Managing Male Acne

By Dr Anil Sharma / 16 Dec 2016

Dr Anil Sharma provides an introduction to the causes of acne and outlines treatment methods suitable for men

Acne is a result of the action of hormones and other substances on the sebaceous glands and hair roots. These variables lead to plugged pores and outbreaks of acne in varying severity. Acne lesions usually appear on the face, neck, back, chest and shoulders. Although acne is not a serious health risk, it can be a source of considerable emotional distress.1 Severe acne often leads to permanent scarring if not treated quickly. While women are statistically more likely to suffer from acne, men are more liable to develop a more severe form of body acne due to the amount of circulating testosterone.2

It is generally accepted that women are more likely to seek medical help for skin-related issues due to societal norms, whereas men are less likely to present these issues to a professional until the disease is more mature. This is where, as health professionals, we must educate men and make skin health a priority.

Acne and hormones

The main difference between male and female skin, apart from the thickness, is the effect that the male sex hormones, known collectively as androgens, have. The primary sex hormone of this group is testosterone. Although amounts vary, adult males secrete ten times the amount of testosterone as women.3 Testosterone acts on androgen receptors, either directly, or by being converted into dihydrotestosterone (DHT), a considerably more potent activator of the androgen receptors. Throughout male childhood, testosterone levels remain relatively constant until puberty. After puberty, men continuously secrete higher amounts of testosterone that result in all the features of an adult male. With middle age, testosterone levels are responsible for the changes in men's hair and skin. In areas sensitive to androgen modulation, such as the face, underarms, and genital area, testosterone triggers the production of terminal body hair. In men, this extends to the arms, legs, chest and back – virtually the remainder of the skin’s surface area – except the soles of the feet and palms of the hands.3

Androgens, including testosterone, lead to the stimulation of a more compact network of collagen fibres than that found in female skin. This firm collagen and elastin network, coupled with the existence of terminal hair follicles, results in the thick skin seen in men.4 As a result of this biological difference, men are more likely to develop acne.4 Acne vulgaris' pathogenesis is multifactorial, with genetics playing a crucial factor, as an individual who is more predisposed is likely to go on to develop the disease.5 Acne develops as a result of the interplay of the following four factors:6

  • Release of inflammatory mediators into the skin
  • Follicular hyperkeratinisation following plugging of the follicle
  • Propionibacterium acnes follicular colonisation
  • Excessive sebum production

Studies indicate that inflammatory tendencies occur before hyperkeratinisation. Cytokines produced by CD4+ T-cells and macrophages activate local endothelial cells to up regulate inflammatory mediators such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and human leukocyte antigen (HLA)-DR inside the vessels around the pilosebaceous follicle.7

Follicular hyperkeratinisation entails enhanced keratinocyte growth and reduced desquamation, resulting in sebum- and keratin-packed microcomedones.8

Excess sebum is another factor affecting the progress of acne vulgaris. Removal and production of oil are managed by way of a quantity of mediators and different hormones. In particular, androgen hormones moderate oil production and release.10 The amount of comedonal acne in pre-pubertal females correlates with circulating levels of the adrenal androgen dehydroepiandrosterone sulfate (DHEAS).11 Numerous additional mediators and receptors, including human growth hormone, insulin-like growth factor and peroxisome proliferator-activated receptors manage the sebaceous gland and could give rise to the progress of acne.12,13 Moreover, the sebaceous gland acts as a neuroendocrine-inflammatory organ that is triggered via corticotrophin-releasing hormones in reaction to anxiety and typical functions.14

What is P. acnes? 

P. acnes or propionibacterium acnes pathogens, is an anaerobic organism contained in acne lesions. Inflammation influences the disease process by creating cell mediators that soften through the follicle wall. Research indicates that P. acnes might also reveal why acne vulgaris develops in some people but not others.9 


Treatment choices

Treatment should be geared toward the known pathogenic factors involved in acne. Included in these are: follicular epidermal hyperproliferation, excessive sebum production, P. acnes, and inflammation. Knowledge in the severity and the grade of the acne 

While women are statistically more likely to suffer from acne, men are more liable to develop a more severe form of body acne

Other treatment options As well as the treatments mentioned above, which, as stated may not be suitable for patients with back acne due to the surface area, there are also studies that suggest that the following can be effective in treating the condition.

Intralesional steroid injections have already been found to be beneficial for inflammatory lesions. Comedone removal doesn't change the course of the disorder, but it does enhance the patient’s appearance.16

Phototherapy (using red or blue light) and photodynamic therapy are being assessed as potential treatments for acne. It is well documented as per the literature that lasers (fractional), blue light and chemical peels are an excellent adjunct therapy once the endogenous sebaceous production is controlled.23

Summary

Body acne in men can, at times, present in a more severe form when compared to the female population, mainly because of the increased effect of circulating androgens. Due to the possibility of a more severe disease process and risk of scarring, oral isotretinoin may be the first line treatment of choice. However, many patients are anxious about the possible side effects. In my own practice in both the Canada and the UK, I have found great benefit in combining a low dose of isotretinoin (20mg once daily), in combination with a low strength of topical tretinoin (0.025% in an ointment base). Patients may be on treatments for longer but they are more likely to adhere to the treatment protocol and thus achieve the end goal of symptom control and less psychological suffering associated with acne. It is important to treat acne quickly and efficiently to avoid permanent scarring, of which men may be more at risk of developing.15

Dr Anil Sharma is the founder of Sharma Skin & Hair Surgery in Canada.

References

  1. B. Archer, S. N. Cohen, S. E. Baron, and British Association of Dermatologists and Royal College of General Practitioners, ‘Guidance on the diagnosis and clinical management of acne,’ Clinical and experimental dermatology, 37(2012).
  2. Haider & J. C. Shaw, ‘Treatment of acne vulgaris,’ JAMA : the journal of the American Medical Association, 292(2004) pp.726–735.
  3. MercèM. Fernández-Balsells, Mohammad H. Murad, Melanie Lane, Juliana F. Lampropulos, Felipe Albuquerque, Rebecca J. Mullan, et al., ‘Adverse effects of testosterone therapy in adult men: A systematic review and Meta-Analysis’, Journal of Clinical Endocrinology & Metabolism, 95(2010) pp.2560–2575.
  4. Ana Maria M. Abreu-Velez and Michael S, ‘Howard. Collagen IV in normal skin and in pathological processes’, North American journal of medical sciences, 4(2012) pp.1–8.
  5. Goulden V, McGeown CH, Cunliffe WJ, ‘The familial risk of adult acne: a comparison between first-degree relatives of affected and unaffected individuals,’ Br J Dermatol, 141(1999) pp.297-300.
  6. Thiboutot D, Gollnick H, Bettoli V, Dréno 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(2009) pp.1-50.
  7. Jeremy AH, Holland DB, Roberts SG, Thomson KF, Cunliffe WJ, ‘Inflammatory events are involved in acne lesion initiation’, J Invest Dermatol, 121(2003) pp.20-7.
  8. Norris JF, Cunliffe WJ, ‘A histological and immunocytochemical study of early acne lesions’, Br J Dermatol, 118(1988) pp. 651-9.
  9. Webster GF, ‘Inflammatory acne represents hypersensitivity to Propionibacterium acnes’, Dermatology, 196(1998) pp. 80-1. 
  10. Pochi PE, Strauss JS, ‘Sebaceous gland activity in black skin’, Dermatol Clin, 6(1988) pp.349-51.
  11. Lucky AW, Biro FM, Simbartl LA, Morrison JA, Sorg NW, ‘Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study, J Pediatr, 130(1997) pp.30-9.
  12. Trivedi NR, Cong Z, Nelson AM, Albert AJ, Rosamilia LL, Sivarajah S, et al., ‘Peroxisome proliferator-activated receptors increase human sebum production, J Invest Dermatol, 126(2006) pp.2002-9.
  13. Smith TM, Cong Z, Gilliland KL, Clawson GA, Thiboutot DM, ‘Insulin-like growth factor-1 induces lipid production in human SEB-1 sebocytes via sterol response element-binding protein-1’, J Invest Dermatol, 126(2006) pp.1226-32.
  14. Zouboulis CC, Böhm M, ‘Neuroendocrine regulation of sebocytes – a pathogenic link between stress and acne,’ Exp Dermatol, 13(2004) pp.31-5.
  15. Gollnick H, Cunliffe W, Berson D, Dreno B, Finlay A, Leyden JJ, et al, ‘Management of acne: a report from a Global Alliance to Improve Outcomes in Acne,’ J Am Acad Dermatol, 49(2003) pp.1-37.
  16. Cunliffe WJ, Goulden V, ‘Phototherapy and acne vulgaris’, Br J Dermatol, 142(2000) pp.855-6.
  17. Zaenglein AL, Pathy AL, Schlosser BJ, Alikhan A, Baldwin HE, Berson DS, et al. ‘Guidelines of care for the management of acne vulgaris’, J Am Acad Dermatol, 74(2016)pp.945-973.
  18. White GM, Chen W, Yao J, Wolde-Tsadik G, ‘Recurrence rates after the first course of isotretinoin’, Arch Dermatol, 134(1998) pp.376-8.
  19. Halvorsen JA, Stern RS, Dalgard F, Thoresen M, Bjertness E, Lien L, ‘Suicidal ideation, mental health problems, and social impairment are increased in adolescents with acne: a population-based study,’ J Invest Dermatol, 131(2011) pp.363-70.
  20. Jacobs DG, Deutsch NL, Brewer M, ‘Suicide, depression, and isotretinoin: is there a causal link?’, J Am Acad Dermatol, 45(2001) pp.168-75.
  21. Fabbrocini, Izzo, Faggiano, Del Prete, Donnarumma, Marasca , Marciello , Savastano, Monfrecola, Colao, ‘Low glycaemic diet and metformin therapy: a new approach in male subjects with acne resistant to common treatments’, Clin Exp Dermatol, 41(2016), pp. 38-42. <https://www.ncbi.nlm.nih. gov/pubmed/26053680>
  22. Hywel C. Williams, Robert P. Dellavalle, and Sarah Garner. Acne vulgaris. Lancet, 379(2012) pp.361–372.
  23. Randie H. Kim and April W. Armstrong, ‘Current state of acne treatment: highlighting lasers, photodynamic therapy, and chemical peels’, Dermatology online journal, 17(2011). 

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