Acne Vulgaris Nelson

8/22/2019 Acne Vulgaris Nelson

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ACNE VULGARIS

NE L S ON P. TAN D AY U

0 9 - 1 0 0F A K U L T A S K E D O K T E R A N

U N I V E R S I T A S K R I S T E N I N D O N E S I A


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DEFINITION

Acne vulgaris is a self-limited

disorder of the pilosebaceous

unit that is seen primarily inadolescents.

Zaenglein et al, 2008.


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PILOSEBACEOUS UNIT


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LESION (1)

Cases of acne present with apleomorphic variety of lesions,

consisting of comedones,

papules, pustules, and nodules.


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LESION (2)

Although the course of acne maybe self-limiting, the sequelae

can be lifelong, with pitted or

hypertrophic scar formation


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EPIDEMIOLOGY

Acne is often an earlymanifestation of puberty

The greatest numbers of cases areseen during the middle-to-lateteenage period. Afterward, theincidence steadily decreases.


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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 hormoneAcromegaly due to excessive growth hormone productionAdenoma of the adrenal gland especially prolactinoma

Obesity and the metabolic syndrome

Medication-phenytoin, steroids, barbiturates, OC Pills.


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ETIOLOGY

Keratinization

Sebum

Bacteria

Hereditary

HormonalDiet

Weather


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INITIAL PATHOGENESIS:follicular hyperkeratinization

proliferation +

decreased desquamation of keratinocytes

hyperkeratotic plug

(microcomedone)


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PATHOGENESISSebaceous glands enlarge

Sebum production increases

Growth medium forP. acnes

Plugs provide anaerobic

Lipid-rich environment


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PATHOGENESISBacteria thrive

Inflammation results

Chemotactic factors attract neutrophils

Depending on conditions

Non-inflammatory

open/closed comedonesInflammatory

papule/pustule/nodule


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1. FOLLICULAR PLUGGING

Proliferation ofductal keratinocytes,with altereddifferentiation

Result in comedones

First observed atadrenarchy

Probably androgenmediated


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2. SEBORRHOEA

Increased sebum

production and

release

May be mediated byAndrogens

Growth hormone


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3. BACTERIAL OVERGROWTH

Colonization withProprionibacter ium

acnes

Normal commensal,

anaerobic Increased growth in

blocked sebum-filled follicles


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4. INFLAMMATION

Mediated by activationof monocytes and

neutrophils by P.

acnes

Release ofinflammatory

cytokines Interleukins

TNF


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GRADING

Plewig & Kligman (1975)1:

Comedones:50 comedones

Papulopustular lesions:

30 papulopustular lesions

Wasitaatmadja (1982)1:

Ringan, bila:

Beberapa lesi tak beradang pada 1predileksi

Sedikit lesi tak beradang padabeberapa tempat predileksi

Sedikit lesi beradang pada 1predileksi

Sedang, bila: Banyak lesi tak beradang pada 1predileksi

Beberapa lesi tak beradang padalebih dari 1 predileksi

Beberapa lesi beradang pada 1predileksi

Sedikit lesi beradang pada lebihdari 1 predileksi

Berat, bila: Banyak lesi tak beradang pada

lebih dari 1 predileksi Banyak lebih beradang pada 1 atau

lebih predileksi


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WHITEHEAD AND BLACKHEADS


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CLOSED COMEDONES (WHITEHEAD)
http://www.dermnetnz.org/common/image.php?path=/acne/img/comed2.jpg


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CLOSED COMEDONES (WHITEHEADS)


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OPEN COMEDONES (BLACKHEAD)

open comedo (a

blackhead): when

follicular orifice is opened

+ distended.

Melanin + packed

keratinocytes + oxidized

lipids dark colour


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OPEN COMEDONES (BLACKHEAD)


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OPEN COMEDONES (BLACKHEADS)


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CLOSE UP OF BLACKHEAD


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INFLAMMATORY LESIONS

Papules (small red bumps)

Pustules (white or yellow squeezable

spots)

Inflamed nodules (large red lumps)


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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 largemacrocomedones and cysts that arefilled with smelly pus.


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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.


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DIFFERENTIAL DIAGNOSIS

Acneiform eruption

Acne Venenata

Rosacea

Perioral dermatitis


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ACNEIFORM ERUPTION

A drug induced acne.


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GENERAL PRINCIPLES OF MANAGEMENT

Prevention

Treatment


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PREVENTION OF ACNE

Avoid the increasing amount of lipid sebum

Avoid the triggering factors of acne

Inform consent


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TREATMENT OF ACNE

Topical

Systemic

Physical

Diet


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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)


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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 relatedto a decrease in the bacterial population and an

accompanying decrease in the hydrolysis of

triglycerides.


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TOPICAL ANTIBIOTICS

Clindamycin 1%

Erythromycin 2% or 4% with zinc acetate 1.2% -

most useful when inflammatory lesions

predominate


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SYSTEMIC MEDICATIONS

Oral vitamin A dan retinoid

Hormonal therapy

Oral antibiotics


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ORAL ANTIBIOTICS

1st line - Tetracycline, doxycycline, minocycline

2nd line - Erythromycin

Cotrimoxazole


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PHYSICAL TREATMENT

Comedones extraction

Intralesion corticosteroids

Liquid nitrogen

Ultraviolet radiation


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REFERENCES

Djuanda A, Hamzah M, Aisah S, editor. Ilmu penyakit kulit dan kelamin. Edisi keenam. Jakarta: BadanPenerbit FKUI; 2013. Hal. 254-9.

Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ. Fitzpatrick's dermatology in generalmedicine. 7th Ed. New York: McGraw-Hill; 2008. p. 692-702.

Buxton PK. ABC of dermatology. 4th Ed. London: BMJ Group; 2003. p. 47-9.

Weller R, Hunter J, Savin J, Dahl M. Clinical Dermatology. 4 th Ed. UK: Blackwell Publishing; 2008. p. 162-70.

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 ofdermatology 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 ofDermatology Paris Ju ly 2002. p.7-9.

James WD, Berger TG, Elston DM. Acne. In: James W, Berger T, ElstonDM , editor. Andrews disease ofthe 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 itstherapy. London:Informa Healthcare; 2007. p. 1-5.

Zouboulis, Christos C. Update and future of systemic acne treatment. Dermatology, Acne Sympo sium atthe World Congres of Dermatology Paris July 2002. p. 37-42.

Acne Vulgaris Nelson

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