ACNE VULGARIS

N E L S O N P. TA N D AY U 09-100
FA K U LTA S K E D O K T E R A N U N I V E R S I TA S K R I S T E N I N D O N E S I A

DEFINITION

Acne vulgaris is a self-limited disorder of the pilosebaceous unit that is seen primarily in adolescents.
Zaenglein et al, 2008.

PILOSEBACEOUS UNIT

LESION (1)

Cases of acne present with a pleomorphic variety of lesions, consisting of comedones, papules, pustules, and nodules.

LESION (2)

Although the course of acne may be self-limiting, the sequelae can be lifelong, with pitted or hypertrophic scar formation

EPIDEMIOLOGY

Acne is often an early manifestation of puberty The greatest numbers of cases are seen during the middle-to-late teenage period. Afterward, the incidence steadily decreases.

ETIOLOGY
Normal physiological reaction in puberty Disease of the ovaries
Polycystic ovarian syndrome Benign or malignant ovarian tumors

Disease of the adrenal gland

Partial deficiency of the adrenal enzyme 21 Hydroxylase Benign or malignant adrenal tumors

Disease of the pituitary gland

Cushings syndrome due to excessive adrenocorticotrophic hormone Acromegaly due to excessive growth hormone production Adenoma of the adrenal gland especially prolactinoma

Obesity and the metabolic syndrome Medication-phenytoin, steroids, barbiturates, OC Pills.

ETIOLOGY

Keratinization Sebum Bacteria Hereditary Hormonal Diet Weather

INITIAL PATHOGENESIS: follicular hyperkeratinization proliferation + decreased desquamation of keratinocytes hyperkeratotic plug (microcomedone)

PATHOGENESIS Sebaceous glands enlarge Sebum production increases

Growth medium for P. acnes

Plugs provide anaerobic Lipid-rich environment

PATHOGENESIS
Bacteria thrive Inflammation results Chemotactic factors attract neutrophils Depending on conditions
Non-inflammatory open/closed comedones Inflammatory papule/pustule/nodule

1. FOLLICULAR PLUGGING
Proliferation of ductal keratinocytes, with altered differentiation Result in comedones First observed at adrenarchy Probably androgen mediated

2. SEBORRHOEA Increased sebum production and release May be mediated by

Androgens Growth hormone

3. BACTERIAL OVERGROWTH Colonization with Proprionibacterium acnes Normal commensal, anaerobic Increased growth in blocked sebumfilled follicles

4. INFLAMMATION Mediated by activation of monocytes and neutrophils by P. acnes Release of inflammatory cytokines
Interleukins TNF

GRADING
Plewig & Kligman (1975)1: Comedones: <10 comedones on 1 side of the face 10-24 comedones 25-50 comedones >50 comedones Papulopustular lesions: <10 papulopustular lesions on 1 side of the face 10-20 papulopustular lesions 21-30 papulopustular lesions >30 papulopustular lesions
Wasitaatmadja (1982)1: Ringan, bila: Beberapa lesi tak beradang pada 1 predileksi Sedikit lesi tak beradang pada beberapa tempat predileksi Sedikit lesi beradang pada 1 predileksi Sedang, bila: Banyak lesi tak beradang pada 1 predileksi Beberapa lesi tak beradang pada lebih dari 1 predileksi Beberapa lesi beradang pada 1 predileksi Sedikit lesi beradang pada lebih dari 1 predileksi Berat, bila: Banyak lesi tak beradang pada lebih dari 1 predileksi Banyak lebih beradang pada 1 atau lebih predileksi

WHITEHEAD AND BLACKHEADS

CLOSED COMEDONES (WHITEHEAD)

CLOSED COMEDONES (WHITEHEADS)

OPEN COMEDONES (BLACKHEAD)

open comedo (a blackhead): when follicular orifice is opened + distended.

Melanin + packed keratinocytes + oxidized lipids dark colour

OPEN COMEDONES (BLACKHEAD)

OPEN COMEDONES (BLACKHEADS)

CLOSE UP OF BLACKHEAD

INFLAMMATORY LESIONS Papules (small red bumps) Pustules (white or yellow squeezable spots) Inflamed nodules (large red lumps)

ACNE CONGLOBATA
Unpleasant form of nodulocystic acne Interconnecting abscesses and sinuses, which result in unsightly hypertrophic (thick) and atrophic (thin) scars. There are groups of large macrocomedones and cysts that are filled with smelly pus.

WHAT TESTS SHOULD BE DONE? In general, laboratory workup is not indicated for patients with acne unless hyperandrogenism is suspected. Many patients report that their acne flares during periods of stress.

DIFFERENTIAL DIAGNOSIS

Acneiform eruption Acne Venenata Rosacea Perioral dermatitis

ACNEIFORM ERUPTION
A drug induced acne.

GENERAL PRINCIPLES OF MANAGEMENT

Prevention
Treatment

PREVENTION OF ACNE
Avoid the increasing amount of lipid sebum Avoid the triggering factors of acne Inform consent

TREATMENT OF ACNE
Topical Systemic

Physical
Diet

TOPICAL MEDICATION
Retinoid (tretinoin 0.1-0.25%, isotretinoin 0.05%, adapalene 0.1%)

take out the mature comedones anti-inflammatory effect

prevents comedone formation

Salicylic acid

 Azelaic acid (20% cream or 15% gel)

has both antimicrobial and comedolytic properties.

Additionally, it is a competitive inhibitor of tyrosinase, thus decreasing pigmentation.

Benzoyl peroxide
a powerful antimicrobial agent. This effect is related

to a decrease in the bacterial population and an

accompanying triglycerides. decrease in the hydrolysis of

TOPICAL ANTIBIOTICS
Clindamycin 1% Erythromycin 2% or 4% with zinc acetate 1.2% most useful when inflammatory lesions predominate

SYSTEMIC MEDICATIONS

Oral vitamin A dan retinoid Hormonal therapy Oral antibiotics

ORAL ANTIBIOTICS
1st line - Tetracycline, doxycycline, minocycline
2nd line - Erythromycin Cotrimoxazole

PHYSICAL TREATMENT Comedones extraction Intralesion corticosteroids Liquid nitrogen Ultraviolet radiation

REFERENCES
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Weller R, Hunter J, Savin J, Dahl M. Clinical Dermatology. 4th Ed. UK: Blackwell Publishing; 2008. p. 16270.
Batra, Sonia. Acne. In: Ardnt KA, Hsu JT, editor. Manual of dermatology therapeutics. 7th Ed. Massachusetts: Lippincot Williams and Wilkins; 2007. p. 4-18. Schalock PC. Rosaceae and perioral (periorificial) dermatitis. In: Ardnt KA, Hsu JT, editor. Manual of dermatology therapeutics. 7th Ed. Massachusetts: Lippincot Williams and Wilkins; 2007. p.175-180 Dreno B, Poli F. Epidemiology of Acne. Dermatology, Acne Symposium at the World Congres of Dermatology Paris July 2002. p.7-9.

James WD, Berger TG, Elston DM. Acne. In: James W, Berger T, ElstonDM, editor. Andrews disease of the skin Clinical Dermatology 10th Ed. Canada: Elsevier; 2000. p. 231-44.
Gupta AK, Swan JE. Perioral dermatitis. In: Williams H, Bigbi MC, Diepgen T, Herxheimer H, Nalgi L, Rzany B. Evidence-Based Dermatology. London: BMJ Books; 2003. p. 125-131. Webster, Guy. Overview of the pathogenesis of acne. In: Webster GF, Rawlings AV, editor. Acne and its therapy. London:Informa Healthcare; 2007. p. 1-5. Zouboulis, Christos C. Update and future of systemic acne treatment. Dermatology, Acne Symposium at the World Congres of Dermatology Paris July 2002. p. 37-42.