DEFINITION

EPIDEMIOLOGYAt birth – neonatal period: mild degree of

acne( follicular stimulation by adrenal androgens)

• Puberty: often occur significant problems comedones (predominant lesion)

• Women : may persist through the 30th decade

ETIOLOGY & PATHOGENESISMultifactorial 4 basic steps:

1. follicular epidermal hyperproliferation

2. excees sebum production

3. inflammation

4. the presence & activity of Propionibacterium acnes

Microcomedo-Hyperkeratotic infundibulum-Cohesive corneocytes-Sebum secretion

Comedo-Accumulation of shed corneocytes & sebum-Dilatation of follicular ostium

Inflammatory papule/pustule-further expansion of follicular unit-Proliferation of P.acne-Perifollicular inflammation

Nodule-Rupture of follicular wall-Marked perifollicular inflammation-scarring

CLINICAL FINDING

DIFFERENTIAL DIAGNOSISClosed comedonal acne

MiliaSebaceous hyperplasia

Open comedonal acne Favre-Racouchot syndrome

Inflammatory acneRosaceaPerioral dermatitis

TREATMENTLocal Therapy cleansingTopical AgentsSystemic TherapyHormonal TherapyDietSurgeryIntralesional GlucocorticoidsPhototherapy & Lasers

ACNE VARIANTSNeonatal AcneInfantile AcneAcne ConglobataAcne Fulminans

ACNEIFORM ERUPTIONSSteroid FolliculitisDrug-Induced Acne

GlucocorticoidsPhenytoinLithiumIsoniazidHigh –dose vit.B complexHalogenated compounds

COMPLICATIONTransient macular erythemaPost-inflammatory hyperpigmentationPermanent scarring

PROGNOSIS & CLINICAL COURSEFavorableSpontaneous remissionPrepubescent females with comedonal acne

+ high DHEAS levels predictors of severe or long-standing nodulocystic acne

Th/ regimens initiated earlyPrevent permanent sequelae