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ACNE VULGARIS

dr. IGA SUMEDHA PINDHA, Sp.KK(K) dr. IGAA ELIS INDIRA, SpKK dr.NLP RATIH V KARNA, SPKK
Lab/SMF Ilmu Kesehatan Kulit dan Kelamin FK UNUD/RS Sanglah Denpasar

Acne vulgaris a chronic inflammatory disease of the pilo-sebaceous follicles

characterized by:

comedones (open comedo or blackhead, closed comedone or whitehead), papules, pustules, nodules, and often scars

Pathogenesis
Acne is follicular disease with comedo formation

Comedones reveal: thinned epithelium, dilated follicular canal filled with lamelar lipidimpregnated keratinous material.

Four key element of pathogenesis :


1. 2. 3. 4. Follicular epidermal hyperproliferation Excess sebum production Inflamation The presence and activity of Propionibacterium acnes

primarily affect: face, neck, upper trunk and upper arms

begins at puberty the first sign of increased sex hormone production

Infantile acne : cases that persist after the first 4 weeks of life

ACNE
disease of the adolescent (85% of all teenagers)

Neonatal acne develops few days after birth

Predisposing factors - comedogenic greasy or occlusive products acne cosmetica - mechanical or frictional forces - overexuberant washing - chin straps, violins, hats, surgical tape - acne venenata - drug-induced acne - endocrinologic disorder

Hyperandrogenic state
- woman and children - irregular menses and hirsutism - acne resistant to conventional therapy - relapse quickly after a course of isotretinoin - sudden onset of severe acne

Screening test for virilizing tumor (adrenal tumors, congenital adrenal hyperplasia, ovarian tumor)

- serum dehydro epiandrosterone sulfate (DHEAS) - testosterone

Polycystic ovarian syndrome (PCOS)

- serum testosteron - LH/ FSH ratio (>2-3) - ovulation < 9 periods per year or period >40 days apart - sign of hyperandrogenism

Gradation of acne
Comedonal acne Papulopustular acne Conglobate acne

ACNE CLASIFICATION
KOMEDO MILD MODERATE < 20 20-100 PAPUL/PUSTUL NODUL <15 15-50 <5

SEVERE

>100

>50

>5

Acne neonatorum

Differential diagnosis
1.1. Acneiform eruption Characterized by papules and pustules No comedone Associated to certain drugs glucocorticoid, isoniazid, high dose of vit B complex, phenobarbital, tetracycline, iodides, bromides - Sudden onset - Different distribution to acne vulgaris (Appear on wide distribution)

2. 2.Rosacea
- Chronic eruption of the central face

- Burning or stinging sensation


- Characterized by : persistent erytheme, flushing, telangiectasis, papule,pustule, cyste, progressive hyperplasia of sebaceous glands

- No comedones
- Thickened skin of nose (rhynophyma)

3. Perioral dermatitis
- Confined inflammation of perioral & perinasal regions - Predominant in child-bearing woman - No exact etiology (sensitivity of sun exposure, acne, rosacea, infection of candida or demodex folliculorum, misuse of potent topical steroid ) -Clinnical findings : persistent erytheme, scale with small papule and pustules in the perioral and nasolabial regions -There is five millimeter clear zone at the vermilion edge

TREATMENT
- Avoidance of specific foods is not necessary - Scrubbing of the face worsen acne

Medical therapy
1.

Systemic & topical antimicrobials

2.

Systemic & topical retinoids

3. hormonal therapy 4. intralesional corticosteroids 5. physical modalities


comedo extractor photodynamic therapy Laser Dermabrasi Bedah Skalpel

Complications
pitted scars

Scarring

keloids

wide-mouthed depressions

MELASMA (CHLOASMA FACIEI)

dr. IGA SUMEDHA PINDHA, Sp.KK(K)


dr. IGAA ELIS INDIRA, SpKK dr. NLP.RATIH V KARNA, SPKK
Lab/SMF Ilmu Kesehatan Kulit dan Kelamin FK UNUD/RS Sanglah Denpasar

Visible pigmentation of the skin or hair is a combination of

amount of melanin type of melamin (eumelanin = brown, pheomelanin = yellow or red) degree of vascularity presence of carotene thickness of the stratum corneum

Melanin is formed from tyrosine, via the action of tyrosinase, in the melanosomes of melanocyte

Pigmentation require
the adequate manufacture of melanin appropriate transport of melanosomes within the melanocyte

The melanosomes are transferred from a melanocyte to a group of 36 keratinocytes called the epidermal melanin unit

Melasma is characterized by brown patches typically on the malar prominences and forehead quite sharply demarcated

MELASMA

Clinical patterns: centrofacial malar mandibular

Affect darker-complexioned individuals (Fitzpatrick skin types IV and V) Most frequently in young women, men 10%

Pregnancy

Use of dilantin PREDISPOSING FACTORS hormonal : ingestion of estrogen (oral contraceptives or hormone replacement therapy [HRT] at menopause)

Endocrinologic disorders

Melasma classified as
Epidermal based : Dermal based : Mixed :
woods light lesion

woods light lesion

epidermal and dermal

Pathology
1. Epidermal type Increasing of melanin disposition on basal, suprabasal and epidermal layers. Vacuolar degeneration in basal cells. Dermal type Perivascular melanin contained macrophag on superfisial dermis and middermis layers Mixed type Both of histologic findings Electron mic. : scattered melanosomes in keratinosit. Dopa staining : increasing of melanocytes count.

2.

3.

Differential diagnosis
Drug induced hyperpigmentation Hyperpigmentation post inflamation Ochronosis exogen Mercury deposition on the skin

Treatment

Avoid exposure to sunlight Use sunblock with broad-spectrum UV

Gold standard bleaching cream with hydroquinone 2% - 4% Treatment Tretinoin cream increase efficacy

Kligmans formula : combination of hydroquinone, tretinoin and topical steroid Glycolic acid added to hydroquinone to Treatment enhance efficacy

Complication from use high concentration of hydroquinone


satellite pigmentation local ochronosis

Other topical therapy


azelaic acid, kojic acid N-acetyl-4-cysteaminyphenol, licorice extract, arbutil

Surgical procedures
peels laser treatment pretreatment with hydroquinone result