Adult Acne

By Dr Anjali Mahto / 01 May 2015

Dr Anjali Mahto details the prevalence and pathophysiology of acne in post-adolescent women, with an overview of the treatment options available

Introduction

Acne is one of the most common skin disorders amongst the general population, with research estimating that it affects up to 80% of people at some point during their lives.1 It is well-recognised that acne can cause both long-term physical and mental scarring, making it imperative that a treating practitioner assesses disease severity and psychological distress in individual patients, while creating a tailor-made treatment plan to suit their requirements. Within the past decade, scientific data, in addition to anecdotal evidence, has suggested that acne has become an increasing problem in one particular group – namely, the post-adolescent female.2

What causes acne?

Acne is a disorder of the pilosebaceous unit in skin which is composed of a sebaceous gland, hair follicle and hair. These are found all over the body except the palms, soles, top of the feet and the lower lip, while the face, neck and upper chest contain the largest number of pilosebaceous units. Sebum is produced by sebaceous glands and functions to keep skin well-lubricated and waterproof. During adolescence, under the influence of hormones (particularly androgens), sebaceous glands enlarge.3 The pathophysiology of acne is complex and multifactorial but a number of factors are thought to play a role, including interplay between hyperkeratinisation, excess sebum production and colonisation of the hair follicle
by Propionibacterium acnes (P acnes).4 Hyperkeratinisation is a disorder of the
cells lining the hair follicle. Under normal circumstances, these cells desquamate every 21 days. The growing hair usually pushes these cells out of the follicle. With hyperkeratinisation, this process fails and excess keratin is produced. Keratin is a sticky protein, which will cause dead skin cells to adhere to each other. This in turn can block the follicle or sebaceous gland in a process known as comedogenesis. Comedones (blackheads or whiteheads) can then develop.5If a comedone continues to grow under the skin surface, its contents of keratin and sebum will expand. Eventually, this will lead to rupture of the comedo wall and its contents will be extruded resulting in inflammation.6 This is visualised as pustular or papular acne. P. acnes can also proliferate at this stage contributing to the problem. Depending on the severity of inflammation, deeper, more painful nodules and cysts can develop which leave a risk of skin scarring.5

Epidemiology of female adult acne

Outpatient visits for patients with acne over the age of 25 are increasing, and women seem to make up the majority of patients with adult acne.7 The spectrum of acne as a disease is also showing some interesting trends. Cases are developing both earlier and later than what has previously been seen.7 There are also a large number of people in whom acne is continuing for longer, beyond the teenage years.7

Two distinct subtypes of adult female acne may be defined according to onset: ‘persistent’ and ‘late-onset’. Persistent disease is that which develops in the teenage years and fails to spontaneously resolve by the third decade of life. Patients who suffer from persistent acne have lesions intermittently or continuously during this time. They make up about 80% of cases of female adult acne.8 Late- onset disease is defined as acne that initially begins after the age of 25 years and has been reported to occur in about 18.4% of women.1 Most patients with post- adolescent acne present at 24 years of age.1 Some studies suggest that acne in later life is associated with a strong family history of the disorder. Data from one study has shown that 50% of patients had a first-degree relative with post-adolescent acne.9,10 There appears to be no link for the development of female adult acne with exogenous factors such as cosmetics, skin care products or occupation.2

Androgens

Androgens are steroid-based hormones present in both men and women. In women, they are produced primarily in the adrenal glands and ovaries; however, peripheral tissues such as skin and fat also play a role in converting weak androgens into their more potent counterparts. Women with high androgenic states are more likely to have acne, due to increased size of their sebaceous glands in addition to increased sebum production.7 Androgens are thought to be a major causative factor in female adult acne. The majority of women with acne in their post-adolescent years are likely to have a hormonal component to their disease.7 However, interestingly, most adult women will have normal circulating androgen levels upon blood tests.11 The possible explanation for this observation is that androgen levels are higher at the local cutaneous or skin level, rather than in the bloodstream. Certainly, data is consistent with this hypothesis and studies have shown increased levels of tissue-derived androgens acting locally on target tissues promoting acne in females.11,12,13
One also needs to consider, however, the possibility of disorders causing excess circulating androgen in women. Of these, polycystic ovarian syndrome (PCOS) and congenital adrenal hyperplasia (CAH) are most common.2 PCOS affects how a woman’s ovaries work and is one of the most common endocrine disorders in women of a reproductive age, with a prevalence of 6%.14 It can be associated with irregular menstruation, weight gain and hirsutism. Approximately 25% of women with PCOS will have acne.15 One review of data indicates severe acne or resistant acne in women is highly suggestive of PCOS and the discerning clinician should think about screening for this.12 CAH is a genetic disorder characterised by enzyme deficiencies that is much more rare, but important to consider in refractory cases.1 Patients may have precocious or failure of puberty, excessive facial hair, ambiguous genitalia, or menstrual irregularities. It may be diagnosed by blood tests and occurs more frequently in those of Eastern European Jewish descent.16 If there is any concern about these conditions, then suggest your patient sees their GP and is referred appropriately to a specialist (dermatologist, endocrinologist, gynaecologist).

Clinical features

Late onset acne has usually been associated with a distinctive clinical pattern, however, not all studies have confirmed this finding and many report that late onset disease may be similar to that in adolescence.17-18
Adult women often have a cyclical pattern to their disease, with peri-menstrual flares of acne. There can often be deep, tender, inflammatory lesions concentrated along the lower half of the face, jawline, chin and neck. Female adult acne sufferers have been reported to have comparatively low number of comedonal lesions compared to teenagers, although this finding is variable.7,17,18

Psychological aspects

There is no doubt that acne can have a significant impact on a patient’s emotional and psychological well-being. A recent study of approximately 2,000 acne sufferers, commissioned by the British Skin Foundation, revealed that 63% of respondents felt that the condition had affected their self-confidence and 20% had considered or attempted suicide.19 Adults may be more self-conscious of their disease, and experience more social anxiety and isolation, as acne is still largely considered a disease that primarily affects teenagers. It is important to assess how a patient’s acne is affecting their quality of life and ask pertinent questions relating to this. A specialist should review disease that is causing severe psychological distress.

Treatments

Female adult acne patients seem to exhibit higher treatment failure rates with traditional acne therapies. One study showed that 82% of persistent acne sufferers failed therapy with multiple courses of antibiotics, and 32% had relapsed after treatment with one or more courses of isotretinoin.20 Bearing this in mind, if your patient falls into this category, has nodules or cysts, evidence of scarring, or post-inflammatory change in pigmented skin, it is prudent to refer them to a dermatologist early. In my experience, these patients are much more likely to have resistant, unresponsive disease where treatment delay is likely to result in unnecessary further scarring. Acne therapies for the adult woman are likely to involve a combination of conventional therapies in association with adjunctive cosmetic treatments. Specifically this will be influenced by factors such as the predisposition of older skin to irritation, whether they are of child-bearing age, psychosocial impact, possible slow response to treatment and high likelihood of good adherence.2

Common treatment options for acne will now be discussed, but please note that this does not aim to be an exhaustive list. 

1) Comedo extraction21,22

Physical removal of comedones has been popular with dermatologists and aestheticians alike. It can be carried out in a number of ways including use of a comedone extractor, steam extraction, or electrosurgery (using a hyfrecator). It will cause a reduction in the number of future in amed lesions and can create an immediate sense of improvement. The procedure is also a useful adjunct prior to treatment with isotretinoin. There is a risk that it can cause tissue damage and make cystic lesions worse,21 so it is important that the practitioner is properly trained.

Open comedones (blackheads) reappear clinically after 20-40 days and closed comedones (whiteheads) within 30-50 days.22 The treatments therefore need to be repeated on a regular basis for optimum results.

2) Topical preparations

A number of topical therapies are available, including those containing benzoyl peroxide, antibiotics (e.g. clindamycin), salicylic acid, retinoids and azelaic acid.
These agents work in a number of ways aiming to reduce comedone formation and inflammation, or decreasing the activity of P. acnes. They are suitable for the treatment of comedonal or mild to moderate in ammatory acne.

3) Chemical peels23,24,25

The most commonly used agents are salicylic and glycolic acid-based products
but there is a much wider range of acid-based products available on the market. The chemical peel is applied to the skin surface to induce an accelerated form of exfoliation. Light peels will cause sloughing of the cells in the top layer of the skin or stratum corneum, while deeper peels can penetrate the dermis. Peels are useful to treat active comedones, post-inflammatory change and superficial scars. They are not suitable for inflammatory cystic acne, as they are unlikely to provide long-term control of disease.

4) Intralesional steroid

This is a useful method for treating large, stubborn, solitary acne cysts, or if a rapid response is required by the patient. Concentrations of 5mg/ml or less of triamcinolone acetonide can be injected directly into the acne lesion until subtle blanching is observed. This results in flattening of the nodule within 42-72 hours.26 There are risks of skin atrophy and pigmentary change with this procedure, and caution is advised.27

5) Photodynamic therapy (PDT)28,29,30

This is a developing area where a light source is combined with the application of a photosensitising agent to the skin. It is safe and effective but there is no consensus regarding which photosensitising agent should be used, the type of light source, or the optimum dosing schedule.28 Blue light can improve acne temporarily due to its anti- inflammatory effects but red light may provide the best long-term results. Side effects that can be a problem include pain, redness lasting 3-5 days, swelling or oedema, and pigmentation change. The data is still lacking for best practice.29,30

6) N-lite31,32

This is a type of pulsed dye laser that uses yellow light at 585 nm. It is thought to increase TGF-beta production in skin. TGF-beta is a potent stimulus for neocollagenesis and also reduces in ammation. Anecdotal evidence suggests that it may have a role in mild to moderate acne but may not be as efficacious as PDT.31,32 It can be of use in conjunction with other agents.

7) Oral treatments

If a patient has moderate to severe active acne with scarring, they should see a dermatologist. A dermatologist is likely to use one of a number of oral systemic agents such as antibiotics, spironolactone and isotretinoin for treatment. Spironolactone has anti-androgenic properties and is an effective drug for female adult acne that has failed to respond to other treatments. It has been used for more than two decades in a dermatological setting and is generally well tolerated.7 Isotretinoin is a retinoid drug of great value for nodulo-cystic acne. Despite its well-publicised side-effect profile, it is an extremely safe and effective drug when prescribed by a specialist.33 

 

References
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  2. Goulden V, Clark SM, Cunli e WJ. ‘Post-adolescent acne: a review of clinical features’, Br J of Dermatol, 140 (1999), p. 672-676.

  3. Friedlander SF, Eichen eld LF, Fowler JF et al. ‘Acne epidemiology and pathophysiology’, Semin Cutan Med Surg 29(2 Suppl 1) (2010), p. 2-4.

  4. Thiboutot D, Gollnick H, Bettoli V, Dre?no B, Kang S, Leyden JJ, et al. ‘New insights into the management of acne: an update from the Global Alliance to Improve Outcomes in Acne group’, J Am Acad Dermatol, 60(5 Suppl) (2009), p. 1-50.

  5. Zaenglein A, Thiboutot D. Acne vulgaris. In: Dermatology (Bolognia J, Jorizzo J, Rapini R, eds) (USA: Elsevier Ltd, 2003) p. 531-544.

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  7. Kim G, Del Rosso J. ‘Oral spironolactone in post-teenage female patients with acne vulgaris’, J of Clin Aesthet, 5(31) (2012), p. 37-50.

  8. Dreno B, Layton A, Zouboulis C, et al. ‘Adult female acne: a new paradigm’, J Eur Acad Dermatol Venereol 27(9) (2013), p. 1063-70

  9. Cunli e W, Gould D. ‘Prevalence of facial acne vulgaris in late adolescence and in adults’, BMJ, 26 (1979), p. 931-935.

  10. Gouden V, Mc Geown CH, Cunli eW. ‘The familial risk of adult acne: comparison between first-degree relatives of affected and unaffected individuals’, Br J of Dermatol, 141(2) (1999), p. 297-300.

  11. Carmina E, Lobo RA. ‘Evidence for increased androsterone metabolism in some normoandrogenic women with acne’, J Clin Endocrinol Metab, 76 (1993), p. 1111-1114.

  12. Looking bill DP, Horton R, Demers L Metal. ‘Tissue production of androgens in women with acne’, J Am Acad Dermatol, 12 (1985), p. 481-487.

  13. Thiboutot D, Harris G, Iles V et al. ‘Activity of the type 1 5-alpha-reductase exhibits regional differences in isolated sebaceous glands and whole skin’, J Invest Dermatol, (1995), p. 209-214.

  14. Azziz R, Woods KS, Reyna R, et al. ‘The prevalence and features of the polycystic ovary syndrome in an unselected population,’ J Clin Endocrinol Metab, 89(6) (2004) p. 2745-9.

  15. Lowenstein E J. ‘Diagnosis and management of the dermatological manifestations of the polycystic ovary syndrome’, Dermatol Ther, 19(4) (2006), p. 210-223.

  16. O’Brien RF, Emans SJ. ‘Polycystic ovary syndrome in adolescents’, J Ped Adolesct Gyn, 21 (3)(2008), p. 119-128.

  17. Lucky AW. ‘Quantitative documentation of a premenstrual are of facial acne in adult women,’ Arch Dermatol, 140 (2004), p. 423-424.

  18. Dre?no B, Thiboutot D, Layton AM, et al. ‘The Global Alliance to Improve Outcomes in Acne. Large- scale international study enhances understanding of an emerging acne population: adult females’, J Eur Acad Dermatol Venereol,Oct (2014).

  19. British Skin Foundation. Over half of acne sufferers experience verbal abuse from friends &family due to their condition (UK: British Skin Foundation, 2015) http://www.britishskinfoundation.org.uk/LinkClick.aspx?leticket=i2bE2n4c8m0%3D&tabid=172 [Accessed 15 April 2015]

  20. Goulden V, Stables G, Cunliffe W. ‘Prevalence of facial acne in adults’, J Am Acad Dermatol, 41(4) (1999), p. 577-580.

  21. Lowney ED, Witkowski, Simons H Metal. ‘Value of comedo extraction in treatment of acne vulgaris’, JAMA, 189 (1964), p. 1000-1002.

  22. Plewig G. ‘Follicular keratinisation’, J Invest Dermatol, 62(3) (1974), p. 308-320.

  23. Lee HS, Kim IH. ‘Salicylic acid peels for the treatment of acne vulgaris in Asian patients’, Dermatol Surg, 29(12) (2003), p. 1196-1199.

  24. Kaminaka C1, Uede M, Matsunaka H, et al. ‘Clinical evaluation of glycolic acid chemical peeling in patients with acne vulgaris: a randomized, double-blind, placebo-controlled, split-face comparative study’, Dermatol Surg, 40(3) (2014), p. 314-22

  25. Dreno B, Fischer TC, Perosino E, et al. ‘Expert opinion: efficacy of superficial chemical peels in active acne management--what can we learn from the literature today? Evidence-based recommendations’, J Eur Acad Dermatol Venereol, 25(6) (2011), p. 695-704

  26. Levine RM, Rasmussen JE. ‘Intralesional corticosteroids in the treatment of nodulocystic acne’, Arch Dermatol, 119(6) (1883), p. 480-481.

  27. Callen JP. ‘Intralesional corticosteroids’, J Am Acad Dermatol , 4(2) (1981) p.149-151.

  28. American Academy of Dermatology. Photodynamic therapy for acne, a workin progress (US: American Academy of Dermatology, 2011) https://www.aad.org/dw/monthly/2011/march/photodynamic-therapy-for-acne-a-work-in-progress [Accessed 15 April 2015]

  29. Kim RH, Armstrong AW. ‘Current state of acne treatment: highlighting lasers, photodynamic therapy, and chemical peels’, Dermatol Online J, 1(3) (2011), p. 2.

  30. Smith EV, Grindlay DJ, Williams H. ‘What’s new in acne? An analysis of systematic reviews published in 2009-2010’, Clin Exp Derm, 36(2) (2011), p. 119-122.

  31. Seaton ED1, Charakida A, Mouser PE, et al. ‘Pulsed-dye laser treatment for inflammatory acne vulgaris: randomised controlled trial’, Lancet, 25;362(9393) (2003), p. 1347-52.

  32. Seaton ED1, Mouser PE, Charakida A, et al. ‘Investigation of the mechanism of action of nonablative pulsed-dye laser therapy in photorejuvenation and in ammatory acne vulgaris’, Br J Dermatol, 155(4) (2006), p. 748-55.

  33. Good eld M, Cox N, Bowser A et al. ‘Advice on the safe introduction and continued use of isotretinoin in acne in the U.K. 2010’, Br J Dermatol, 162 (2010), p. 1172-1179. 

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