Acne

ACNE
By Daphne Gima
18th February 2009
OUTLINE
 Introduction
 Pathogenesis of Acne
 Classification of Acne
 Management of Acne
 Summary
 References
INTRODUCTION
 Inflammatory disease of the pilosebaceous
follicles marked by comedones, papules or
pustules on the face, chest and upper back.
 Has high prevalence, particularly in
adolescence, but can occasionally occur even
until 4th decade of life.
 Affects more males than females
 Although not fatal, produces physical

scarring as well as psychological stress.
PATHOGENESIS OF ACNE VULGARIS
 Four main pathogenetic factors:
(i) Increased sebum production

(ii) Follicular hyperkeratinization, leading to hyperkeratotic
plug of sebum and keratin (microcomedone)
(iii) Follicular colonization with anaerobe Propionibacterium
acnes
(iv) Inflammation
PATHOGENESIS OF ACNE (2)
 Depending on degree of the factors, the
microcomedone will form
- Closed comedone (whitehead) with further
accumulation of sebum
- Open comedone (blackhead) with further
follicular orifice distension, and oxidized
lipids.
- Inflammatory lesions (cysts) develop when
follicular contents rupture, forming superficial
pustule, deeper papule and even deeper
nodule.
 External factors that may also contribute to
acne:
(i) Cosmetics
(ii)Diet
(iii)Stress
(iv)Medications
- azathioprine, barbiturates, corticosteroids,

cyclosporin, isoniazid, lithium etc
CLASSIFICATION OF ACNE
Generally divided into 4:
 Type 1: Mainly comedones with occasional
small inflamed papule or pustule, no scarring
 Type 2: Comedones and more facial papules
and pustules; mild scarring
 Type 3: Numerous comedones, papules and
pustules, spreading to back, chest and
shoulders, with occasional cyst and nodule;
moderate scarring
 Type 4: Numerous large cysts on the face,
neck and upper trunk; severe scarring
CLASSIFICATION OF ACNE
DIFFERENTIAL DIAGNOSIS: ACNE
FULMINANS
 Rare form of severe cystic acne usually seen
in young males age 12 to 17.
 Onset of severe cystic involvement and
concomitant ulceration is acute.
 Besides cysts, patients also usually presents
with fever, malaise, fatigue and arthralgias.
 Ulcerations have a characteristic
overhanging, ragged border which surrounds
an exudative necrotic plaque.
DIFFERENTIAL DIAGNOSIS: ACNE
CONGLOBATA
 Severe form of acne that is uncommon and
produces disfigurement.
 Characterized by paired and grouped
comedones, primarily seen on neck and
trunk.
 Nodules can increase in size or coalesce to
eventually degenerate to discharge foul-
smelling pus and ulcerate.
 As cyst or nodule breaks down, crusts can
form over deep ulcers which are very slow to
heal.
MANAGEMENT OF ACNE
 Acne treatment involves targeting of the 4
factors involved in the pathogenesis of acne
 Aim: Reduce/eliminate microcomedones
 Treatment is based on severity of acne and

the agents used include the retinoids,
antibiotics & anti-inflammatory agents.
 Given either topically or orally.
 Acne lesions take at least 2 months to

mature, so any treatment should be given for
2-3 months.
TOPICAL TREATMENT: BENZOYL
PEROXIDE
 Preparations available in 2.5%, 5% & 10%, Use OD
or BD.
 Strong antibacterial effects, moderate anti-
inflammatory and slight anticomedogenic effects
 Reduces P. acnes colonization by releasing free-
radical oxygen that oxidizes bacterial proteins in
the sebaceous follicles
 Most common SE is skin irritation, also can bleach
hair and clothing.
 Combination with topical antibiotic or retinoid more
effective than benzoyl peroxide alone.
 Advantage: Does not cause bacterial resistance, as
seen with antibiotics
TOPICAL TREATMENT: RETINOIDS
 Topical preparations of retinoids include tretinoin,
adapalene and tazarotene.
 Chemically related to vitamin A and exerts function via
the retinoic acid receptor and the retinoid receptor,
exact MOA unknown.
 Effects include:
- Normalization of desquamation to decrease

microcomedones formation.
- Anti-inflammatory effects by inhibiting activity of
leukocytes, release of pro-inflammatory cytokines and
other mediators.
- Helps penetration of other active agents.
TOPICAL TREATMENT: RETINOIDS (2)
 Potential SE include excessive desquamation,
burning, increased photosensitivity,
erythema, irritation, abnormal pigmentation
and teratogenicity.
 3rd generation retinoids e.g. adapalene
produces less irritation and has faster onset
of action than older generations retinoids.
 Topical retinoids can be used OD or BD. In OD
regimens, preparation should be applied at
bedtime with concurrent use of sunscreen
during daytime.
TOPICAL TREATMENT: ANTIBIOTICS
 Act as bacteriostatic and specifically reduce
P. acnes growth and decrease percentage of
pro-inflammatory free fatty acids in surface
lipids.
 Most frequently used are clindamycin,
erythromycin and occasionally
metronidazole, all used BD.
 Most common SE are irritation with
erythema, itching, peeling, dryness and
burning.
 Also risk of pseudomembranous colitis in
clindamycin use.
SYSTEMIC TREATMENT: ANTIBIOTICS
 For management of moderate and severe
acne, particularly in pustular acne.
 Oral antibiotics produce more rapid clinical
improvement than topical preps, but also
associated with GI upset, vaginal candidiasis,
and also decrease efficacy of oral
contraceptives.
 Normal regimens include:
- Tetracycline 500-1000mg in 2 divided doses.
- Erythromycin 250-750mg BD.
- Doxycyline 100mg BD.
- Minocycline 50-100mg BD.
- Azithromycin 250mg 3 times/week
SYSTEMIC TREATMENT: ANTIBIOTICS
(2)
 Resistance of P. acnes is problem,
erythromycin most common, followed by
tetracycline and doxycyline.
 Recommendations to limit resistance:
- Avoid antibiotics if nonantibiotic agents eg.

benzoyl peroxide are effective.
- Antibiotics should be prescribed for a
minimum of 2 months and max 6 months.
- Avoid concomitant use of topical and oral
antibiotics.
- Educate patient on compliance.
SYSTEMIC TREATMENT: ISOTRETINOIN
 Only treatment that targets all 4 pathogenic
factors leading to acne, so indicated for
severe recalcitrant nodular acne.
 Dose (adults) : 0.5-1mg/kg/day in 2 divided
doses for 15 to 20 weeks
 However, highly teratogenic and is
contraindicated in pregnancy, lactation and
severe hepatic and renal dysfunction.
 Also causes hypertriglyceridemia, linked to
suicide & depression, possibly due to
decreased brain metabolism in the
orbitofrontal cortex.
SYSTEMIC TREATMENT: ISOTRETINOIN
(2)
 Patients should be counselled to use two

forms of contraception due to teratogenic
risk.
 Monitoring parameters:
- Monthly pregnancy tests
- Lipids (particularly triglycerides)
- Liver function tests

MISCELLANEOUS TREATMENT
 Patients may also benefit from oral anti-
androgens that act at peripheral receptor level to
reduce sebum production.
- Spironolactone 50-150mg daily.
- Flutamide 125mg OD.
 Estrogen-containing oral contraceptives are also

useful.
- Diane 35 (Cyproterone acetate 2mg &
ethinyloestradiol 0.035mg)
 Salicylic acid preparations (including facial wash)
may also be used though they are moderately
effective.
SUMMARY
 Acne is an inflammatory disease of the
pilosebaceous follicles caused by abnormal
keratinization, increased sebum production,
P. acnes colonisation and inflammation.
 Classified into 4 types depending on clinical
presentation of lesions.
 Treatment includes benzoyl peroxide, topical
and oral preparations of retinoids and
antibiotics.
SUMMARY (2)
ACNE SEVERITY TREATMENT
Non-inflammatory comedonal Topical retinoids

acne
Mild to moderate inflammatory Benzoyl peroxide + a topical

acne antibiotic or combination of
both
Moderate to severe Benzoyl peroxide + topical/oral
inflammatory acne antibiotics + topical retinoids
Severe nodulocystic acne Benzoyl peroxide + oral

isotretinoin
REFERENCES
1. P. Rutter, Community Pharmacy: Symptoms, Diagnosis and Treatment. 1st edn, Churchill-
Livingstone 2004.
2. UpToDate: Approach to Acne Vulgaris
3. Lacy et al. Drug Information Handbook, 17th edn, Lexi-Comp. 2008.
4. Kumar A. et al. Treatment of acne with special emphasis on herbal remedies. Expert Rev
Dermatol. 2008;3(1):111-122
5. Piskin S. & Uzunali E. A review of the use of adapalene for the treatment of acne
vulgaris. Therapeutics & Clinical Risk Management 2007:3(4) 621-624
6. Bardazzi et al. Azithromycin: A new therapeutical strategy for acne in adolescents.
Dermatol Online J. 2007; 13(4):4
7. Swanson J. Antibiotic resistance of Propionibacterium acnes in acne vulgaris. Dermatol
Nurs 2003; 15(4): 359-362
8. National Guideline Clearinghouse. Guidelines of care for acne vulgaris management.
From www.guideline.gov.
9. Woodard I. Adolescent acne: a stepwise approach to management. Topics in Advanced
Practise Nursing eJournal. 2002;2:2.

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What is acne and what causes it?

What is acne and what causes it?

How is acne classified?

How is acne classified?

ACNE

 Although not fatal, produces physical

(i) Increased sebum production

- azathioprine, barbiturates, corticosteroids,

 Treatment is based on severity of acne and

 Acne lesions take at least 2 months to

- Normalization of desquamation to decrease

- Avoid antibiotics if nonantibiotic agents eg.

 Patients should be counselled to use two

- Monthly pregnancy tests

- Lipids (particularly triglycerides)

- Liver function tests

- Flutamide 125mg OD.

 Estrogen-containing oral contraceptives are also

Non-inflammatory comedonal Topical retinoids

Mild to moderate inflammatory Benzoyl peroxide + a topical

Severe nodulocystic acne Benzoyl peroxide + oral

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