus R, Katta R. Diet and acne: an exploratory survey study of patient beliefs. Dermatol pract Concept 2015; 6(2): 21 – 27.
– Smith RN, Mann NJ, Braue A, Makelainen H, Varigos GA. A low-glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial. Am J Clin Nut 2007; 86(1): 107 – 15.
– Magin P, Pond D, Smith W, Watson A. A systematic review of the evidence for ‘myths and misconceptions’ in acne management: diet, face-washing and sunlight. Fam Pract 2005; 22: 62 – 70.