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)
http://www.dermnetnz.org/common/image.php?path=/acne/img/comed1.jpg -
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CLOSE UP OF BLACKHEAD
http://www.dermnetnz.org/common/image.php?path=/acne/img/comed3.jpg -
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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.
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