Acne can affect people of all ages and is one of the 10 most common diseases in the world. Acne is virtually universal in young people and many will experience mild physiological acne. A study of young people in the UK aged 14-16 years found the prevalence of examined acne in 50% and moderate to severe acne in 11%. The prevalence is just as high in women over 25 years old as it is in those under 15 years of age.
A large multi-national cross-sectional study looked at the presence of acne in women aged 0-70 years. Of the women studied, 55% had some form of acne. This peaked in teenage years, although clinical acne was seen in 45% of women aged 21–30, 26% aged 31–40, and 12% aged 41–50. Post-menopausal women have less acne. Studies have shown that males have more severe acne in late adolescence than females, but over the age of 40 years, male acne is not as predominant as female acne.
Acne vulgaris is the most common type, but other clinical variants include infantile acne (transient form due to maternal hormonal transfer). Other acne forms include:
- Acne conglobata (a severe nodulo-cystic acne with abscesses and sinus). This is a severe form of acne that can become the rare acne fulminans which is associated with systemic symptoms;
- Drug-induced, including corticosteroids, synthetic androgens, psychotropic drugs (lithium, amineptine), immunosuppressants (azathioprine and ciclosporin) and vitamin B (B12);
- Cosmetic-induced (including pomades, bleaching agents, over-use of grease and detergents);
- Occupational acne (exposure to chlorace-inducing chemicals in the workplace);
- Acne associated with psychological problems (acne excoriee, body dysmorphic disorder and anorexia).
This article will discuss the management of acne vulgaris in primary care.
Acne is predominantly seen on the face (99% of all cases), as well as the back (60% of all cases) and the chest (15% of all cases). Acne is usually classified as mild, moderate or severe and can vary from mild comedonal (the presence of whiteheads and blackheads only) acne, where non-inflammatory and inflammatory lesions can arise as papules, pustules or deep-seated pustules and nodules. These may develop sinus tracts (see Table 1).
The clinical presentations of acne related to severity are outlined in Table 1.
As lesions regress, inflammatory macules may present. In patients with skin types IV-VI (brown, dark brown or black skin), post inflammatory pigmentation presents as acne hyper-pigmented macules. This is believed to be a pathological response of the skin to injury in skin of colour. Scarring is a consequence of any type of untreated acne, due to the loss of tissue in atrophic scarring or excessive tissue growth in hypertrophic and keloid scarring. In darker skin types keloid scarring is more common, due to differences in collagen production (fibroblast size and activity and immune mechanisms).
The emergence of acne is generally hormonal, with the surge of androgens at puberty for males and females, and pre-menstrual flares and anti-androgen-responsive acne in females explained by associated hormonal diseases (for example, polycystic ovary syndrome, late-onset congenital adrenal hyperplasia and hypercortisolism).
During puberty, in the case of acne vulgaris, the androgen glands stimulate the sebaceous glands to produce sebum. Hypercornification (increased keratinisation of the cell lining) of the pilosebaceous ducts of the sebaceous glands is also under the control of androgens. This causes partial or total obstruction of the ducts. The obstructed pilosebaceous ducts are colonised by bacteria, including propionibacterium acnes, staphylococcus epidermidis and pityrosporum ovale. P. acnes has the ability to break down triglycerides in sebum to free fatty acids producing lipase. Cytokines as inflammatory mediators are also released. The release of inflammatory mediators causes inflammation, and polymorph and lymphocyte infiltration results in pus formation. Rupture of the ducts contributes to large inflammatory pustules, nodules and cysts.
Scarring may occur in up to 90% of patients with any acne lesions, although some people are more prone to scarring than others. The duration of inflammation correlates to scar production, and can be the direct result of a delay in appropriate acne management.
Triggers and myths
Acne vulgaris does have some triggers, but the cause (unlike other acne variants) remains hormonal. This explains why 70% of women report acne flares two-seven days before menstruation. However, a genetic link has been established too. Large cohort studies have shown that the risk of acne in a first-degree relative of someone who has acne is approximately four-five times higher than in relatives of unaffected individuals. Overuse of cosmetics, especially products that are not non-comedogenic, can exacerbate mild acne.
There is no evidence that alcohol or smoking exacerbates acne in young people, but there is a link with non-inflammatory acne and comedones in middle-aged women who are heavy smokers.
The link between diet and acne has been the subject of a large number of studies in the last 20 years, but no absolute conclusions have been established to date. Five studies show a link between high glycaemic index (GI) diets and acne, but two studies found no link with high GI, while three of the five studies found that increased milk consumption worsens acne (although there was no consensus on whether whole or skimmed milk was better or worse). Any link with dairy products, chocolate and cheese is unproven.
Acne can have an enormous psychosocial burden for the sufferer. A study comparing psychiatric co-morbidity in atopic dermatitis, alopecia areata, acne and psoriasis highlighted the importance of recognising depression among dermatology patients.8 The study also indicated that in some instances even clinically mild to moderate disease, such as noncystic facial acne, can be associated with significant depression and suicidal ideation.8 For more insight into the psychosocial effects on young people visit: http://www.healthtalk.org/young-peoples-experiences/acne/topics.
Patients who are distressed by their facial appearance should be informed about Changing Faces (https://www.changingfaces.org.uk), who may be able to offer the patient additional support.
Current management of acne vulgaris
Patient history should include examination of the face, chest and back, recording the skin change, number and type of acne lesions, and any visible scarring.
Examine the skin by looking for the classical acne lesions, open and closed comedones, papules, pustules and nodules, and recording the distribution. There are several recording scores of acne symptoms, including the Leeds Acne grading scale. However, a good practical scale for primary care is the comprehensive acne severity scale, outlined in Table 2.
You should ask about experience and success with past and current treatments (including over-the-counter preparations). Assess and record psychological concerns and social effects for the patient (the Cardiff Acne Disability Index (CADI) and Assessment of Psychological and Social Effects (APSEA) are useful tools).
Primary care treatment guidance
Acne is treatable and the aim of acne management should be to:
- Alleviate symptoms
- Clear existing lesions
- Limit disease progression by preventing new lesion forming and scars developing, and
- Avoiding any negative impact on quality of life.
To achieve these aims, early recognition of mild acne is crucial, as is intervening before it develops to moderate acne. The golden rule is that any acne treatment should be used for eight weeks before reassessment. If acne has responded, continue with the treatment for a further eight weeks. If there has been no response, move up to the next treatment step.
Mild acne can usually be controlled with a topical preparation. Moderate acne usually requires a prescribed topical preparation and some form of oral therapy. Patients with severe acne should be referred to a dermatology specialist for management. The European Dermatology Forum Guidelines provide an evidence-based treatment pathway for acne. The NICE Clinical Knowledge Summaries provide UK guidance based on the European guidelines.
Mild acne can usually be treated with over-the-counter preparations. There is a wide range available containing the following ingredients:
- Benzoyl peroxide 5-10% (an antimicrobial which reduces duct cornification and p.acnes)
- Nicotinamide (this reduces sebum and pigmentation)
- Salicylic acid (keratolytic)
- Chlorhexidine (antiseptic)
- Hydrogen peroxide (oxidising agent).
- Sulphur/resorcinol (antiseptic and keratolytic)
- Zinc (anti-inflammatory).
For mild acne, NICE recommends topical retinoids for comedones and benzoyl peroxoide (2.5%-10%) for papules. If the mild acne does not respond to these preparations after two months, then topical retinoids, benzoyl peroxide or azelaic acid should be prescribed in primary care.
In moderate acne, the guidelines recommend first-line topical combination therapy with antibiotics (for example, benzoyl peroxide 5% and clindamycin 1% or tretinoin 0.025% and erythromycin 4%) or retinoids if comedones present (Adapalene and benzoyl peroxide).
Oral antibiotic should be considered if moderate acne does not respond to topical treatments (first line options are tetracycline, oxytetracyline, doxycyline or lymecyline), and for practical purposes such as treating the chest and back. Success is dependent on correct administration. Antibiotics need to be prescribed for at least three months as therapeutic effects are generally not observed until six-eight weeks. NICE guidance states that a topical and oral antibiotic should not be combined to prevent development of bacterial resistance.
However, an oral antibiotic should not be prescribed alone, so topical treatment (retinoids and benzoyl peroxide) should be prescribed with oral antibiotics.
Combined oral contraceptives are recommended for females with moderate to severe acne as there is good evidence they reduce lesion count.[11,12] Anti-androgen therapy (cyproterone acetate with ethinylestradiol) should only be prescribed for a short course (three-four cycles) for women of reproductive age in the treatment of severe acne (or hirtutism) when topical or systemic therapy has failed. This follows a safety review by the European Medicines Agency (EMA), the Medicines and Healthcare Products Regulatory Agency (MHRA), which identified a higher risk of venous thromboembolism with anti-androgen therapy.
Patients with severe acne should be referred to a dermatology specialist as the majority of patients will be treated with oral isotretinoin.[11,12]
General skin care tips and patient information
General skin care tips are outlined in Table 4. People with acne should be directed to reputable information sources. The British Association of Dermatologists provides patient information that can be downloaded (http://www.bad.org.uk/shared/get-file.ashx?id=65&itemtype=document).
There is no UK acne support group, but the TalkHealth Partnership provides information and a patient forum at Talk Acne (http://www.talkhealthpartnership.com/talkacne/).
Referral to secondary care
NICE recommends the following referral pathway for people with moderate acne that is unresponsive to primary care treatment, and severe acne.
- People who have severe psychosocial problems, including a morbid fear of deformity (body dysmorphic disorder) should be referred to a psychiatrist
- The following people should be referred to a dermatologist:
- Those who are developing scarring, or are at risk of developing it, despite primary care interventions
- Those with moderate acne that has failed to respond adequately to treatment over a period of at least six months, and treatment failure should be judged on the person’s perception of their condition
- Those with an uncertain diagnosis.
- Women who potentially have an underlying endocrinological cause of acne (such as polycystic ovary syndrome) that needs assessment should be referred to an endocrinologist or gynaecologist.
Treatment options in secondary care include oral isotretinoin, a teratogenic drug only prescribed under the supervision of a dermatology consultant or GPwER in dermatology, according to local protocol.