Clinical SKILLS

Acne vulgaris — diagnosis,

management and optimising
patient care
Isabel Lavers

Acne vulgaris is deemed the most common skin condition worldwide (Pommerville, 2010). Often regarded
as a self-limiting disease of adolescence acne, it is in fact a chronic disease with pathogenic factors that may
persist for decades, patterns of recurrence and relapse, acute outbreaks and detrimental psychological effects.
Acne requires potentially long-term therapy and has a significant impact on a patient’s quality of life.The major
goals of treating acne are to heal existing skin lesions, stop new lesions from forming, prevent irreversible
scarring and reduce the psychological distress that acne can cause by improving the skin’s appearance.
Antibiotic resistance is increasing in acne therapy and requires careful review of prescribing habits. Acne
is treatable and early evidence-based intervention is crucial to the successful management of acne and the
prevention of lifelong scarring.This article will outline current knowledge of the condition in general and will
explore evidence-based treatments and issues concerning antibiotic resistance in acne vulgaris.

care account for 3.5 million annually

Key words
Acne vulgaris
Chronic skin disorder
Scarring
Psychological distress
Evidence-based treatment
Antibiotic resistance
Acne vulgaris
Acne vulgaris is a prevalent and non-
discriminatory condition affecting
individuals of almost all ages and
ethnicities. It may begin as early as
the neonatal period and peaks in
adolescence. For some acne will even
persist into the fourth or fifth decade
of life, thus the majority of the world’s
population will either have personally
experienced acne at some point
in their lives, or know of someone
who has. According to Buxton and
Morris-Jones (2009) 80-100% of
adolescents are affected, therefore
it is not surprising that in the United
Kingdom acne consultations in primary
Isabel Lavers is a Specialist Nurse in
Dermatology at Salford Royal NHS
Foundation Trust
(Dawson, Dellavalle, 2013).
This requires the healthcare
professional to diagnose acne vulgaris
correctly, have knowledge of the
different types of acne treatments
available, interpret current evidence-
based guidance on acne prescribing
correctly and treat without delay.
Acne vulgaris is a chronic skin
disorder of the pilosebaceus unit
(PSU) (Figure 1), which is made up
The majority of the world’s
population will either
have personally experienced
acne at some point in their
lives or know of someone
who has.
of the hair follicle and accompanying
sebaceous glands. It is characterised
by open and closed comedones,
inflammatory papules, pustules, cysts
and nodules. It is a polymorphic skin
disease most commonly affecting
the face in 99% of patients and less
frequently the trunk (back 60%); chest
(15%); shoulders and buttocks.
Hair
Skin surface
Sebum
Sebaceous
gland
Follicle
Figure 1. Normal pilosebaceus unit.
The clinical picture embraces a
spectrum of symptoms, ranging from
mild comedonal acne, with or without
inflammatory lesions, to severe acne
and rarer forms of acne such as ‘acne
fulminans’, which presents with severe
inflammation, nodules and potentially
associated systemic symptoms.
For the treatment of acne several
therapeutic strategies are currently
available, alone or as fixed-dose
combinations, including benzoyl
peroxide, topical or systemic antibiotics,
anti-inflammatories, azelaic acid and
topical or systemic retinoids.
Acne, regardless of clinical severity
but particularly when severe, can
significantly impact on an individual’s
quality of life and psychological wellbeing.

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Acknowledging the potentially long-term

physical and emotional scars caused
by acne vulgaris, attention has focused
Skin surface on early intervention to limit disease
severity and progression. Timely and
efficacious treatment of acne using fixed-
Blockage of dose (two therapies combined into
follicle opening one formulation) topical combination
Bacteria therapy (for example, benzoyl peroxide
(enlarged) and an antibiotic, or benzoyl peroxide
and a retinoid) has been shown to
Sebaceous gland be more effective than monotherapy
in addressing the pathogenic factors
Follicle
of acne, and the safety and efficacy
of combining topical treatments has
become well established over recent
years (Nast et al, 2011).

Figure 2. Microcomedone. Pathogenesis

Acne develops in the pilosebaceus unit
(PSU) (Figure 1). In the healthy PSU,
3a Skin surface the sebaceous gland produces sebum,
essential for the integrity and normal
Whitehead functioning of the skin. Shedding of
keratinocytes through desquamation is a
normal process of the healthy follicular
duct. The dead cells are moved out of
Enlargement of the follicular duct by the movement of
follicle opening the growing hair and sebum.

Acne vulgaris has a multifactorial

pathogenesis, of which the key factors
Sebaceous gland
are:
Follicle  Increased sebum production
 Follicular hyperkeratosis
 Proliferation and inflammation
associated with Propionibacterium
acnes
 Reactive inflammation
3b Skin surface
 Heredity.

Blackhead Patients with seborrhoea and acne

who are genetically prone have a
significantly greater number of lobules
per sebaceous gland. The sebaceous
Enlargement of gland is a target of androgens; and
follicle opening hormonal influences play an important
role in the pathogenesis of acne. People
who get acne are particularly sensitive
Sebaceous gland to normal or increased plasma levels
of androgen hormones. In the patient
Follicle
with acne, circulating androgen leads
to increased sebum production and
abnormal keratinocyte proliferation is
observed, resulting in ductal obstruction
and the development of the primary
Figure 3. Non-inflammatory lesions in acne: open comedone/blackhead (3a); closed comedone/ acne lesion, the microcomedone
whitehead (3b). (Figure 2).

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Papule Pustule immune systems and inflammatory

Epidermis
events (Nast et al, 2011).

Bacteria Bacteria Clinical characteristics

Dermis
Dead Dead The patient with acne can present with
skin cells skin cells a spectrum of lesions and the range
White blood cells of symptoms can fluctuate over time
with regard to types of lesions present,
distribution and severity. Depending
Nodule Cyst

Epidermis
on the severity of the acne, there may
be non-inflammatory comedones, or
in inflammatory acne a mixture of
Bacteria Bacteria

Dermis
Epithelial
Dead Dead cell lining comedones and inflamed lesions in the
skin cells skin cells form of papules and pustules. Severe
acne tends to be extensive, often
White blood cells White blood cells
showing evidence of nodules and cysts
Figure 4. Inflammatory lesions in acne: papule; pustule, nodule, cyst. (Figures 4 and 5). Patients report the
lesions to be painful and may experience
rupture of lesions upon pressure or
rubbing of clothing.
5a 5c 5e
Range of clinical features in acne
vulgaris:
 Seborrhoea (excessive oiliness of the
skin)
 Non-inflammatory lesions, open and
closed comedones (blackheads and
whiteheads)
5b 5d 5f
 Inflammatory lesions, including
papules and pustules
 Scarring of varying severity
 Post-inflammatory pigmentation.

Grading acne is essential as it not

Mild acne (5a, b)
Characterised by non-inflammatory
open and closed comedones and
few, if any, inflammatory lesions.
These types of lesion are unlikely
to result in scarring and are
typically limited to the face
Figure 5. Clinical characteristics of mild, moderate and severe acne.
The continuous build-up of debris
in the follicular duct subsequently
causes the development of open
comedones (blackheads) and closed
comedones (whiteheads) (Figure 3)
and is independent of the colonisation
with P. acnes, though the increased
production of sebum serves as the ideal
environment for bacterial growth.
Propionibacterium acnes (P. acnes)
lives as a commensal bacterium in the
Moderate acne (5c, d) Severe acne (5e, f)
Characterised by a mixture Characterised by increased
and increased numbers of non- numbers of inflammatory papules,
inflammatory comedones, and pustules and the possibility of
inflammatory papules and pustules. nodules and cysts, commonly with
Lesions commonly affect the face evidence of scarring
and often the trunk. There is a risk
of scarring
PSU, but if the follicular environment in
the PSU alters as a result of increasing
bacterial count and subsequent rupture
of the debris-filled PSU, an immune
response is triggered and the release
of inflammatory cytokines occurs,
causing inflammatory lesions — in
the first instance papules and pustules
(Figure 4). The improved understanding
of acne development on a molecular
level suggests that acne is a disease
that involves both innate and adaptive
only informs therapeutic strategies
but also helps to monitor treatment
response and could trigger a prompt
referral to a dermatologist if the acne
is severe, is not responding or the
psychological impact is detrimental
(Clinical Knowledge Summaries, 2014).
Grading acne into mild, moderate and
severe is most commonly used in clinical
practice, a simple, reproducible and rapid
means of assessing the patient with acne
(O’Brien et al, 1998) (Figure 5). For more
detailed acne grading, scales such as the
Leeds acne grading system (O’Brien et
al, 1998) are available. Alongside clinical
assessment of acne, assessment of the
psychological impact via a questionnaire
is recommended. If the psychological
impact seems severe or even
disproportionate, the patient-reported
Dermatology Life Quality Index (DLQI)
or Assessments of the Psychological
and Social Effects of Acne (APSEA)
questionnaire are useful to monitor the

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Figure 6. Patient with hypotrophic scars.
Figure 7. Patient with post-inflammatory
hyperpigmentation.
person’s psychological state before or
during treatment.
Acne scarring and post-inflammatory
hyperpigmentation
Scarring generally indicates previous
episodes of severe acne, usually
following deep-seated inflammatory
lesions or occurring in ‘scar prone’
patients or those with a hereditary
background of severe acne scarring.
Acne scarring is for life and
psychologically severely damaging.
Even after the disease has ended,
acne scars and hyperpigmentation
are not uncommon permanent
negative outcomes. The body produces
collagen to repair the damaged scar
tissue. Scars may show increased
collagen (hypertrophic and keloid
scars) or be associated with collagen
loss (hypotrophic scars) (Figure 6).
Acne scarring will occur in 30% of
those with moderate to severe acne
and early treatment at every stage
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is key to prevention (Van Onselen,
2010). Its presence warrants a more
aggressive treatment to prevent further
scarring and HCPs in primary care
should consider early referral to a
dermatologist as recommended in the
EDF guidelines (Nast et al, 2011) and
Clinical Knowledge Summaries (2014).
Scars may also be the result of self-
Acne scarring is for
life and psychologically
severely damaging. Even
after the disease has
ended, acne scars and
hyperpigmentation are not
uncommon permanent
negative outcomes.
manipulation and the patient needs to
be counselled against such habits.
Of special concern among darker
skinned patients with acne is the
occurrence of keloid scarring and
post-inflammatory hyperpigmentation
(PIH) (Figure 7). Inflammatory acne
lesions disrupt the epidermal basal
layer causing melanocytes to increase
melanin production, resulting in PIH.
PIH is common in patients with skin of
colour and can persist for months or
years, as described by Callender (2004).
Diagnosis
A careful physical examination should
be carried out, assessing all acne-
prone areas. This is important, as some
patients present with mild-to-moderate
acne affecting one area and severe
acne affecting another. Diagnosis of
acne is (commonly) based on clinical
findings. The presence of some or all
of the following symptoms indicates
the presence of acne: greasy skin,
comedones (open and closed), inflamed
lesions (papules, pustules and nodules)
and scarring.
Investigations are generally not
required but a detailed medical history,
which includes the psychological impact
of the disease, is essential. Genetic
factors have been recognised and,
according to Friedmann (1984) and
studies conducted by Savage and Layton
in Harrogate (2010), there is a high
concordance among identical twins.
There is also a tendency towards severe
acne in patients with a positive family
history of acne (Dreno, Poli, 2003).
At time of clinical assessment the
HCP should discuss and document:
 Clinical appearance of the acne,
duration, distribution and severity of
the acne
 Occupation, hobbies and family
history
 Current or previous over-the-
counter or prescribed products,
response to treatment and patient
satisfaction
 Patients diagnosed with severe acne
or those presenting with severe
psychological problems should be
referred to a dermatologist for
treatment (Nast et al, 2011).
Without the presence of
comedones, an alternative clinical
diagnosis needs to be considered
(Roebuck, 2006). Table 1 shows possible
differential diagnoses for acne vulgaris.
Not all acne forms are hormone-
driven and some may be due to
external triggers. Furthermore the HCP
should be aware of important acne
variants, as these often require prompt
and aggressive treatment (see Table 2).
Some drugs can induce acne and
a detailed medical history is therefore
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of possible side-effects and how to

Table 1. manage these?
Differential diagnoses for acne vulgaris.  Is the patient motivated and
does the patient have realistic
expectations?
Differential diagnosis Key features
Rosacea Absence of comedones, telangiectasia and Patient education
erythema; affects older adults The following information should be
Perioral/periorbital Monomorphic papular eruptions, sparing the provided to all patients to enhance
dermatitis vermilion border, occurs around the mouth and concordance and improve therapy
sometimes around the eyes outcomes:
Keratosis pilaris Commonly affects the back of the upper arms and sometimes the buttocks and front Avoid picking at spots because this
of the thighs.Thought to be linked to atopic dermatitis (DermNet NZ, 2014) can cause permanent damage and
scarring
Gram-negative More common in males, often complication of Vigorous washing and scrubbing
folliculitis long-term antibiotic therapy can irritate the skin and make acne
worse
Washing the skin with a gentle skin
Table 2. cleanser twice-daily is recommended
Use cosmetics, toiletries and
Acne variants. sunscreens that do not clog pores.
These products may be labelled
Acne variants Key features non-comedogenic or oil-free
Acne conglobata A severe form of acne, which tends to present in young male adults, causing Use medication as directed (time
interconnecting abscesses and sinuses resulting in deep scars, cysts filled with of day, amount, frequency and, for
foul smelling pus, and requires aggressive treatment with oral isotretinoin, often example, antibiotics with/without
accompanied by a concomitant course of oral steroids food) as this can alter effectiveness
Use medication as directed and
Acne fulminans A dermatological emergency of sudden onset, presenting with necrotising acne
allow time to take effect; this may be
lesions. Patients feel systemically unwell and inpatient care is required with a systemic
several weeks or months
combination treatment of isotretinoin and steroids
All previously purchased acne
Steroid acne A monomorphic rash to the trunk and often upper arms, and less commonly the face, treatments should be discontinued
caused by oral, systemic, inhaled or even topical application of steroids unless specified by the health
Neonate/infantile acne Usually self-limiting but can be treated topically and seldom requires systemic practitioner
treatment There is little evidence that food
causes acne — a healthy balanced
diet is generally advised. Some
essential. The following drugs are Index (DLQI) or Assessments of the research suggests a diet with a
known to cause acne: corticosteroids, Psychological and Social Effects of low glycaemic index is beneficial,
bromides, lithium, certain antiepileptics Acne (APSEA) questionnaire. Simpson although further research is needed
and iodide-containing drugs. and Cunliffe (2004) consider the use (Steventon, Cowdell, 2013).
of quality of life and psychosocial
Psychological impact and patient motivation questionnaires essential to adequately Antibiotic resistance
Psychological change does not understanding just how the disease A recent call to limit antibiotic use in
necessarily correlate to disease severity is affecting the patient. To effectively acne urges all Healthcare Professionals
and, according to Savage and Layton support the patient with acne through (HCPs) to carefully review their
(2010), even mild to moderate disease this potentially difficult time, prior to prescribing habits, as many utilise
can be associated with significant treatment the following should be antibiotics as a primary treatment.
psychological morbidity and suicidal considered, acted upon and referral HCPs should familiarise themselves
ideation. The individual with acne, to a dermatologist considered if with current guidance and prescribe
according to evidence, can become appropriate: antibiotic agents in a judicial manner,
so concerned about their body image  What is the psychological impact of as suggested by Thiboutot et al (2013).
that body dysmorphobia can become disease on the patient? Although current acne guidelines
a significant factor (Schofield et al,  Will the patient be able to comply discourage the use of antibiotics as
2009). A questionnaire to assess the with the treatment? prolonged monotherapy (Thiboutot et
psychological impact is useful when  Does the patient understand the al, 2009), about 5 million prescriptions
assessing impact, such as the patient- suggested therapy? for oral antibiotics are still written each
reported Dermatology Life Quality  Does the patient understand the risk year for the treatment of acne. The

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ductal blockage and commensal

To treat
the 4 pathological
factors effectively
To educate people
about expectations
To treat without delay
and encourage drug
concordance
The goals of
patient-centred
acne treatment
To reduce To reduce or
increasing antibiotic clear skin lesions, with
resistance minimal side-effects
To prevent
physical and
emotional scarring
Figure 8. The goals of patient-centred acne treatment (Lavers, 2014).
key issues with antibiotic resistance is increasing” and there is “cross-
are that there is significant and often resistance between erythromycin and
prolonged antibiotic use in acne. Some clindamycin”. To avoid development of
patients present with acne for a decade resistance the prescriber is advised:
or more and will have had numerous
courses of topical and systemic “When possible, use non-antibiotic
antibiotics. Thiboutot et al (2013) urge antimicrobials (such as benzoyl
us to consider the following: peroxide or azelaic acid); if a particular
P. acnes is only one of the 4 antibacterial is effective, use it for
pathogenic factors repeat courses if needed”.
Retinoid + antimicrobial agents such
as benzoyl peroxide (BPO) is now In addition, Humphrey (2012)
first-line treatment advises prescribers to: review their
More than 50% of P. acnes strains current practice and prevent increasing
are resistant resistance by avoiding topical or
Do not use antibiotics as oral antibiotics as monotherapy or
monotherapy or combine topical maintenance therapy; limit duration of
and systemic antibiotics antibiotic use and assess response at
Oral antibiotics are generally 6 to 12 weeks, use concomitant BPO
considered to be more effective (leave-on or wash); avoid simultaneous
than topical antibiotics use of oral and topical antibiotics
BPO and systemic antibiotics should without BPO and using topical retinoid
be combined with a topical retinoid. +/- BPO as maintenance in lieu of
antibiotics.
This is further supported by
recommendation from the British Therapeutic options
National Formulary (BNF) 68 (2014), It is important to stress that acne is
which states that “antibacterial not an infection but an inflammatory
resistance of Propionibacterium acnes reaction to an internal process of
bacterial growth, rather than an
external causative organism, and
treatment is aimed at preventing and
reversing this process. Treating the
early signs and symptoms of acne
may help to control its progression
and severity. Individuals with acne
should seek advice and support from
a health professional at the earliest
possible time. A study found that 74%
of patients waited over 1 year before
seeking medical attention (Hannah et
al, 2003). Acne treatments should be
selected on presenting symptoms, acne
severity, distribution and psychological
impact, thus matching an effective
management plan with an individual.
How well a patient will respond to
treatment is difficult to predict, nor
is there an easy way to predict how
long a patient’s acne will be likely to
last. Factors that link to poor prognosis
include early onset, hyperseborrhea,
truncal acne and scarring, according to
Dreno et al (2003), as well as a strong
family history of acne.
The overall goal of acne
management for all patients is to select
treatments that effectively address as
many pathogenic factors as possible,
as recommended by Katsambas et al
(2004), while minimising side-effects
(as summarised in Figure 8).
Promotion of adherence
Acne treatment can last several
years and thus is deemed a chronic
condition, which can be challenging
for the patient. Patients’ acceptance
of the disease process, recommended
treatment and a pragmatic approach
to drug therapy are factors found
to improve adherence to the drug
regime, especially those required over
long periods of time. This is especially
true for pre-teens and adolescents,
who have the most difficulty complying
with long-term plans (Eichenfield et
al, 2005). Current guidelines take this
into consideration and not only offer
effective treatment but treatments
that support therapeutic adherence.
Adherence is facilitated by knowledge
of the product being used, for
example, correct application, treatment
duration, the expected onset of effect,

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Table 3.
Actions of topical and systemic acne therapies in relation to the four pathogenic factors.
SEBUM HYPER
PRODUCTION KERATINISATION
Topical therapies
Retinoids - ++
Benzyl peroxide - +
Antibiotics - +
Azelaic acid - +
Nicotinamide - +
Systemic therapies
Antibiotics - +
Hormonal ++ ++
therapy
Retinoids +++ ++
the sequence of the healing process,
the maximal achievable average effect,
expected adverse events, and the
benefit to quality of life (Nast et al,
2011). Many products now come with
mobile phone apps to educate the
patient in the correct use of the drug
and allow uploading of images to track
treatment progress.
Following on from assessment
and diagnosis a treatment plan
is developed. The 2011 EDF
Guidelines (Nast et al, 2011) set out
recommended treatments for each
level of severity. Based on the strength
of current evidence, treatments are
deemed as highly recommended
through to negative and open
recommendation. Tables 3 and 4
illustrate how the different agents used
reduce the pathological factors of acne
vulgaris and provide a summary of the
2011 EDF guideline recommendations.
To be effective, acne therapies
need to treat as many of the key
pathological factors as possible at the
same time, always with the focus on
scar prevention. Topical treatments
are the first step in acne therapy as
they aim to unblock the PSU and
thus reduce bacterial load. All acne
treatments should in the first instance
consist of a topical treatment or
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INFLAMMATION REDUCTION IN
P. ACNES
+ -
++ +++
++ +++
+ +/-
+ +/-
+++ +++
Indirect Indirect
++ ++
Many products now come
with mobile phone apps to
educate the patient in the
correct use of the drug and
allow uploading of images to
track treatment progress.
combination of topical treatments with
a systemic agent added as and when
required. Summary of treatments
for mild, moderate and severe acne
vulgaris include topical agents, systemic
antibiotics, hormonal agents and
isotretinoin as illustrated in Table 4.
Putting current guidelines into practice —
insight into an acne clinic
The need for medicines optimisation
and how this can improve patient
outcomes in practice is paramount.
After taking a detailed patient history,
including physical and psychological
assessment, one needs to categorise
the presenting condition into non-
inflammatory and inflammatory acne
and its severity. Laboratory tests
for acne are generally not required,
however laboratory testing may be
indicated in the following situations:
Female patients with dysmenorrhea
or hirsutism
4Investigations: levels of total
and/or free testosterone,
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dehydroepiandrosterone sulfate,
luteinizing hormone, and follicle-
stimulating hormone
Cases refractory to treatment
or when improvement is not
maintained
4Investigations: skin culture to rule
out gram-negative folliculitis.
Non-inflammatory acne does not
require treatment with antibiotics
but is aimed at unblocking the PSU
and preventing the inflammatory
cascade from occurring. The patient
is prescribed a topical treatment
(adapalene) to be applied to all acne-
prone areas.
Honesty is vital and patients need
to understand that treatment is there
to manage the condition but it is not
a cure. There is little point in reviewing
the patient before 3-4 months to allow
for the drug/s to take effect. There is no
benefit in moving on to an alternative
drug in the hope of a quick fix.
Inflammatory acne requires an
antimicrobial but not necessarily an
antibiotic. BPO has been an effective
antimicrobial in acne treatments for
centuries. Mild to moderate acne
is treated with a topical treatment.
Skin irritation and bleaching of
textiles is common. Skin irritation
can be overcome by using a stepped
approach of applying the treatment
every couple of days or once irritation
has settled. Eventually the patient will
be able to apply the treatment daily.
Using a gentle non-comedogenic
cleanser and moisturiser further
reduces irritation. Bleaching of textiles
cannot be avoided, but using old or
white towels, bedding and sleepwear
can overcome any objections.
When a topical or systemic
antibiotic is used, it should be used
in conjunction with benzoyl peroxide
or topical retinoid to reduce the
emergence of resistance. Topical
antibiotics used include clindamycin
and erythromycin, though resistance
to erythromycin favours the use of
clindamycin. Azelaic acid has been
shown to help reduce inflammation
and may aid in treatment of post-
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is rarely associated with a lupus-

Table 4. like syndrome, minocycline-induced
Summary of EDF 2011 guidelines. hyperpigmentation; due to these risks
it is no longer a first-line systemic
Mild acne Moderate acne Severe acne antibiotic for acne. Systemic antibiotics
Acne severity
can be discontinued after a good
High strength of Adapalene + benzoyl Isotretinoin improvement (ie, few inflammatory
recommendation peroxide (FDC) lesions present) has been observed.
– or Remember never to prescribe topical
Benzoyl peroxide + and systemic antibiotics together
clindamycin (FDC) or as monotherapy. All antibiotics
Moderate strength of Topical retinoids Azelaic acid Systemic antibiotics should be used for limited periods
recommendation (adapalene to be Benzoyl peroxide (doxycycline and only (BNF online, 2014). If no
preferred over tretinoin/ Topical retinoid lymecycline) + improvement with systemic treatment
isotretinoin) Systemic antibiotic adapalene is achieved check for concordance,
(doxycycline and Systemic antibiotics consider antibiotic resistance and, if
lymecycline) + (doxycycline and required, choose alternative systemic
adapalene lymecycline) + azelaic antibiotic as per guideline/BNF. Advise
acid patients to use sun protection SPF
Systemic antibiotics 30+ as tetracyclines can make the
(doxycycline and skin sensitive to UV radiation. For
lymecycline) + females foundations containing an SPF
adapalene + benzoyl
peroxide (FDC)
Oral isotretinoin has been
Alternatives for Hormonal Hormonal antiandrogens* used for almost 50 years and
females antiandrogens* + +
topical treatment systemic antibiotics
is the only treatment that
or can treat all key pathogenic
Hormonal * A standard Combined factors of acne.
antiandrogens* + Oral Contraceptive (COC)
systemic antibiotics is suitable for most women
– are useful. Remember that you can
with moderate to severe acne
prescribe sunscreens, as per BNF.
refractory to other treatments,
or who also wish to receive
Hormonal therapies can be
contraception.
used in females with acne, especially
Co-cyprindiol (non-
those with premenstrual acne
proprietary) and branded
flares in whom other therapies
preparations contain an anti-
have failed. Patients may also have
androgen (BNF online, 2014)
signs of hyperandrogenism (eg,
Source: European Dermatology Forum (Nast et al, 2011). FDC = fixed-dose combination hirsutism, irregular menses, menstrual
dysfunction). Serum androgen levels
may or may not be elevated.
inflammatory hyperpigmentation. pregnancy and children under 12 years
Apply twice daily. Improvement may of age. Risk or signs of scarring and severe
be seen within 4 weeks. psychological impact should trigger a
Systemic treatment with antibiotics prompt referral to a dermatologist.
Adapalene is the recommended is added if the acne is moderate Equally if no improvement with
topical retinoid-like drug. It is licensed to severe or the patient struggles topical and systemic treatment has
from 9 years of age. Patients must to reach affected areas with the been achieved over the period of
inform the HCP in the event of topical treatment. Again, review 9-12 months (unfortunately no exact
pregnancy and stop using a topical after 3-4 months, at which point an timeframe is recommended), consider
retinoid. It inhibits microcomedone improvement should be noticeable. seeking a second opinion.
formation, decreases cohesiveness Systemic antibiotics for acne are
of keratinocyesin sebaceous follicles, all equally effective but generally Oral isotretinoin has been used
which allows for easy removal, and lymecycline and doxycycline are for almost 50 years and is the only
has anti-inflammatory properties. preferred for ease of use (once daily) treatment that can treat all key
Erythromycin is an alternative in and good tolerability. Minocycline pathogenic factors of acne. It is an

24 Dermatological Nursing, 2014, Vol 13, No 4 www.bdng.org.uk

16-25_Acne.mjjp2C.indd 22 03/12/2014 15:14


oral retinoid indicated for recalcitrant,
nodulocystic acne and patients
who suffer greatly psychologically.
Treatment is still predominately
initiated in secondary care, although
some Trusts are trialling treatment in
the community. Treatment is weight-
based, usually dosed initially 0.5mg/
kg and increased to 1mg/once daily
for 15-20 weeks. Oral isotretinoin is
teratogenic and contraindicated in
women of childbearing potential unless
all of the conditions of the Pregnancy
Prevention Programme are met. There
is an associated risk of depression and
suicide and patients are counselled
carefully for suitability for treatment
and reviewed for mood changes at
each consequent appointment.
Isotretinoin is contraindicated in
patients with hepatic insufficiency,
excessively elevated blood lipid
values, hypervitaminosis A, allergy
to hydrogenated soya-bean oil and
refined soya-bean oil and those
receiving concomitant treatment with
tetracyclines. These must be stopped
prior to commencement of treatment
with isotretinoin.
Summary
Evidence-based guidance supports
health professionals to plan and review
acne treatment, manage this long-term
condition effectively and minimise its
potentially disfiguring results. Effective
prevention and reduction of the four
pathogenic factors in acne requires
early and aggressive treatment without
delay, to achieve successful treatment
and reduce the risk of irreversible
scarring. There is a clear association
between acne, depression and anxiety,
independent of disease severity.
Good therapeutic adherence can be
achieved by involving the patient in
the treatment selection and through
education.
The increasing emergence of
resistant bacteria in acne challenges
the HCP to review current prescribing
patterns, limit antibiotic prescribing
and use antimicrobial alternatives. The
benefits of fixed-dose combination
therapy are recommended to aid
efficacy and adherence and should be
www.bdng.org.uk
16-25_Acne.mjjp2C.indd 23
considered during patient consultation
and at the point of prescribing. DN
Conflict of interest
Isabel Lavers RGN, BSc, INP is
employed by Galderma UK; however,
this article was written in the capacity
of her clinical role, working for Salford
Royal NHS Foundation Trust as a
Specialist Nurse in Dermatology. This
article has not been endorsed by
Galderma UK.
Acknowledgements
Images are courtesy and with the
permission of the Primary Care
Dermatology Society (PCDS).
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