ACNE & ADNEXAL
DISORDERS
Arief Budiyanto
Bagian/ SMF IK Kulit dan Kelamin
FK-UGM/ RSUP Sardjito
Yogyakarta
DISORDER OF ADNEXAL
ADOLESCENS SKIN
SEBACEOUS GLANDS
APOCRINE GLANDS
ECCRINE GLANDS
PHYSIOLOGY OF REGULATORY MECHANISM
Acne vulgaris
Is it important or just
Trivial ?
Is it a disease ?
INSURANCE ?
Embarrasing
MOST FREQUENT QUESTION
DIET CHOCOLATE
-SPICY
-FRIED FOODS
-MILK
STRESS
SEXUAL ACTIVITY
What is ACNE
Not an infection but
Inflammatory skin condition
Common, chronic, recurring disease
Self limited disease
Influences Quality of Life
Constitute a socioeconomic problem
Why it is important serious disease
1. The morbidity - the prevalence 85% 95%
(100% teenager)
adult acne- women > 21th
-the most
commondermatologic
disorder in US, RSS the II
nd
2. The embarrasing disease
3. The cost - skin care
- treatment of complication - scar
Prevalence
( 85 %) mild
( 15 %) need medical treatment
PREVALENCE
-THE MOST COMMON VISIT DERMATOLOGIST AGE 15-45
-MAN > WOMAN ------- VISIT OF WOMEN 80% > FREQUENT
> AGE 19 YRS
-US DATA PRESCRIPTION ANTIBIOTICS $ 5 MILLION
ISOTRETINOIN $ 1.4 MILLION
PATHOGENESIS:
ANDROGE
N
5ar type 1
MICROCOMEDONE
Linoleic acid
IL-1 alpha
ABNORMAL KERATINIZATION
Acroinfundibulum
INFLAMMATION
RUPTURE FOLLICLE WALL
TNF
-ALPHA
P.ACNE
LIPASE
SEBUM SECRETION
DHT
Gollnick H et al J.Am.Acad.Dermatol 2003:;49(1 Sup
MICROBIOLOGY OF PILOSEBACEOUS UNIT
STAPHYLOCOCCI, MICROCOCCI
GRAM (+), COAGULASE (-)
SUPERFICIAL AEROBIC
PORTION OF SEBACEOUS
UNIT
PITYROSPOSPORUM OVALE,
PITYROSPORUM ORBICULARE.
LIPOFILIC YEAST
PROPIONEBACTERIUM ACNES,
ANEROBIC PLEOMORHIC DIPHTEROID.
MOST PREVALENT ORGANISM IN
FOLLICULAR
INFRAINFUNDIBULUM
ANAEROBIC CONDITION
OF SEBACEOUS UNIT
INFLAMATORY
REACTION OCCURS IN
ACNE
PATHOGENESIS:
THE DEVELOPMENT
OF ACNE LESSION
MIKROCOMED
O
COMEDO
INFLAMMATION
LESSION
CLINICAL SIGN:
PRIMARY LESSION
COMEDO
1.OPEN
2.CLOSED
Regional consensus of acne
management (2003)
Ringan:
< 20 komedo, atau < 15 lesi
inflamasi,
atau lesi total < 30
Sedang:
20-100 komedo, atau 1510 lesi inflamasi,
atau lesi total 30-125
18
Regional consensus of acne management
(2003)
Berat:
15 kista, atau total
komedo > 100,
atau lesi inflamasi
total > 50
19
ACNE VULGARIS
DEFINITION:
1. CHRONICALLY INFLAMMATION OF
SEBACEOUS FOLLICLE
2. LESSION COMEDONE-PAPULE-PUSTULENODULE-CYST-SCAR (PLEOMORPHIC)
3. PREDILECTION SEBORRHOIC AREA
4. AGE -PUBERTY
DIAGNOSE OF ACNE VULGARIS:
1. PREDILECTION
2. LESSION
3. SEBORRHOE
4. TEENAGE
CLINICAL VARIATION:
NEONATAL ACNE
ADULT ACNE
ACNE IN COLORED SKIN
SUBTYPES OF ACNE:
CYSTIC ACNE
SUBTYPE ACNE :
ACNE FULMINAN
SUBTYPES ACNE:
MECHANICAL ACNE
ACNE COSMETICA POMADE ACNE
ACNE EXCORIEE
DIFFERENTIAL DIAGNOSIS:
ROSACEA
ERYTHEMATOTELANGIETATIC
PAPULOPUSTULAR
DIFFERENTIAL DIAGNOSIS:
PHYMATOUS
OCULAR
DIFFERENTIAL DIAGNOSIS
ACNEIFORM ERUPTION
* CORTICOSTEROID
* INH
* BROMIDE. IODIDE
* PHENYTOIN
DIFFERENTIAL DIAGNOSIS
PERIORAL DERMATITIS
Perioral Dermatitis, Corticoid Damage
DIFFERENTIAL DIAGNOSIS:
GRAM NEGATIVE FOLLICULITIS
TREATMENT:
ANTI -ANDROGEN
ABNORMAL KERATINIZATION
RETINOIC ACID
INFLAMMATION
P.ACNE
ANTI INFLAMMATION
ANTIBIOTIK
SEBUM SECRETION
Actions of Anti-Acne
Therapies
Topical retinoids:
Normalize follicular
hyperproliferation
and cohesiveness
Reduce
inflammatory
response
Antibiotics:
Reduce
microorganisms
Reduce
inflammatory
response
Benzoyl
peroxide:
Reduces
Oral
Isotretinoin:
Reduces sebum
Normalizes
hyperkeratinizatio
n
Inhibits P. acnes
growth (indirect)
Reduces
inflammatory
response
Hormones:
Reduce sebum
production
Reduce
proliferation
of follicular
keratinocytes
CURRENT ACNE
TREATMENT
TOPICAL -RETINOIDS
-ANTIBIOTICS : CLINDAMYCIN, ERYTHROMYCIN,
NADIFLOXACIN, NA
SULFACETAMIDE,
DAPSONE
-BENZOYL PEROXIDE
-AZELAIC ACID
-SALICYLIC ACID, SULFUR
-NICOTINAMIDE, ASCORBIC ACID
SYSTEMIC -ANTIBIOTICS
-HORMONAL
-ISOTRETINOIN
ADJUVANT -CHEMICAL PEELING
-LASER & LIGHT
-CRYO THERAPY
-DIET
Therapies
Actions of Anti-Acne
Therapies
HyperSebum
Inflammati Reduction
keratinizati
production on
Topical therapies
on
in P.acnes
Retinoids
++
Benzyl
peroxide
++
+++
Antibiotics
++
+++
Azelaic acid
+/-
Nicotinamide
+/-
Systemic therapies
Antibiotics
+++
+++
Hormonal
therapy
++
++
Indirect
Indirect
Retinoids
+++
++
++
++
Layton AM. A review on the treatment of acne vulgaris. Int. J. Clin. Pract. 60(1), 6472 (2006).
TREATMENT:
NON INFLAMMATION
TOPICAL
KERATOLYTIC
COMEDOLYTIC
BACTERICIDAL
TREATMENT:
INFLAMMATION
TOPICAL
= ACNE NONINFLAMMATION
BENZOIL PEROKSIDE
ANTIBIOTIC
SYSTEMIC
ANTIBIOTIC
ANTI INFLAMMATION
HORMON
RingkasanManajemen
Acne
Tujuan Pengobatan
Menormalkan hiperaktifitas keratinosit pada
folikel
Menurunkan aktifitas kel sebasea,
menurunkan produksi sebum
Menurunkan populasi P. Acne
Mencegah inflamasi
44
Ringkasan Manajemen
Acne
Prinsip penatalaksanaan
1. Pencegahan
2. Pengobatan
Topikal
Sistemik
Kombinasi topikal & sistemik
Tindakan khusus
3. Perawatan
45
PERTIMBANGAN KLINIS
1. DERAJAT BERAT PENYAKIT ( luas lesi, derajat
perkembangan lesi/ tipe lesi, lama sakit, dampak
penyakit terhadap psikologi pasien)
2. PENETAPAN
FAKTOR
PREDISPOSISI
PENENTU
(penting untuk pemilihan kombinasi obat/tehnik
terapi yang dipergunakan)
3. Tidak ada satu monoterapi/ tehnik terapi yang bisa
menekan seluruh jalur patogenesis acne ( Terapi
kombinasi hampir selalu lebih unggul)
4. Jelaskan ekspektasi yang bisa diperoleh ( sesuai
program terapi, jenis obat, kondisi penyakit)
BROMHIDROSIS
APOCRINE
ECCRINE
BROMHIDROSIS
EXCESSIVE ABNORMAL BODY ODOR
FOUL SMELLING SWEAT-MALODOR
ARISE FROM THE APOCRINE GLAND
BROMHIDROSIS
YOUNG ADULTS
BLACK
SUMMER
FAMILY HISTORY
CULTURAL
SUBJECTIVE -RACES
BROMHIDROSIS PATHOGENESIS
Increase number & size apocrine
glands, increase ratio
apocrine/eccrine -----increase
production
Axillary bacteria ------- methyl 2
hexenoic acid
Short chain fatty acids & ammonia.
Trimethylaminuria- FISH ODOR
PHYSIOLOGY OF REGULATORY MECHANISM
PREDISPOSING FACTOR
HYPERHYDROSIS
OBESITY
INTERTRIGO
DIABETES MELLITUS
FOODS - GARLIC
- ALCOHOL
HERITABLE AMINOACIDURIA
BROMHIDROSIS TREATMENT
HYGIENE SOAP & WATER
DEODORANT
REDUCING BACTERIA
REDUCING APOCRINE /ECRINE SWEAT
-ANTIPERSPIRANT
-ABSORBENT POWDERS
-SURGERY- CURRETAGE SUBCUTANEOUS
- EXCISION
- SYMPATHECTOMY
-BOTULINUM TOXIN INJECTION
-IONTOPHORESIS
ANTIPERSPIRANT
Aluminum chloride hexahydrate
Aluminum chlorhydrate
Aluminum sesquichlorohydrate
Aluminum chlorohydrex
Aluminum zirconium tetrachlorohydrate
Formaldehyde 10%
Glutaraldehyde 10%
Methenamine 8%
Glycopyrrolate
Metal ions form precipitating complexes with mucopolysaccharides
--damage to luminal epithelial cell
-- obstructive conglomerate
-- completely plugs the acrosyringium..
DEODORANT
Triclosan
Benzalkonium chloride,
Chlorhexidine.
Propylene glycol
Fragrances
Iontophoresis with tap water by producing a physical
blockage of the sweat ducts at the level of the stratum
Botulinum toxin injection
Botulinum toxin, a neurotoxin, acts by
blocking the release of acetylcholine from
the presynaptic terminal of the
neuromuscular junction. It enters the
cytosol and very specifically cleaves
protein components of the
neuroexocytosis apparatus; consequently,
acetylcholine cannot be released. The use
of Botulinum toxin to block sympathetic
innervation of eccrine sweat glands
