Narrative review
Modern management of acne
Victoria Rebecca Harris, Alan J Cooper
A
cne vulgaris is an inflammatory skin condition with an
estimated global prevalence of 9.4% and is the eighth most
prevalent disease in the world.1 Although perceived as a
disease of adolescence, it can persist — with women typically more
affected than men — beyond the teenage years.2 Acne is increas-
ingly a reason for dermatologic consultation among adult women.3
Risk factors
The factors that contribute to acne, particularly the role of diet, are
an area of changing ideas with ongoing research that is of imme-
diate clinical relevance. There exists plausible theoretical research
that elements of contemporary Western diets may be associated
with acne.4 For example, androgens and hormonal mediators, such
as the insulin-like growth factor 1 found in milk, can survive pro-
cessing and may contribute to the excess sebum production seen in
acne.5 A recent large prospective cohort study found that skim milk
contains hormonal constituents in quantities that are sufficient to
have biological effects in teenage boys.6
The high glycaemic index foods found in the typical adolescent
Western diet have also been investigated for their contribution to
the development of acne. A recent randomised controlled trial that
involved adolescent boys with acne vulgaris found an improve-
ment in acne and insulin sensitivity after a diet with a low
glycaemic load.7 However, further research is required to confirm
this study and to identify the underlying pathophysiological
mechanisms of diet and weight loss in acne.
Hereditary factors have also been attributed to the pathogenesis of
acne, with a positive family history observed in severe cases of
acne.8 In addition, observations in the study of twins suggest a
genetic component of the disease.9 More recently, a large scale
genetic study in the United Kingdom compared the genetics of
patients with severe acne with that of the subjects in the control
group and provided information on predicting who is prone to acne
by establishing the loci of possible causative genes.10 This study
provides the basis for new research into the genetic basis of acne.
Clinical features
The clinical features of acne include seborrhoea and a spectrum
of lesions, including non-inflammatory lesions (comedones),
inflammatory lesions (pustules), various degrees of scarring, and
in very severe cases, nodules and cysts.11 The distribution of acne
follows the areas of greatest density of pilosebaceous units, such as
the face, neck, chest and back.12 Acne typically affects adolescents
around adrenarche (aged 9e17 years) as this coincides with an
increase in sebum production of sebaceous glands (Box 1, Box 2 and
Box 3).13
Impact on quality of life
In addition to the physical symptoms of inflammation, scarring
and disfigurement, there are also long lasting psychosocial effects.
Patients with acne may experience tremendous impairment to
quality of life that is comparable with that experienced by patients
Royal North Shore Hospital, Sydney, NSW. alanjco@tpg.com.au j doi: 10.5694/mja16.00516
Summary
 Acne is a chronic inflammatory disease of the pilosebaceous
unit resulting from androgen-induced increased sebum
production; altered keratinisation; bacterial colonisation of hair
follicles on the face, neck, chest and back by Propionibacte-
rium acnes; and an inflammatory response in the skin. The
exact way these processes interact and the order in which they
occur in the pathogenesis of acne are still unclear.
 Scarring that occurs from acne, particularly severe acne, can
persist a lifetime and have long lasting psychosocial effects.
Depression, social isolation and suicidal ideation are frequent
comorbidities in acne.
 Despite the plethora of topical and systemic treatments
available for acne, there is a relative lack of quality evidence
for its application. Of the systemic treatments available, oral
isotretinoin remains the most effective well established
treatment for acne that targets all the aetiological factors.
 Current guidelines for the treatment of acne are based largely on
expert consensus and advocate a combination of topical agents
in mild to moderate cases and reserve the use of systemic
therapies for moderate to severe or refractory cases of acne.
However, given the psychosocial impacts of acne, there is a
strong argument for early, effective treatment with systemic
therapy when topical and general measures have failed.
with chronic illnesses, such as asthma, epilepsy, diabetes, back pain
or arthritis.14 Irrespective of the degree of severity of acne, patients
are at an increased risk of anxiety and depression compared with
the non-affected population.15 Additionally, the emotional
components of the disease might not be immediately recognised or
volunteered by the patient. It is therefore important for clinicians to
be aware of the established psychological sequelae of acne and be
alert for and elicit a spectrum of psychological symptoms and signs
as clinically appropriate.
Pathogenesis
Acne is a multifactorial, inflammatory disease of the pilosebaceous
unit. It involves the interplay of four distinct processes:16
 excess sebum production caused by increased androgen
production;
 altered keratinisation within the follicle and ductal occlusion;
 proliferation and colonisation of the pilosebaceous duct by
Propionibacterium acnes (P. acnes); and
MJA 206 (1)
 release of inflammatory mediators into the skin.
The exact sequence of events and how they are interconnected
remain unknown; however, recent research suggests that these
factors are more interrelated than previously understood.17
j
16 January 2017
Treatment
The mainstays of an acne treatment regimen should include general
measures, such as face hygiene with soap-free face wash, use of oil-
free moisturisers to minimise the side effects of topical treatments,
41
 Narrative review
1 Clinical photograph of a 16-year-old male patient with
severe nodulocystic acne affecting the chest
and avoidance of triggers. Examples of reported triggers of acne
include makeup, sunscreens and medications, such as corticoste-
roids and anabolic steroids.18 The aim of pharmacological treatment
of acne is to maximally suppress the aetiological factors, clear the
acne and minimise scarring. The role of combining topical agents is
to target more of the pathogenic factors of acne and promote a more
effective clearance of acne.19 The main topical treatments include
keratinolytics (sulphur, salicyclic acid), antiseptics (benzoyl
peroxide), retinoids and antibiotics. These agents are available in a
variety of strengths and vehicles; therefore, a tolerable regimen can
usually be found for most skin types.
While there is a plethora of topical options available, there is
a paucity of quality studies comparing relative efficacy among the
different topical agents. Current guidelines are instead reliant on
expert consensus for treatment rather than on evidence-based
treatment and include the Global Alliance to Improve Outcomes in
Acne,20 the European Dermatology Forum,21 and the guidelines of
care from the American Academy of Dermatology.11
16 January 2017
Another factor that contributes to the difficulty of treating acne is
the lack of a singular global assessment standard in clinical practice
or research.22 An assessment of acne severity is multifactorial and
dependent on physical assessment (eg, lesion type, number, size,
distribution and location)23 in addition to an assessment on the
j
MJA 206 (1)
impact of acne on the quality of life of the individual (eg, the
Dermatology Life Quality Index).24
Benzoyl peroxide (BPO)
BPO is an effective bactericidal agent that causes peeling of the skin
42 and is beneficial for acne with mild and transient irritation. It is also
conveniently available for patients as an over-the-counter treatment.
2 Clinical photograph of a 16-year-old male patient with
severe nodulocystic acne affecting the face
It is currently the strongest antimicrobial agent that has no known
association with development of resistance.25 The current thera-
peutic guidelines in Australia recommend BPO 5% as initial therapy
for mild to moderate acne.26 It can be used in combination with
topical antibiotics or a topical retinoid. However, the side effects of
BPO can make its use intolerable; they include cutaneous irritation or
dryness, which can be minimised by application to dry skin to
reduce irritation; contact urticaria; contact dermatitis; and bleaching
of clothes and bed linen. If irritation occurs, then lower strengths and
less frequent application may be suggested to ensure compliance.
Topical retinoids
Topical retinoids, including tretinoin, adapalene, isotretinoin
and tazarotene, work by reducing obstruction within the follicle
through action on abnormal keratinisation and are also anti-
inflammatory.12 The Australian therapeutic guidelines recom-
mend either adapalene 0.1% in cream or gel topically, or tretinoin
0.025% in cream topically for 6 weeks and then review.26 Side
effects for topical retinoids include local irritation and photosen-
sitivity and should be discontinued in rare cases of severe
cutaneous irritation. The gradual introduction of retinoids in
combination with a low irritant, pH balanced, soap-free cleanser
may avoid irritation.
The current Australian therapeutic guidelines warn that topical
retinoids are teratogenic and state that they should be avoided in
women who are planning to become pregnant, are pregnant
or breastfeeding.26 The regulatory concern of the teratogenic
potential of topical tretinoin is contrary to previous human
percutaneous absorption studies. A human study that examined
the percutaneous absorption of tretinoin in various formulations
indicated that it was minimally absorbed and did not affect the
endogenous levels of the drug or its metabolites in the subjects
studied.27 There has also been a study that examined the incidence

3 Clinical photograph of a 16-year-old male patient with
severe nodulocystic acne affecting the back
of major congenital anomalies for 215 exposed women versus
430 non-exposed age-matched women, and concluded that topical
tretinoin is not associated with increased risk for major congenital
disorders.28
Antibiotics
Topical. The primary topical antibiotics used for acne are clinda-
mycin and erythromycin and they have similar efficacy. However,
there is growing concern about P. acnes resistance, particularly with
erythromycin.16 Therefore, the current Australian therapeutic
guidelines suggest the use of a combination of BPO and topical
retinoid gel (benzoyl peroxide/adapalene 2.5%/0.1%) or clinda-
mycin gel (benzoyl peroxide/clindamycin 5%/1%).26 Antibiotic
topical monotherapy is to be avoided; nevertheless, clindamycin
alone can be used if the patient’s skin is prone to irritation with
other acne treatments.
Oral. Despite the growing concerns surrounding antimicrobial
resistance, initial treatment for moderate to severe acne is an
oral antibiotic — for both antimicrobial and anti-inflammatory
effects — in combination with topical retinoid and benzoyl
peroxide.29 To prevent recurrence when oral antibiotics are ceased,
it is important to establish a tolerable long term topical treatment
when commencing oral antibiotics. Doxycycline (50e100 mg
orally once daily for 6 weeks) is the first agent of choice, and if it is
not tolerated, then minocycline (50e100 mg orally once daily for
6 weeks), and if tetracyclines are contraindicated (eg, pregnancy),
then erythromycin (250e500 mg daily for 6 weeks).26
Side effects of antibiotic treatment are a concern for both patients
and clinicians and, therefore, the choice of antimicrobial agent may
vary among dermatologists based on preference and experience.
For example, photosensitivity caused by doxycycline may be
intolerable or impractical as a first line treatment for some patients.
Narrative review
Rare serious effects exist within both tetracycline and macrolide
antibiotic classes. Minocycline, for example, has been associated
with drug reaction with eosinophilia and systemic symptoms,30
vestibular disturbances, benign intracranial hypertension, and
pigment deposition in the teeth, skin and mucous membranes.31
Macrolides are not without serious adverse effects either, with
reports of cardiac conduction abnormalities and hepatotoxicity.32
The efficacy of antibiotic therapy should be reviewed after 6 weeks
and if no improvement is observed, a change in antibiotic should be
considered. The prolonged use of antibiotics is questionable in light
of resistance concerns from the long term use of low dose
antibiotics.33
Antiadrenergics
Combined oral contraceptive pill (COCP). Hormonal therapies
are useful adjunctive treatment options. A recent Cochrane review
reaffirmed the efficacy of COCP for treatment of inflammatory and
non-inflammatory acne, but found few differences in efficacy
between the different types of COCP that are currently available.34
The Australian guidelines, however, suggest that the COCP most
likely to improve acne is one that contains cyproterone acetate.26
The benefit from COCP is slow and may not be apparent for
3 months, so a 6 month trial is recommended.
Spironolactone. Spironolactone is a diuretic and anti-androgen
drug that works by blocking androgen receptors when adminis-
tered at increased doses. Spironolactone is useful to treat acne in
female patients when COCP is contraindicated, not tolerated or
desired, or insufficient as monotherapy.35 It can be used in male
patients, but may have the adverse effect of feminisation, as seen in
a recent Japanese trial that involved 23 men treated initially with
200 mg spironolactone daily for 8 weeks, but ceased in men
prematurely due to the side effect of gynaecomastia.36 The
common adverse effects of treatment are irregular menstrual
bleeding, diuresis, breast tenderness, fatigue, headache and
dizziness.37 Pregnancy should be excluded before commencing
therapy, as there is a risk of defective virilisation of the male fetus.
Hyperkalaemia is a concerning side effect; however, it is rare in
young healthy females and it was recently stated in the American
guidelines for the treatment of acne that testing potassium in young
healthy females on spironolactone is unnecessary.11
Oral retinoids
Since isotretinoin (13-cis retinoic acid) was introduced in 1982, it
has been the most effective treatment for acne and the only
treatment that offers remission.
Its efficacy is due to the fact that it targets all four known
components involved in the development of acne.38
MJA 206 (1)
A widely accepted standard dosing of isotretinoin in severe cases
of acne is a starting dose of 0.5 mg/kg/day for the first 4 weeks,
increase to 1 mg/kg/day, then continuation until a cumulative
dose of 120e150 mg/kg is reached and tolerated by the patient.39
j
For very severe cases that involve large areas of inflammatory
16 January 2017
lesions, a course of prednisone 20e40 mg a day and starting at
lower doses of isotretinoin to prevent severe flares may also be
warranted (Box 4 and Box 5).40
Considerably higher doses of isotretinoin than those used histori-
cally, including up to 220 mg/kg, were examined in a recent
prospective interventional study and it was found that there was a
significantly decreased risk of relapse and that rash was the only 43
adverse effect in patients.41 Conversely, a low dose isotretinoin
 Narrative review

4 Clinical photograph of a 14-year-old male patient with 5 Clinical photograph of an 18-year-old male patient
severe nodulocystic acne and scarring of the face and following treatment of isotretinoin at 135 mg/kg
chest before treatment cumulative dose

Salicylic acid (a b-hydroxy acid) and glycolic acid (an a-hydroxy

acid) are two chemical peels currently available as an adjuvant
treatment for acne affecting the face.49 Chemical peels improve
acne by minimising the abnormal pattern of keratinisation by
causing desquamation, which reduces corneocyte cohesion and
keratinocyte blockage, and allowing the promotion of normal
epidermal differentiation.50 A downside to this is that it requires
multiple treatments to be efficacious, which is costly and can have
side effects of redness and irritation to the skin. Therefore, chemical
peels do not replace the existing topical and systemic treatment
available for acne.11
(0.3e0.4 mg/kg/day) treatment has also been found to be a safe and
effective management of patients with early recurrent disease.42 Lasers and light-based devices for acne have been increasingly
used over the past few years. Light therapy, in the form of blue light
Use of oral isotretinoin is tightly regulated because of its well
and blue and red light, can treat active acne causing the destruction
known teratogenic effects and is available in many countries only
of the propionibacteria through targeting the porphyrins produced
through specialist care.43 A recent population-based study of
by these bacteria.51 Evidence exists that light therapy is a safe and
incidence rates of pregnancy, abortions and birth deformities
efficacious treatment of acne.52
incurred by women on isotretinoin found that the incidence of
major malformations while on isotretinoin was 11%, which is lower
than what was previously reported.44
6 Clinical photograph of an 18-year-old male patient with
Depression and suicide have been reported and well publicised extensive hypertrophic scarring over the shoulders
in patients taking isotretinoin.45 However, a causal relationship
between isotretinoin and suicidal thoughts or depression has never
been established.46 Conversely, there have been studies that
showed reduced anxiety and depression in patients with cystic
acne after a successful treatment with oral isotretinoin.47
16 January 2017

Adjuvant and newer procedures for acne and

acne scarring
j
MJA 206 (1)

Scarring is an unwanted complication of acne that should be

treated seriously (Box 6). The psychological effects of acne can be
long lasting, and the association between acne and depression and
anxiety is independent of the disease severity.48 As a consequence,
newer treatment modalities and adjuvant therapies for acne and
scarring, while costly, are a growing market in both medical and
44 cosmetic practices. Examples of these adjuvant modalities include
chemical peels, light, laser and radiofrequency.

Radiofrequency and photodynamic therapy are examples of other
new therapies for the treatment of acne and scarring. While there
has been a recent plethora of research on the efficacy of the different
modalities, there is still a lack of long term follow-up to prove their
efficacy in the treatment of acne.53
Conclusion
Acne is a chronic disease prevalent in the adolescent population
and, without appropriate treatment, it may cause potentially
serious psychological damage and physical scarring. In order to
effectively and rapidly reduce acne lesions, a combination therapy
Narrative review
that targets as many of the underlying factors as possible should be
considered. The emergence of P. acnes resistance requires a com-
bination topical therapy and a low therapeutic threshold to intro-
duce oral isotretinoin, which is a highly effective, well established
treatment of acne and the only therapy that targets all of the
aetiological factors of this disease.
Competing interests: Alan Cooper was a member of the Roaccutane Advisory Board, a group of
Australian dermatologists brought together by Roche Products Pty Ltd. The preparation of this
document was not supported in any way by Roche Products Pty Ltd.
Provenance: Commissioned; externally peer reviewed. n
ª 2017 AMPCo Pty Ltd. Produced with Elsevier B.V. All rights reserved.

1 Tan JK, Bhate K. A global perspective on the
epidemiology of acne. Br J Dermatol 2015; 172
Suppl 1: 3-12.
2 Collier CN, Harper JC, Cafardi JA, et al. The prevalence of
acne in adults 20 years and older. J Am Acad Dermatol
2008; 58: 56-59.
3 Dreno B, Thioboutot D, Layton AM, et al. Large-scale
international study enhances understanding of an
emerging acne population: adult females. J Eur Acad
Dermatol Venereol 2015; 29: 1096-1106.
4 Spencer EH, Ferdowsian HR, Barnard ND. Diet and acne: a
review of the evidence. Int J Dermatol 2009; 48: 339-347.
5 Davidovic BB, Wold R. The role of diet in acne: facts and
controversies. Clin Dermatol 2010; 28: 12-16.
6 Adebamowo CA, Spiegelman D, Danby FW, et al. Milk
consumption and acne in teenage boys. J Am Acad
Dermatol 2008; 58: 787-793.
7 Smith RN, Mann NJ, Braue A, et al. A low-glycemic-
load diet improves symptoms in acne vulgaris
patients: a randomized controlled trial. Am J Clin Nutr
2007; 86: 107-115.
8 Dreno B, Poli F. Epidemiology of acne. Dermatology
2003; 206: 7-10.
9 Bastille V, Snieder H, MacGregor AJ, et al. The influence
of genetics and environmental factors in the
pathogenesis of can: a twin study of acne in women.
J Invest Dermatol 2002; 119: 317-322.
10 Navarini AA, Simpson MA, Weale M, et al. Genome-wide
association study identifies three novel susceptibility loci
for severe acne vulgaris. Nat Commun 2014; 5: 4020.
11 Zaenglein AL, Pathy AL, Schlosser BJ, et al. Guidelines of
care for the management of acne vulgaris. J Am Acad
Dermatol 2016; 74: 945-973.
12 Williams HC, Dellavalle RP, Garner S. Acne vulgaris.
Lancet 2012; 379: 361-372.
13 Zouboulis C. Acne and sebaceous gland function.
Clin Dermatol 2004; 22: 360-366.
14 Mallon E, Newton JN, Klassen A, et al. The quality of life
in acne: a comparison with general medical conditions
using generic quality of life questionnaires. Br J Dermatol
1999; 140: 672-676.
20 Gollnick H, Cunliff W, Berson D, et al. Management of
acne: a report from global alliance to improve outcomes
in acne. J Am Acad Dermatol. 2003; 49 Suppl 1: S1-S37.
21 Nast A, Dreno B, Bettoli V, et al. European evidence
based (S3) guidelines for the treatment of acne. J Eur
Acad Dermatol Venereol 2012; 26 Suppl 1: 1-29.
22 Barratt H, Hamilton F, Car J, et al. Outcome measures in
acne vulgaris: systematic review. Br J Dermatol 2009;
160: 132-136.
23 Tan JK, Tang J, Gupta AK, et al. Development and
validation of a comprehensive acne severity scale.
J Cutan Med Surg 2007; 11: 211-216.
24 Finlay AY, Khan GK. Dermatology Life Quality Index
(DLQI) e a simple practical measure for routine clinical
use. Clin Exp Dermatol 1994; 19: 210-216.
25 Gollnick HPM, Dreno B. Pathophysiology and management
of acne. J Eur Acad Dermatol Venereol 2015; 29 Suppl 4: 1-2.
26 eTG complete [website]. Melbourne: Therapeutic
Guidelines Limited; 2016. https://tgldcdp.tg.org.au/
etgcomplete (accessed Apr 2016).
27 Latriano L, Tzimas G, Wong F, et al. The percutaneous
absorption of topically applied tretinoin and its effect
on endogenous concentrations of tretinoin and its
metabolite after single doses or long term use. J Am
Acad Dermatol 1997; 36(3 Pt 2): S37-S46.
28 Jick SS, Terris BZ, Jick H. First trimester topical tretinoin
and congenital disorders. Lancet 1993; 341: 1181-1182.
29 Tan J, Humphrey S, Vender R, et al. A treatment for
severe nodular acne: a randomized investigator-blinded,
controlled, noninferiority trial comparing fixed-dose
adapalene/benzoyl peroxide plus doxycycline vs. oral
isotretinoin. Br J Dermatol 2014; 171: 1508-1516.
30 Shaughnessy KK, Bouchard SM, Mohr MR, et al.
Minocycline-induced drug reaction with eosinophilia and
systemic symptoms (DRESS) syndrome with persistent
myocarditis. J Am Acad Dermatol 2010; 62: 315-318.
31 Goulden V, Glass D, Cunliff WJ. Safety of long-term
high-dose minocycline in the treatment of acne.
Br J Dermatol 1996; 134: 693-695.
32 Glassman AH, Bigger T. Antipsychotic drugs: prolonged
QTc interval, torsade de pointes, and sudden death.
37 Shaw JC, White LE. Long-term safety of spironolactone
in acne: results of an 8-year follow up study. J Cutan
Med Surg 2002; 6: 541-545.
38 Cunliff WJ, Hughes BR, Layton AM, et al. Retinoids today
and tomorrow. The isotretinoin mechanism of action. In:
Proceedings of the Satellite Symposium to the First
Congress of the European Academy of Dermatology and
Venereology (EAVD). Florence: Roche, 1989: 5-13.
39 Strauss JS, Rapini RP, Shalita AR, et al. Isotretinoin
therapy for acne: results of a multicenter dose-response
study. J Am Acad Dermatol 1984; 10: 490-496.
40 Webster G. Acne vulgaris. BMJ 2002; 325: 475-479.
41 Blasiak R. High-dose isotretinoin treatment and the
rate of retrial, relapse, and adverse effects in patients
with acne vulgaris. JAMA Dermatol December 2013;
149: 1392-1397.
42 Amichai B, Semer A, Grunwald MH. Low dose
isotretinoin in the treatment of acne vulgaris. J Am Acad
Dermatol 2006; 54: 644-646.
43 Cooper A. Treatment of acne with oral isotretinoin:
recommendations based on Australian experience.
Australas J Dermatol 2003; 44: 97-105.
44 Bérard A, Laurent A, Gideon K, et al. Isotretinoin,
pregnancies, abortions and birth defects: a
population-based perspective. Br J Clin
Pharmacol 2007; 63: 196-205.
45 Sundström A, Alfredsson L, Sjölin-Forsberg G, et al.
Association of suicide attempts with acne and acne
treatment with isotretinoin: retrospective Swedish
cohort study. BMJ 2010; 341: c5812.
46 Jacobs DG, Deutsch NL, Brewer M. Suicide, depression,
and isotretinoin: is there a causal link? J Am Acad
Dermatol 2001; 45: S168-S175.
47 Rubinow D, Peck G, Squillace K, et al. Reduced anxiety and
depression in cystic acne patients after successful treatment
with oral isotretinoin. J Am Acad Dermatol 1987; 17: 25-32.
48 Gieler U, Gieler T, Kupfer JP. Acne and quality of life -
impact and management. J Eur Acad Dermatol Venereol
2015; 29 Suppl 4: 12-14.
49 Kessler E, Flanagan K, Chia C, et al. Comparison of
a- and b-hydroxy acid chemical peels in the treatment
MJA 206 (1)

15 Gieler U. Acne and Quality of Life e impact and
management. J Eur Acad Dermatol Venereol 2015; 29
Suppl 4: 12-14.
16 Thiboutot D, Gollnick H, Bettoli V, et al. New Insights
into the management of acne: an update from the
Am J Psychiatry 2001; 158: 1774-1782. of mild to moderately severe facial acne vulgaris.
33 Eady AE, Cove JH, Layton AM. Is antibiotic resistance in Dermatol Surg 2008; 34: 45-51.
cutaneous propionibacteria clinically relevant? 50 Lee HS, Kim IH. Salicylic acid peels for the treatment
Implications of resistance for acne patients and of acne vulgaris in Asian patients. Dermatol Surg:
prescribers. Am J Clin Dermatol 2003; 4: 813-831. 2003; 29: 1196-1199.
j
16 January 2017

global alliance to improve outcomes in acne group. J Am
Acad Dermatol 2009; 60 Suppl 5: S1-S37.
17 Suh DH, Kwon HH. What’s new in the physiology of
acne? Br J Dermatol 2015; 172 Suppl 1: 13-19.
18 Walker J, Adams B. Cutaneous manifestations of
anabolic- androgenic steroid use in athletes.
Int J Dermatol 2009; 48: 1044-1048.
19 Gollnick HPM. From new findings in acne pathogenesis
to new approaches in treatment. J Eur Acad Dermatol
Venereol 2015; 29 Suppl 5: 1-7.
34 Arowojolu AO, Gallo MF, Lopez L M, et al. Cochrane
Review: combined oral contraceptive pills for treatment
of acne. Evid-Based Child Health 2011; 6: 1340-1433.
35 Shaw J. Low dose adjunctive spironolactone in the
treatment of acne in women: a retrospective analysis of
85 consecutively treated patients. J Am Acad Dermatol
2000; 43: 498-502.
36 Sato K, Matsumoto D, Iiuka F, et al. Anti-androgenic
therapy using oral spironolactone for acne vulgaris in
Asians. Aesthetic Plast Surg 2006; 30: 689-694.
51 Lee W, Shalita A, Poh-Fitzpatrick M. Comparative
studies of porphyrin production in Propionibacterium
acne and Propionibacterium granulosum. J Bacteriol
1978; 133: 811-815.
52 Papageorgiou P, Katsambas A, Chu A. Phototherapy
with blue (415 nm) and red (660 nm) light in
treatment of acne vulgaris. Br J Dermatol 2000; 142:
973-978.
53 Taub AF. Procedural treatments for acne vulgaris. 45
Dermatol Surg 2007; 33: 1005-1026. -