1. ACNE & ADNEXAL DISORDERS
Diany Nurdin

2. DISORDER OF ADNEXAL ADOLESCENS SKIN
SEBACEOUS GLANDS
APOCRINE GLANDS
ECCRINE GLANDS

3. PHYSIOLOGY OF
REGULATORY
MECHANISM

5. INSURANCE ? Acne vulgaris Is it important or just Trivial ?
Is it a disease ?
INSURANCE ?

6. Embarrasing Devastating

7. Why it is important – serious disease
The morbidity - the prevalence 85% – 95%
(100% teenager)
adult acne- women > 21th
-the most common dermatologic
disorder in US, RSS the II nd
The embarrasing disease
The cost - skin care
- treatment of complication - scar

8. MOST FREQUENT QUESTIONS
DIET –CHOCOLATE
-SPICY
-FRIED FOODS
-MILK
STRESS
SEXUAL ACTIVITY

9. What is ACNE ? Not an infectious but Inflammatory skin condition
Common, chronic, recurring disease
Self limited disease
Influences Quality of Life
Constitute a socioeconomic problem

10. ACNE VULGARIS DEFINITION: CHRONICALLY INFLAMMATION OF
SEBACEOUS FOLLICLE
2. LESSION COMEDONE-PAPULE-PUSTULE-
NODULE-CYST-SCAR (PLEOMORPHIC)
3. PREDILECTION SEBORRHOIC AREA
4. AGE -PUBERTY

11. Prevalence
( 85 %) mild
( 15 %) need medical treatment

12. 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

13. PATHOGENESIS: ANDROGEN DHT 5ar type 1 MICROCOMEDONE Linoleic acid
IL-1 alpha
ABNORMAL KERATINIZATION
Acroinfundibulum
INFLAMMATION
RUPTURE FOLLICLE WALL
TNF -ALPHA
LIPASE
P.ACNE
SEBUM SECRETION

14. Gollnick H et al J.Am.Acad.Dermatol 2003:;49(1 Suppl) S1-S37

15. 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
MICROBIOLOGY OF PILOSEBACEOUS UNIT

16. PATHOGENESIS:
THE DEVELOPMENT
OF ACNE LESSION
MIKROCOMEDO
COMEDO
INFLAMMATION
LESSION

17. CLINICAL SIGN:
PRIMARY LESSION
COMEDO
1.OPEN
2.CLOSED

18. DIAGNOSE OF ACNE VULGARIS:
1. PREDILECTION
2. LESSION
3. SEBORRHOE
4. TEENAGE

19. CLINICAL VARIATION:
NEONATAL ACNE

20. ADULT ACNE

21. ACNE IN COLORED SKIN

22. SUBTYPES OF ACNE:
CYSTIC ACNE

23. SUBTYPE ACNE :
ACNE FULMINAN

24. SUBTYPES ACNE:
MECHANICAL ACNE
ACNE COSMETICA – POMADE ACNE

25. ACNE EXCORIEE

26. ROSACEA
DIFFERENTIAL DIAGNOSIS:
ERYTHEMATOTELANGIETATIC
PAPULOPUSTULAR

27. DIFFERENTIAL DIAGNOSIS:
PHYMATOUS
OCULAR

28. DIFFERENTIAL DIAGNOSIS:
ACNEIFORM ERUPTION
* CORTICOSTEROID
* INH
* BROMIDE. IODIDE
* PHENYTOIN

29. DIFFERENTIAL DIAGNOSIS
PERIORAL DERMATITIS

30. Perioral Dermatitis, Corticoid Damage

32. GRAM NEGATIVE FOLLICULITIS
DIFFERENTIAL DIAGNOSIS:
GRAM NEGATIVE FOLLICULITIS

33. TREATMENT: ANTI -ANDROGEN RETINOIC ACID ANTIBIOTIK ANTI INFLAMMATION
ABNORMAL KERATINIZATION
RETINOIC ACID
ANTI INFLAMMATION
INFLAMMATION
P.ACNE
ANTIBIOTIK
SEBUM SECRETION

34. Actions of Anti-Acne Therapies
Topical retinoids:
Normalize follicular hyperproliferation and cohesiveness
Reduce inflammatory response
Oral Isotretinoin:
Reduces sebum
Normalizes hyperkeratinization
Inhibits P. acnes growth (indirect)
Reduces inflammatory response
Antibiotics:
Reduce microorganisms
Reduce inflammatory response
Hormones:
Reduce sebum production
Reduce proliferation of follicular keratinocytes
Benzoyl peroxide:
Reduces microorganisms

35. 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

36. Actions of Anti-Acne Therapies
Sebum production
Hyper- keratinization
Inflammation
Reduction in P.acnes
Topical therapies
Retinoids - ++ +
Benzyl peroxide
+++
Antibiotics
Azelaic acid
+/-
Nicotinamide
Systemic therapies
Hormonal therapy
Indirect
Layton AM. A review on the treatment of acne vulgaris. Int. J. Clin. Pract. 60(1), 64–72 (2006).

37. TREATMENT:
NON INFLAMMATION
TOPICAL
KERATOLYTIC
COMEDOLYTIC
BACTERICIDAL

38. TREATMENT:
INFLAMMATION
TOPICAL
= ACNE NONINFLAMMATION
BENZOIL PEROKSIDE
ANTIBIOTIC
SYSTEMIC
ANTIBIOTIC
ANTI INFLAMMATION
HORMON

41. BROMHIDROSIS
APOCRINE
ECCRINE

44. BROMHIDROSIS
APOCRINE : BROMIDROSIS OSMIDROSIS ECCRINE : KERATINOGENIC-- BACTERIAL DEGRADATION OF MACERATED STRATUM CORNEUM--ODOROGENIC FATTY ACID

45. BROMHIDROSIS EXCESSIVE –ABNORMAL BODY ODOR FOUL SMELLING SWEAT-MALODOR
ARISE FROM THE APOCRINE GLAND

46. BROMHIDROSIS YOUNG ADULTS BLACK SUMMER FAMILY HISTORY CULTURAL
SUBJECTIVE -RACES

47. BROMHIDROSIS PATHOGENESIS
Increase number & size apocrine glands, increase ratio apocrine/eccrine -----increase production
Axillary bacteria e-3-methyl 2 hexenoic acid
Short chain fatty acids & ammonia.
Trimethylaminuria- FISH ODOR

48. PREDISPOSING FACTOR HYPERHYDROSIS OBESITY INTERTRIGO DIABETES MELLITUS
FOODS - GARLIC
- ALCOHOL
HERITABLE AMINOACIDURIA

49. BROMHIDROSIS TREATMENT
HYGIENE –SOAP & WATER
DEODORANT
REDUCING BACTERIA
REDUCING APOCRINE /ECRINE SWEAT
-ANTIPERSPIRANT
-ABSORBENT POWDERS
-SURGERY- CURRETAGE SUBCUTANEOUS
- EXCISION
- SYMPATHECTOMY
-BOTULINUM TOXIN INJECTION
-IONTOPHORESIS

51. 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..

52. DEODORANT Triclosan Benzalkonium chloride, Chlorhexidine.
Propylene glycol
Fragrances

53. Iontophoresis with tap water by producing a physical blockage of the sweat ducts at the level of the stratum

54. 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