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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.
Types of acne lesions
Typically, a patient with acne presents with the following lesions:
Severe acne will be more widespread with lots of inflammatory lesions, as well as:
Author: Rod Tucker