DEPARTMENT OF DERMATO-VENEREOLOGY

JOURNAL READING
MEDICAL FACULTY
SEPTEMBER 2016
PATTIMURA UNIVERSITY

Acne: Etiopathogenesis and its management

Wina Asriani
(2010 83 037)

Advisor:
dr. Hanny Tanasal, Sp.DV

DERMATO-VENEREOLOGY DEPARTMENT
FACULTY OF MEDICINE PATTIMURA UNIVERSITY
AMBON
2016
Abstrack
Acne vulgaris
is.
One of the commonest skin disorders and
have to treat

chronic inflammatory disease of

pilosebaceous units

can present as seborrhea, comedones, erytematous papules,

pustules and nodules

to better understanding of the etiopathogenesis of acne,new

therapeutic modalities have been designed

The purpose of this article is to review the etiopathogenesis

and treatment options avaliable with us in the present
scenario
 Introduction
Acne vulgaris the most common skin pilosebaceous unit

Characterized by seborrhea, comedone formation, inflammatory lesions and

increased colonization by propionibacterium spp. staphylococcus spp. and
yeast of malassezia spp.within the follicular canal

It is common enough to be called a physiological process, It is better

regarded as a disease

The disorder can cause significant emotional distress and physical scarring if
untreated. Underestimating its importance is of serious consequences
Definition

Inflammatory disease of pilosebaceous

unit
Etiopathogenesis

Increased sebum production by the sebaceous gland.

Alteration in the keratinization process.
Follicular colonization by propionibacterium spp.
Release of inflammatory mediators into the skin.

Others contributing factors

include hormonal influences from
estrogen and androgens, such as
DHEAS (dehydro epiandrosterone
sulfate)
 irritate the infundibular keratinocytes leading to release of
inflammatory substancereduction of sebaceous linoleic acid and 5-
reductase enzyme levels These changes lead to induction of
FOLLICULAR HYPERKERATOSIS

COMEDOGENESIS occurs when abnormally desquamating corneocytes

accumulate within the sebaceous follicle and form a keratinous plug

Propionibacterium species (p.acne, p.granulosum) bacteria produce more

lipases which are responsible for hydrolysis of triglycerides to free fatty acids
contributing to follicular hyperkeratosis and even rupture of follicle
Inflamatory process initiating comedogenesis through
release
IL-1

Androgens increase sebum secretion and also cause

sebaceous gland hyperplasia

A hot and humid climate aggravates acne due to

increase sweating causing ductal hydration

External application of oil, pomades and other

comedogenic cause acneiform eruption

A high glycemic diethyperinsulinemiaincrease level IGF-

1increase sebum production and synthesis of androgen
 Hallmark
of acne

sebaceous gland hypertrophy

Seborrhea
and hyperplasia

The changes in the

quality of sebum may cause
irritation of the duct
epithelium.
Sequence of events
The microcomedo first clinical lesionblockage of the sebaceous
canal altered keratinization retention of sebum and inflammatory
process PAPULE AND PUSTULE

Further retention of sebum rupture sebaceous gland and spread the

sebum in the dermis NODUL

Confluence of affected glands accumulation of pus, fluid and cyst

formation

SCAR cyst heal after rupture or absorbstion of fluid

The severity of acne can be graded on clinical
grounds as under

Grade 1 (mild) : Comedones, occasional

papules.

Grade 2 (moderate): Comedones, many

papules, few pustules

Grade 3 (severe) : pustules, nodules and

abscesses.

Grade 4 (cystic) : Mainly cysts or abscess,

widespread scarring.
Management of acne vulgaris patients

General Eliminate stress by reassurance

measures
Counseling of the patient regarding nature of illness,
treatment modalities and its outcome.

Advice to avoid scratching of lesions

Assess the endocrinal status and

premenstrual flares
Advise to avoid the use of acnegenic drugs, oils, pomades
and heavy cosmetics

Balanced diet should be advised. Avoid

high glycemic diet.
Spesific measures

Decreasing the sebaceous gland secretion

Correction the ductal hipercornification
Decresasing p.acne population
Producing an inflammatory effect

Topical
therapy

Anticomedogenic
Antiseborrhoeic
Antibacterial
Topical retinoid : Mechanism of action :
tretinoin disturbed keratinization,
isotretinoin increase in cell turn over
Adaplene regulation of
Tazarotene prostaglandin synthesis

Adverse effect :
Primary irritant dermatitis
Benzoyl peroxide
Its broad spectrum antimicrobial agent effective via its
oxidizing activity
Topical antibiotics
Used in inflammatory acne (erytromicyn and clindamycin)

Other topical agent mentioned as below

Azelaic acid
Salicyl acid
Acid lactid
Pcolinic acid gel
Dapsone gel 5%
Topical 5 - fluorouracil
Systemic therapy
Tetracyclines
Sulpha drugs:
Macrolides
Hormonal therapy
Oral zink therapy
Oral Retinoids
Phototherapy
Conclusion
Mild (only comedones)
Benzoil peroxide gel
salicil acid gel as cleanser
azelaic acid

Mild to moderate (comedo, few papules and or pustule)

Benzoil peroxide gel or
Topical retinoid
Topical antibiotiks
Moderate to severe (many inflammatory papules, pustules, 1-2 nodul and or
scarring)
Oral antibiotics
Sebostatic agent hormonal therapy, isotretinoin

Cystic acne (more than 2 nodules, cyst abcess, scar)

Aspiration of the cyst
Systemic antibiotics
Dapsone or sebostatic agent
Adjunctive therapy :
laser and light therapy
Acne surgery
 Any
Question???