FEATURE ARTICLE

Acne Basics
Pathophysiology, Assessment, and Standard
Treatment Options
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Katrina Nice Masterson

ABSTRACT: Acne is a chronic condition affecting the formation and interpretation of the clinical examination
pilosebaceous unit. Presenting almost daily in the typical will help guide initial treatment choices. It will not always be
dermatology practice, the condition poses numerous treat- appropriate to correlate disease severity with the emotional
ment challenges due to the complex interaction of its and psychological impact of the condition on an individual
clinical presentation and unique patient needs. The follow- (Collier et al., 2008). Assessment of the patient’s priori-
ing discussion will provide basic pathophysiology and ties will be equally important in establishing the plan of
describe the clinical presentation of acne vulgaris and many treatment. There is no associated mortality with acne
of its variants. Several of the standard treatment options will treatment, but the psychosocial impact of acne is substan-
be described. Uncommon variants, acute forms, and more tial. Associated morbidity in the form of permanent scarring
complex treatment regimens will not be discussed here. and emotional distress is well documented in the literature
Key words: Acne, Acne Assessment, Acne Pathophysiology, (Zaenglein et al., 2016). Adding to this is the financial
Acne Severity, Acne Treatment burden on healthcare. In 2004, an estimated $398 million
was spent on office visits for acne (Bickers et al., 2006).

A cne is one of the most conspicuous skin

disorders treated in dermatology for ages
15Y40 years (Tanghetti et al., 2014). To some
extent, acne affects nearly everyone at some
point in life. In the United States, estimates
place incidence at around 40Y50 million persons with
85% prevalence in the 12- to 24-year age group (Bhate &
Williams, 2012). Typically, significant acne will sponta-
Approximately $1.740 billion was spent on prescription
acne drugs, and an additional $329 million was spent on
over-the-counter acne medications (Bickers et al., 2006).
A good understanding of acne physiology, thorough assess-
ment skills, and knowledge of treatment options will allow
the dermatology clinician to develop and guide the patient
in successful acne treatment.

neously regress in early adulthood; however, a number of PATHOPHYSIOLOGY

people will experience persistent acne or new-onset acne
The exact cause of acne has not been established. It is
in adulthood. A study by Collier et al. (2008) analyzed
generally accepted that the interplay of multiple factors is
the data from 1,013 completed surveys; the survey asked
subjects to self-report the presence or absence of acne
during their life by decade. In this investigation, a signifi-
cant number of subjects report having acne in adulthood
(see Figure 1). A typical dermatology practice could reason-
ably expect to see multiple patients daily with a primary
complaint of acne. Understanding the process of acne

Katrina Nice Masterson, DNP, Randall Dermatology, West

Lafayette, IN.
The author declares no conflict of interest.
Correspondence concerning this article should be addressed to
Katrina Nice Masterson, DNP, 124 Sagamore Parkway West, West
Lafayette, IN 47906.
E-mail: [email protected]
Copyright B 2018 by the Dermatology Nurses’ Association. FIGURE 1. Acne epidemiology; percentage reported by
DOI: 10.1097/JDN.0000000000000361 decade. Adapted from Collier et al. (2008).

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Copyright © 2018 Dermatology Nurses' Association. Unauthorized reproduction of this article is prohibited.
involved. Although most patients with acne do not have et al., 2016). Increased sebum production is stimulated by
underlying endocrine disorders, it is important to be aware androgen activity in the pilosebaceous unit. This increase
that acne may be a presenting symptom in persons with in sebum production may be related to an excess in andro-
androgen-mediated disease. Presently, research points toward gen hormones or an increase in sebaceous gland sensi-
four main processes that contribute to the development of tivity to normal androgen levels or increased activity of
acne. Keys to the pathogenesis of acne are Propionibacterium 5!-dihydrotestosterone (5!-DHT) in the skin (Ghosh,
acnes (P. acnes), keratinocyte hyperproliferation in the follicle, Chaudhuri, Jain, & Aggarwal, 2014). 5!-DHT is consid-
androgen-mediated increase in sebum production, and, very ered the major proponent of increased sebaceous gland
importantly, inflammation (Collier et al., 2008). activity as the glands contain the necessary enzymes
P. acnes is one in a group of normal bacterial flora involved in the conversion of testosterone to 5!-DHT
found in the follicular unit (Makrantonaki, Ganceviciene, (Makrantonaki et al., 2011). Even in the absence of abnor-
& Zouboulis, 2011). The precise contribution to the skin mal hormone levels or clinically evident hyperandrogenism,
made by this bacterium is not clear. Some studies show adult female acne may still be hormonally responsive
increased bacterial load in those with clinically evident (Ghosh et al., 2014). Endocrinologic testing before acne
acne, but this is not universally confirmed (Makrantonaki treatment is warranted in the presence of clinical signs of
et al., 2011). It is believed that the bacterium can stimulate hyperandrogenism or with a family history hyperandrogenism
tumor necrosis factor-alpha and the interleukins (ILs; (Zaenglein et al., 2016).
Tanghetti, 2013). Specifically, IL-1", IL-8, and IL-12 Inflammation, as a component of acnegensis, is de-
seem to be stimulated by P. acnes (Makrantonaki et al., bated to occur as a result of follicular hyperkeratinization
2011). These cytokines are proinflammatory and may be or, more recently, as the precursor of increased prolifer-
part of an immune response from the pilosebaceous unit. ation of follicular keratinocytes (Makrantonaki et al.,
In healthy skin, P. acnes plays a role in the protective 2011). New research has shown increased IL-1 activity
immune response by contributing to the formation of triggering keratinocyte upregulation in follicles before
short-chain fatty acids and in maintaining a more acidic hyperkeratinization (Layton et al., 2016; Makrantonaki
skin pH (Barnard, Shi, Kang, Craft, & Li, 2016). A lower et al., 2011). Another inflammatory mechanism thought
skin pH promotes keratinocyte growth and is less hospi- to play a role in acne formation involves the synthesis of
table for bacterial growth. In healthy skin, as opposed to leukotrienes, prostaglandins, and 15-hydroxyeicosatetraenoic
acne skin, structural differences have been seen along with acids by the enzymes lipoxygenase and cyclooxygenase
variances in immune modulation carried out by various P. (Makrantonaki et al., 2011). In vivo, sebaceous glands in
acnes strains (Layton, Eady, & Zouboulis, 2016). Recently, active acne lesions will show cyclooxygenase upregulation
new metagenomic research suggests that acne pathogenesis when compared with glands in normal-looking skin
may not be related to the amount, presence, or absence of a (Makrantonaki et al., 2011). S100 calcium-binding protein
bacterial strain but may be more connected to the overall A7, psoriasin, is found in the epidermis and is greatly
balance of the skin microbiome (Barnard et al., 2016). In increased in clinically active sebaceous gland ducts or acne
Barnard et al.’s study, they found that the presence of a lesions (Makrantonaki et al., 2011). The levels of this protein
virulence-linked gene that is involved in bacterial toxin are meaningfully increased in a number of inflammatory skin
production and transport was much higher in acne-involved conditions such as psoriasis, and the levels increase in relation
skin than in healthy skin (Barnard et al., 2016). More to inflammatory stresses (Makrantonaki et al., 2011). Evidence
research in this direction is inevitable and should present of the activation of inflammatory pathways has been shown
new avenues for studies aimed at regulating the unhealthy at all stages of acne development, including before it is clinically
(acne-prone) microbiome and encouraging a microbial evident (Tanghetti, 2013). This increasing evidence of the
balance that contributes to healthy skin. role of inflammation will impact future research on the use
Sebaceous glands are found everywhere on the body of anti-inflammatory modalities in acne treatment.
except for the palmer surface of the hands and the plantar Current evidence shows acne to be a complex process.
surface of the feet. Sebaceous glands secrete oil or sebum. More studies along newly emerging lines will enhance our
Sebum works to protect the skin against friction, reduces understanding of acnegensis and how to improve treat-
moisture penetration through the outer skin layers, and ment success. Our incomplete understanding of acne
acts as part of the healing process (Makrantonaki et al., formation clearly exposes the challenges dermatology
2011). Disrupted follicular keratinization, a component providers face when developing treatment plans. Acne
of pore blockage, can occur with concomitant changes in treatment will need to be individualized, and this will start
sebum. Changes in sebumVproduction, increase, com- with a thorough understanding and assessment of the
position, and oxidant-to-antioxidant ratiosVare all seen morphology of clinically evident lesions.
with acne formation (Makrantonaki et al., 2011).
The androgen hormones are a key part of acnegensis. ACNE LESION TYPES
Elevations in dehydroepiandrosterone sulfate outputs are The American Academy of Dermatology (AAD) defines
seen with comedonal acne in prepubertal children (Layton acne vulgaris as a ‘‘chronic inflammatory dermatosis

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Copyright © 2018 Dermatology Nurses' Association. Unauthorized reproduction of this article is prohibited.
notable for open or closed comedones (blackheads and
whiteheads) and inflammatory lesions, including papules,
pustules, or nodules (also known as cysts)’’ (Zaenglein
et al., 2016, p. 947). The primary lesions in acne can be
divided into two main categories: inflammatory and
noninflammatory. Secondary lesions, those that result as
sequelae from the primary lesion or manipulation of the
primary lesion, are not discussed here (see Table 1).
Noninflammatory acne lesions consist of open and closed
comedones (see Figures 2 and 3). Open comedones are
clearly visible in the skin and often present in the central
face. The closed comedone has no visible opening. They
are usually 1 mm or less in size, so examination may require
good lighting or subtle pressure to stretch the skin. The
closed comedone is flesh-toned or mildly hypopigmented.
These noninflammatory lesions can remain stable and
superficial or progress and become deep and/or inflam-
matory (Layton et al., 2016).
Inflammatory lesions consist of papules, pustules, and
nodules (see Figures 4Y7). Papules typically present as var-
iably erythematous lesions of less than 5 mm. Pustules, FIGURE 2. Open comedone (Skin and Common Disorders
generally, are discrete white fluid-filled papules of 5 mm Anatomical Chart, 2004). B 2004, Anatomical Chart Company.
or less. Larger lesions (5 mm or more), also with variable Permission to reuse must be requested from the rightsholder.
erythema, are termed ‘‘nodules.’’ The deeper structures,
such as pustules, nodules, and cysts, can form tunnels or et al., 2016). The successful treatment of acne is often
sinus tracts and often result in severe scarring especially multifactorial, requiring a trial period of various regimens. The
when they form close to one another (Layton et al., 2016). objectives of acne treatment are to clear and prevent active
Acne appears most often on the face with lesser preva- lesions, reduce the risk of scarring, and minimize psychosocial
lence on the back and then the chest (Layton et al., 2016). impact (Tan, 2008). The choice of regimen will be based first
There are a number of known acne variants. Some present on the clinical presentation or assessment of the morphology
as more severe or acute forms of acne; and some, as a result
of secondary factors such as medications, occupational
exposure, and personal grooming. Recognition of these
variants, some of which are very resistant to treatment, will
often begin with a thorough patient history (see Table 2).

TREATMENT CONSIDERATIONS
Intervention soon after the onset of acne is thought to
significantly reduce the risk of significant scarring (Layton

TABLE 1. Acne Lesions

Primary Lesions Types Features
Noninflammatory
Comedones Open Clearly visible, e1 mm
Closed No visible opening e 1 mm
Inflammatory
Papules Variable erythema e 5 mm
Pustules White fluid-filled papule e 5 mm
Variable erythema on base
Nodular Variable erythema Q 5 mm
Cyst Variable inflammation and pain
Deeper structure
FIGURE 3. Closed comedone (Skin and Common Disorders
& May rupture Anatomical Chart, 2004). B 2004, Anatomical Chart Company.
Permission to reuse must be requested from the rightsholder.

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 FIGURE 6. Nodule (Skin and Common Disorders Anatomical
Chart, 2004). B 2004, Anatomical Chart Company. Permis-
FIGURE 4. Papule (Skin and Common Disorders Anatomical sion to reuse must be requested from the rightsholder.
Chart, 2004). B 2004, Anatomical Chart Company. Permis-
sion to reuse must be requested from the rightsholder. accepted model is recommended (Zaenglein et al., 2016).
of lesions present. Mainly comedonal or noninflammatory The most recent treatment algorithm, updated by the
lesions will respond better to medications with comedolytic AAD in 2016, divides acne into gradesVmild, moder-
properties, whereas with inflammatory lesions, therapy ate, and severeVand suggests first-line and alternate
should include medications with anti-inflammatory proper- treatments (see Tables 4 and 5).
ties (see Table 3). The severity of the acne will also factor into The effects that lifestyle and environmental factors
creating a treatment regimen (see Figures 8Y11). may have on acne are also being studied, and treatment
Using severity as a guide can be complicated by a dis- modalities focusing on various factors are being tested.
cordance between clinician and patient assessments of Dietary changes to reduce high glycemic foods or dairy
severity. At present, there is no consensus on grading products seem promising in preliminary investigations
acne severity by using a scale (Tan, 2008). Using clinical (Layton et al., 2016). This approach may hold particular
judgment to grade severity of acne should help the clini- interest for patients as many perceive diet as a factor in
cian to choose the proper treatment, but this is complicated their acne severity and flares (Bhate & Williams, 2012).
by the variable impact psychosocially on the individual Stress, as a factor in acne severity, is often cited by patients
(Tan, 2008). The AAD suggests that using a classification and may have a foundation in effects by the hypothalamicY
scale can be helpful to clinicians in decision-making and pituitaryYadrenal axis on sebaceous glands (Layton et al.,
assessment of therapeutic response, but no universally 2016). What is not clear is if acne severity can be modified

FIGURE 5. Pustule (Skin and Common Disorders Anatomical FIGURE 7. Cyst (Skin and Common Disorders Anatomical
Chart, 2004). B 2004, Anatomical Chart Company. Permis- Chart, 2004). B 2004, Anatomical Chart Company. Permis-
sion to reuse must be requested from the rightsholder. sion to reuse must be requested from the rightsholder.

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 TABLE 2. Acne Variants
Acne Variants Primary Features Treatment Options
Conglobate & Male 9 female & Oral isotretinoin with oral corticosteroids to reduce
& 18Y30 years old inflammation
& Chronic with subtle progression or acute flare. & Systemic antibiotics for secondary infection and
Unremitting course may continue for decades to reduce inflammation
& Deep, grossly inflammatory nodule and pustules
with sinus tracts
& Possible associated gram-negative bacteria
& Severe scarring likely
Fulminans & Primarily male & Oral isotretinoin with oral steroids
& 13Y22 years old
& Acute flare
& Grossly erythematous nodule with ulceration
and hemorrhagic crust along with arthralgia,
fever, and signs of systemic inflammation
& Laboratory findings: increased WBC and ESR,
anemia, microscopic hematuria, and proteinuria
& Failure of oral antibiotic
Excoriee & Often compulsive picking or real or imagined & Cognitive psychotherapy
lesions & Topical treatmentVyields mixed results if
& Adolescent female predominance (onset) picking behavior is not modified
& Consider underlying psychological disorder
Keloidalis & Chronic follicular inflammation presents most & Early treatment essential to halt scarring
(nuchae) often in the upper neck or lower occiput & Topical steroids for smaller lesions
resulting in scarring and alopecia & Intralesional for larger lesions
& Predominant in African American men & Tetracycline antibiotics for anti-inflammatory
& Initially small firm erythematous papule, often effect
pruritic & Oral isotretinoin
& Some benefits seen with laser hair removal and
laser scar amelioration
Rosacea & Central face papules and pustules with prominent & Topical preparation: metronidazole 0.75%,
perilesional erythema azelaic acid 15%, ivermectin 1% or sodium
& No associated nodules and cysts sulfacetamide 10%, and sulfur 5%
& Typical onset at 30Y50 years old & Oral antibiotic: tetracyclines, submicrobial-dose
& Fair skin types predominate oral doxycycline, less often short-course
erythromycin and trimethoprim
Aestivalis & Monomorphic pruritic papules and pustules & Standard acne treatment ineffective
(actinic folliculitis) after sun exposure & Prevent with photo protection
& Male and female equal & Severe case may respond to oral isotretinoin
& Young to middle adult & Photo desensitization can be considered
& Resolves within 2 weeks but may recur annually
& Negative culture
Drug induced & Monomorphic & Avoidance of known associated drugs
& Absence of comedones ) Anabolic and corticosteroids (oral and topical)
) Human growth hormone
) Epidermal growth factor receptor inhibitors
) Carbamazepine, phenytoin, phenobarbitone,
troxidone, gabapentin, topiramate
) Lithium, sertraline
) Isoniazid, pyrazinamide
) Sodium fluoride, potassium iodine
& Benzoyl peroxide
(continues)

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 TABLE 2. Acne Variants, Continued
Acne Variants Primary Features Treatment Options
Cosmetic & Associated with comedogenic personal care & Avoidance of known agents
products ) Lanolin
) Petrolatum
) Vegetable oils
) Butyl stearate
) Lauryl alcohol
) Oleic acid
& Modification of skin care regimen

TABLE 3. Acne Medications

Strength of
Recommendation/
Treatment Purpose Level of Evidence AAD Recommendations
Benzoyl peroxide (BP) Many formulations & Comedolysis A/I, II & Mild acne monotherapy
& Broad-spectrum & Use with topical and
antimicrobial systemic therapyVreduces
& Anti-inflammatory bacterial resistance
& Safe in preadolescents
Salicylic acid Many formulations & Comedolysis B/II
& Broad-spectrum
antimicrobial
& Anti-inflammatory
Antibiotics
Topical & Reduce bacterial A/I, II & Avoid as monotherapy
& Clindamycin colonization (including because of bacterial
& Erythromycin P. acnes) resistance risk
& Anti-inflammatory
Oral & Reduce bacterial A/I, II & Use in moderate-to-severe
& Tetracyclines colonization (including A/I or topical-resistant acne
& Macrolides P. acnes) B/II & Doxycycline and minocycline
(erythromycin, & Anti-inflammatory are equally effective
clindamycin) & Systemic antibiotic use should
& Trimethoprim be limited to the shortest
(with/without possible duration
sulfamethoxazole) & Monotherapy strongly
discouraged; use in
combination with BP
and/or retinoid
& Use macrolides when
tetracyclines are not
appropriate
Retinoids
Topical & Increased desquamation A/I, II & Primarily comedonal acne
& Tretinoin of keratinocytes use as monotherapy
& Adapalene & Anti-inflammatory & Use in combination with
& Tazarotene & Antimicrobial inflamed lesions
& Important in reducing acne
development
& Useful in maintaining results
& Adapalene and tretinoin
safe in preadolescents

(continues)

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 TABLE 3. Acne Medications, Continued
Strength of
Recommendation/
Treatment Purpose Level of Evidence AAD Recommendations
Oral & Inhibits sebaceous A/I, II & Use in severe nodulocystic
& Isotretinoin gland function acne
& Use in moderate acne
if treatment resistant,
scarring, or psychosocial
distress
& Routine monitoring of liver
function, cholesterol, and
triglycerides
& iPledge risk management
for all patients
& Monitor for inflammatory
bowel disease and depression
Antiandrogen
Oral contraceptives: & Decrease sebum A/I & Effective for inflammatory
estrogen/progesterone production acne in women
combination
& Ethinyl estradiol/
norgestimate
& Ethinyl estradiol/
norethindrone
& Acetate/ferrous
fumarate
& Ethinyl estradiol/
drospirenone
& Ethinyl estradiol/
drospirenone/
levomefolate
Androgen blockers & Decrease sebum B/II, III & Useful for some women
Spironolactone production
Other topicals
Dapsone & Reduction of A/I, II & Useful in inflammatory acne
inflammatory lesions & May be more efficacious in
female adults
Azelaic acid & Comedolytic A/I & Use as an adjunct
& Antibacterial & Improves postinflammatory
& Anti-inflammatory hyperpigmentation

Adapted from Lai, Jacob, and Sandu (2015) and Zaenglein et al. (2016). Recommendation key (adapted from Layton et al. [2016]): A = based
on consistent and good-quality patient-oriented evidence; B = based on inconsistent or limited-quality patient-oriented evidence; C = based
on consensus, opinion, case studies, or disease-oriented evidence; I = good-quality patient-oriented evidence (i.e., evidence measuring
outcomes that matter to patients: morbidity, mortality, symptom improvement, cost reduction, and quality of life); II = limited-quality patient-
oriented evidence; III = other evidence, including consensus guidelines, opinion, case studies, or disease-oriented evidence (i.e., evidence
measuring intermediate, physiologic, or surrogate end points that may or may not reflect improvements in patient outcomes). AAD = American
Academy of Dermatology; P. acnes = Propionibacterium acnes.

in some way by modification of stress. There is much Patient preferences in acne treatment will have major
research underway investigating the effects of modifying influence on adherence to a treatment regimen and therefore
lifestyle or environmental factors, and some of the study may have a significant effect on perceived success of the
reports show contradictory results where an intervention regimen (Davis et al., 2012). In developing a treatment
seems to have a positive effect in one study but no effect in regimen, the clinician should discuss the appropriate
another (Layton et al., 2016). medications and their available forms with the patient.

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 TABLE 4. Sample Grading for Acne
Severity (FDA)
Severity Description
Clear Clear skin with no inflammatory or
noninflammatory lesions
Almost Almost clear; rare noninflammatory lesions
clear with no more than one small inflammatory
lesion
FIGURE 8. Open and closed comedones. Mild Mild severity; greater than Grade 1; some
noninflammatory lesions with no more
than a few inflammatory lesions (papules/
pustules only, no nodular lesions)
Moderate Moderate severity; greater than Grade 2;
up to many noninflammatory lesions and
may have some inflammatory lesions, but
no more than one small nodular lesion
Severe Severe; greater than Grade 3; up to many
noninflammatory and inflammatory
FIGURE 9. Noninflammatory and inflammatory papules. lesions, but no more than a few nodular
lesions

Adapted from Center for Drug Evaluation and Research, U.S.

Department of Health and Human Services (2005). FDA = Food and
Drug Administration.

clinician’s medication choice. The safety of medications in

certain patient groups or the personal preferences of the
FIGURE 10. Pustules and small nodules. individual patient are examples of how patient character-
istics can influence a provider’s treatment choice.
Topical medications that are approved by the Food and
Drug Administration for use in acne include benzoyl peroxide,
salicylic acid, antibiotics, retinoids, combination products
(benzoyl peroxide, retinoid, and antibiotic), azelaic acid,
and sulfone agents. Topical therapy may be used alone or
in combination with oral therapeutic agents. Systemic therapy
approved by the Food and Drug Administration includes
antibiotics, antiandrogens, and isotretinoin. Monotherapy is
usually only appropriate for mild acne; more severe acne
often requires a combination of agents with different
mechanisms to have a meaningful effect on acne (Zaenglein
FIGURE 11. Pustules, nodules, and cysts.
et al., 2016). See Table 3 for standard acne medications
Including the patient in decision-making encourages with their purpose, strength of evidence in the literature, and
trust, which should improve treatment adherence and their place in the latest AAD treatment guidelines. Other
satisfaction (Davis et al., 2012). agents used in acne regimens have been studied and show
limited evidence in support of utilization, including sulfur,
STANDARD ACNE MEDICATIONS nicotinamide, resorcinol, sodium sulfacetamide, aluminum
Acne treatments are available both over the counter and chloride, and zinc (Zaenglein et al., 2016). On the basis of
by prescription. Prescription medications are available in current evidence, it is not clear if dietary modifications
topical and oral forms. Topical medications often have a have a role in acne treatment, so none were included in the
number of formulations available. The decision-making latest AAD treatment guidelines (Zaenglein et al., 2016).
in development of an acne treatment regimen will be based
on both clinical presentation and patient characteristics DISCUSSION
(Zaenglein et al., 2016). Clinical assessment of lesion As a presenting complaint at the dermatology office visit,
morphology and location of the lesions can influence a acne is either the most common or second most common

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 TABLE 5. Acne Treatment Algorithm
Mild Moderate Severe
First line & Benzoyl peroxide (BP) & Topical combination therapy; & Oral antibiotic with combination: BP,
& Topical retinoid BP, retinoid, and/or antibiotic topical retinoid, and topical antibiotic
& Any combination of & Oral antibiotic with topical & Oral isotretinoin
topical: BP, retinoid, retinoid and BP
or antibiotic & Oral antibiotic with topical retinoid
and BP and topical antibiotic
Alternative & Add medication not & Alternate combination of & Change oral antibiotic
already in regimen topical & Add oral contraceptive or
& Alternate retinoid & Change in oral antibiotic or oral antiandrogen (women)
& Topical dapsone antiandrogen for women & Oral
& Oral isotretinoin

Adapted from Zaenglein et al. (2016).

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