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ACNE VULGARIS
JOEL SONY
ACNE VULGARIS
•THE PREVALENCE OF ACNE IN ADOLESCENTS HAS BEEN REPORTED TO BE AS
HIGH AS 95% WITH A 20% TO 35% PREVALENCE OF MODERATE TO SEVERE
ACNE.
•ACNE MAY PERSIST INTO ADULTHOOD IN UP TO 50% OF AFFECTED
INDIVIDUALS.
•ACNE RARELY CAUSE SERIOUS SYSTEMIC PROBLEMS, BUT QUALITY OF LIFE
ISSUES ARE A VERY IMPORTANT CONCERN FOR INDIVIDUALS (ESPECIALLY
TEENAGERS) WITH ACNE.
• DEPRESSION, ANXIETY, AND LOW SELF-ESTEEM ARE MORE COMMON IN
PATIENTS WITH ACNE.
RISK FACTORS
•GENETIC
•OBESITY: HYPERANDROGENISM
• A SIGNIFICANT POSITIVE FAMILY HISTORY OF ACNE HAS BEEN
DEMONSTRATED ESPECIALLY WHEN ACNE IS FOUND IN: TWINS ,MOTHER ,
FIRST DEGREE RELATIVE , MULTIPLE FAMILY MEMBERS
• A SIGNIFICANT ASSOCIATION BETWEEN OBESITY AND ACNE IN CHILDREN
AGGRAVATING FACTORS
• SMOKING
• STRESS
• FACIAL THERAPY OR SALON FACIAL MASSAGE
DIET AND SUPPLEMENTS
A. DIETARY FACTORS THAT MAY EXACERBATE ACNE
1. HIGH GLYCEMIC LOADS DIET
2. MILK AND MILK PRODUCTS
RISK OF ACNE INCREASED BY:
FOUR-FOLD WHEN MILK INTAKE FREQUENCY INCREASED FROM LESS
THAN ONCE A WEEK TO DAILY CONSUMPTION
SEVEN-FOLD WHEN ICE CREAM INTAKE FREQUENCY IS BETWEEN LESS
THAN ONCE A WEEK TO DAILY CONSUMPTION COMPARED TO NO
CONSUMPTION
LOW FIBRE AND HIGH FAT DIET
B. DIETARY SUPPLEMENTS
1.THERE IS NO CONCLUSIVE STATEMENT ON THE EFFECTIVENESS OF ZINC
SUPPLEMENT IN ACNE
2.THERE IS NO RETRIEVABLE EVIDENCE ON THE EFFICACY OF VITAMIN A,
VITAMIN C, VITAMIN E AND OMEGA-3 FATTY ACIDS IN THE MANAGEMENT
OF ACNE
FEATURES OF ACNE
1.COMEDONAL ACNE
• OPEN COMEDONES (BLACKHEADS) WITH A CENTRAL DARK KERATIN
PLUGS.
• CLOSED COMEDONES (WHITEHEADS) WITH NO VISIBLE KERATIN PLUG.
2.PAPULAR/PUSTULAR ACNE
•PATIENTS PRESENTED WITH
INFLAMMED
•2 TO 5 MM PAPULES/PUSTULES
3.NODULAR ACNE
PATIENTS PRESENT WITH RED, FIRM, OR FLUCTUANT NODULES (CYST LIKE)
THAT MAY DRAIN OR FORM SINUS TRACTS.
THESE LESIONS MAY LEAVE PERMANENT SCARS.
PATHOGENESIS
HE PATHOGENESIS OF ACNE IS MULTIFACTORIAL. ACNE VULGARIS CAN BE
DIVIDED INTO NON- INFLAMMATORY (OPEN AND CLOSED COMEDONES) AND
INFLAMMATORY (PAPULES, PUSTULES AND NODULES) LESIONS. THE MOST
IMPORTANT FACTORS INVOLVED ARE:
1. INCREASED SEBUM PRODUCTION
2. BACTERIA – PROPIONIBACTERIUM ACNES
3. ALTERED FOLLICULAR KERATINIZATION
4. INFLAMMATION
INCREASE SEBUM PRODUCTION
WHAT TRIGGERS EXCESS SEBUM?
IN MEN, TESTOSTERONE IS SECRETED BY THE MALE SEXUAL ORGANS, AND
IN WOMEN IT ORIGINATES FROM THE OVARIES AND ADRENAL GLANDS. IN BOTH
SEXES, TESTOSTERONE IS SECRETED INTO THE BODY AND ENTERS INTO THE
SEBACEOUS GLAND, WHERE THE ENZYME 5- ALPHA REDUCTASE CONVERTS THE
TESTOSTERONE INTO DI-HYDROTESTOSTERONE; THIS IN TURN STIMULATES
SEBUM FORMATION IN THE SEBACEOUS GLANDS.
BECAUSE 5-ALPHA REDUCTASE IS SENSITIVE TO HORMONE LEVELS, IT GOES
INTO OVERDRIVE, CAUSING AN EXCESS PRODUCTION OF SEBUM WHEN
TESTOSTERONE LEVELS ESCALATE. THIS IS VERY NOTICEABLE DURING PUBERTY.
HOWEVER, RECENT STUDIES HAVE SHOWN THAT HORMONE LEVELS ALONE
ARE NOT SOLELY RESPONSIBLE FOR SEBUM PRODUCTION. 5-ALPHA REDUCTASE
MAY INCREASE ITS SENSITIVITY TO TESTOSTERONE, TRIGGERING EXCESS SEBUM
PRODUCTION EVEN WHEN LOWER LEVELS OF THE HORMONE ARE PRESENT.
UNFORTUNATELY, THE CAUSE OF THIS PHENOMENON IS UNKNOWN.
ALTERED FOLLICULAR KERATINIZATION
IN PATIENTS WITH ACNE, THE RATE OF KERATINOCYTE DESQUAMATION AT
THE FOLLICULAR INFUNDIBULUM IS ALTERED. THE KERATINOCYTES
ACCUMULATE AND BECOME INTERWOVEN WITH MONOFILAMENTS AND
LIPID DROPLETS. THIS ACCUMULATION OF CELLS AND SEBUM RESULTS IN
THE FORMATION OF MICRO-COMEDONES, THE MICROSCOPIC PRECURSOR
TO ALL ACNE LESIONS.THERE IS ALSO THE PRESENCE OF 5Α-REDUCTASE
ACTIVITY IN THE INFRAINFUNDIBULAR SEGMENTS OF SEBACEOUS
FOLLICLES WHICH INCREASES ANDROGEN PRODUCTION AND
SUBSEQUENT FOLLICULAR HYPERKERATOSIS.
PROPIONIBACTERIUM ACNES
THE PROLIFERATION OF PROPIONIBACTERIUM ACNES IS RESPONSIBLE FOR THE
INITIATION OF INFLAMMATION. PROPIONIBACTERIUM ACNES RELEASES MANY
ENZYMES SUCH AS PROTEINASES, LIPASES AND HYALURONIDASES.
BACTERIA IN THE FOLLICLE EXCRETE A LIPASE ENZYME TO BREAK DOWN THE
SEBUM TRIGLYCERIDES INTO FATTY ACIDS AND GLYCEROL. THE SEBUM IS USED AS
A FOOD SOURCE AND THE FREE FATTY ACIDS ARE MERELY WASTE PRODUCTS THAT
IRRITATE THE LINING OF THE FOLLICLE. AT THIS POINT, THE DISEASE MAY RESULT IN
NON-INFLAMMATORY LESIONS AND SIMPLY PRODUCE CLOSED COMEDONES
(WHITEHEADS – IMAGE B), WHICH MAY TURN INTO OPEN COMEDONES
(BLACKHEADS – IMAGE C) AND EXPEL THEIR CONTENTS.
INFLAMMATION
CELLULAR PRODUCTS FROM P. ACNES STIMULATE THE RECRUITMENT OF CD4
LYMPHOCYTES AND SUBSEQUENTLY NEUTROPHILS. THESE INFLAMMATORY
CELLS PENETRATE THE FOLLICULAR WALL, CAUSING DISRUPTION OF THE
FOLLICULAR BARRIER. THIS LEADS TO THE RELEASE OF LIPIDS, SHED
KERATINOCYTES AND P. ACNES INTO THE SURROUNDING DERMIS, INCITING
FURTHER RECRUITMENT OF INFLAMMATORY CYTOKINES AND NEUROPEPTIDES
INCLUDING SUBSTANCE P.
LINOLEIC ACID HAS ALSO BEEN FOUND TO REGULATE IL-8 SECRETION AND
REDUCE THE INFLAMMATORY REACTION. HENCE, DEFICIENCY OF LINOLEIC ACID
MAY INCREASE HYPER- KERATINISATION OF THE EPIDERMIS.
TWO MAIN FATTY ACIDS ESSENTIAL IN THE DIET ARE LINOLEIC (OR OMEGA-6) FATTY ACID AND
ALPHA-LINOLENIC (OR OMEGA-3) ACID. LINOLEIC ACID KEEPS THE SKIN IMPERMEABLE TO WATER,
BUT TO EXERT OTHER EFFECTS THE COMPOUND MUST UNDERGO SPECIFIC METABOLISM.
TYPES OF ACNE
• ACNE CONGLOBATA
• OCCUPATIONAL ACNE
•COSMETIC ACNE
• DRUG-INDUCED ACNE
• INFANTILE ACNE
•LATE ONSET ACNE
• ACNE EXCORIEE
• ACNE FULMINANS
• POST-FACIAL MASSAGE ACNE
ACNE CONGLOBATA
•SEVERE FORM.
• CHARACTERIZED BY INTERCOMMUNICATING ABSCESSES, CYSTS AND
SINUSES LOADED WITH SEROSANGUINOUS FLUID OR PUS.
• COMEDONES – MULTIPAROUS.
•LESIONS TAKE MONTHS TO HEAL AND ON HEALING LEAVE BEHIND DEEP
PITTED OR HYPERTROPHIC SCARS, JOINED BY KELOIDAL BRIDGES.
• MAY BE A/W FOLLICULAR
• OCCLUSION SYNDROME
OCCUPATIONAL ACNE
• CAUSED BY EXPOSURE TO INDUSTRIAL CHEMICALS.
•PREDOMINANTLY COMEDONES.
•SUSPECTED IN : A. UNUSUAL SITES OF INVOLVEMENT E.G. FOREARMS. B.
UNUSUAL AGE E.G. MIDDLE AGE MALES.
COSMETIC ACNE
•ERUPTION SEEN IN WOMEN USING COSMETICS, ESPECIALLY OIL- BASED
ONES.
•ALMOST ALWAYS COMEDONES.
•LESION FREQUENTLY ON THE CHIN.
DRUG-INDUCED ACNE
•STEROIDS, ANDROGENS, ANABOLIC STEROIDS, OCPS, ANTI-TB DRUGS,
IODIDES, BROMIDES AND ANTICONVULSANT CAN CAUSE ACNEIFORM
ERUPTION.
• LESIONS – MONOMORPHIC, CONSISTING OF PAPULES AND PUSTULES.
• TRUNK ESPECIALLY BACK AND FACE MAY BE INVOLVED.
INFANTILE ACNE
• DUE TO PRESENCE OF MATERNAL HORMONES IN THE CHILD.
• HIGHER IN MALES.
• MAY PRESENT AT BIRTH AND MAY LAST FOR UP TO 3 YEARS.
• LESIONS SIMILAR TO THOSE OF ADOLESCENT ACNE.
LATE ONSET ACNE
•ACNE WITH ONSET AFTER 25 YEARS OLD.
•PREDOMINANTLY WOMEN.
• PRESENTS AS DEEP SEATED, PERSISTENT LESIONS ON LOWER HALF OF FACE.
ACNE EXCORIEE
•SEEN IN YOUNG GIRLS, WHO EXCESSIVELY PICK THEIR OTHERWISE MILD
ACNE.
•RESULTS IN DISCRETE EXCORIATIONS ON THE FACE, WHILE COMODONES
AND PAPULES (PRIMARY LESIONS OF ACNE) ARE FEW AND FAR IN BETWEEN
ACNE FULMINANS
•ACUTE ONSET
• PRESENTS AS CRUSTED, ULCERATED LESIONS.
•ASSOCIATED WITH FEVER, MYALGIA AND ARTHRALGIA
POST-FACIAL MASSAGE ACNE
• FACIAL MASSAGE MAY BE FOLLOWED (3-6 WEEKS LATER) BY AN ACNEIFORM
ERUPTION IN ABOUT 30% PATIENT.
• INDOLENT DEEP SEATED NODULES WITH VERY FEW (OR NO) COMEDONES.
• HEAL WITH HYPERPIGMENTATION AFTER SEVERAL WEEKS.
• PREDOMINANTLY ON CHEEKS, ALONG THE MANIBLE
DIFFERENTIAL DIAGNOSIS
MILIA.
• RESEMBLE CLOSED COMEDONES AND HAVE THE APPEARANCE OF A TINY,
WHITE, FIRM BEAD. THEY ARE MORE COMMON IN YOUNG CHILDREN AND
OLDER ADULTS.
KERATOSIS PILARIS.
• VERY COMMON FINDING IN PRE-PUBESCENT CHILDREN AND MAY PERSIST
INTO ADULTHOOD. IT PRESENTS WITH 1- TO 2- MM KERATOTIC PAPULES
TYPICALLY ON THE CHEEKS AND UPPER ARMS. INFLAMMATORY PAPULES
AND PUSTULES ARE USUALLY NOT SEEN
PRINCIPAL MANAGEMENT
PRINCIPLE MANAGEMENT THE AIMS OF ACNE MANAGEMENT ARE:
•TO INDUCE CLEARANCE OF LESIONS
• TO MAINTAIN REMISSION AND PREVENT RELAPSE
• TO PREVENT PHYSICAL AND PSYCHOLOGICAL COMPLICATIONS
ASSESSEMENT
A NEW GRADING SYSTEM NAMED COMPREHENSIVE ACNE SEVERITY SCALE
– CASS (MODIFICATION OF AN INVESTIGATOR GLOBAL ASSESSMENT [IGA]
OF ACNE SEVERITY) IS A VALIDATED TOOL WHICH SIGNIFICANTLY
CORRELATES WITH THE LEEDS TECHNIQUE FOR FACE, CHEST AND BACK.IT IS
SIMPLER TO USE IN CLINICAL PRACTICE.
INSPECTION IS DONE AT A DISTANCE OF 2.5 METERS AWAY FOR ACNE ON
FACE, CHEST AND BACK.
• CHEST AREA DEFINED AS: ANTERIOR TORSO SUPERIORLY DEFINED BY
SUPRASTERNAL NOTCH EXTENDING LATERALLY TO SHOULDERS AND
INFERIORLY BY A HORIZONTAL LINE DEFINED BY THE XIPHOID PROCESS.
•BACK AREA DEFINED AS: (IS DEMARCATED BY THE) SUPERIOR ASPECTS OF
THE SHOULDERS EXTENDING TO THE NECK AND INFERIORLY BY THE COSTAL
MARGINS.
TREATMENT
AS ACNE IS A CHRONIC DISEASE, PHARMACOLOGICAL TREATMENT CAN
BE DIVIDED INTO TWO PHASES:
1. INDUCTION THERAPY THIS PHASE OF TREATMENT AIMS TO INDUCE
ACNE REMISSION WHICH CAN BE ACHIEVED USING TOPICAL OR SYSTEMIC
AGENTS
2. MAINTENANCE THERAPY RECURRENCE OF ACNE LESIONS AFTER
SUCCESSFUL TREATMENT IS COMMON. HENCE, MAINTENANCE THERAPY
IS AN IMPORTANT MODALITY AS PART OF A COMPREHENSIVE
MANAGEMENT OF ACNE. THE MAINSTAY OF MAINTENANCE TREATMENT
IS TOPICAL THERAPY.
NON-PHARMACOLOGICAL TREATMENT INCLUDES PHYSICAL THERAPY
SUCH AS LASER, PHOTOTHERAPY, CHEMICAL PEELS AND COMEDONE
EXTRACTION. HOWEVER, THESE ARE NOT THE MAINSTAY OF ACNE
TREATMENT.
PHARMACOLOGICAL TREATMENT
1.COMEDONAL ACNE
• TOPICAL RETINOID ARE THE FIRST-LINE TREATMENT FOR COMEDONAL ACNE.
• THERAPY IS USUALLY INITIATED WITH THE LOWEST STRENGTH RETINOID TO
MINIMIZE REDNESS AND DRYNESS. THE STRENGTH OF THE RETINOID MAY BE
INCREASED IF NEEDED.
• ALTERNATIVE THERAPIES INCLUDE BENZOYL PEROXIDE, AZELAIC ACID, OR
SALICYLIC ACID.
2.PAPULAR/PUSTULAR ACNE
• MILD DISEASE
FIRST LINE THERAPIES INCLUDE A TOPICAL RETINOID + A TOPICAL ANTIBIOTIC
BEZOYL PEROXIDE MAYBE ADDED AZELAIC ACID IS THE ALTERNATIVE THERAPY
• MODERATE TO SEVERE DISEASE
MODERATE DISEASE CAN BE TREATED WITH THE SAME FIRST-LINE THERAPY AS
MILD DISEASE. IF THE PATIENT DOES NOT RESPOND OR IF THE PATIENT HAS
SEVERE DISEASE, ORAL ANTIBIOTICS+ A TOPICAL RETINOID+BENZOYL PEROXIDE
GEL OR WASH ARE FIRST-LINE THERAPIES. ALTERNATIVE THERAPIES INCLUDE
SWITCHING TO ANOTHER TYPE OF TOPICAL RETINOID PLUS ANOTHER TYPE OF
ANTIBIOTIC PLUS BENZOYL PEROXIDE.
3.NODULAR ACNE
•THE FIRST-LINE THERAPY FOR NODULAR ACNE INCLUDES AN ORAL
ANTIBIOTICS+ A TOPICAL RETINOID+BENZOYL PEROXIDE
• PATIENTS WHO DO NOT RESPOND TO THERAPY COULD BE SWITCHED TO
ANOTHER ORAL ANTIBIOTIC OR ANOTHER TYPE OF TOPICAL RETINOID.
• IF THE PATIENT STILL HAS PERSISTENT NODULAR ACNE, THEY MAY NEED A
REFERRAL TO DERMATOLOGY FOR MANAGEMENT THAT MIGHT INCLUDE
THE USE OF ORAL ISOTRERINOIN THERAPY.
BENZOYL PEROXIDE
TOPICALMEDICATIONSUSEDINTHETREATMENTOFACNE
NON- PHARMACOLOGICAL
1. Laser, phototherapy, chemical peels and comedone extraction. However,
these are not the mainstay of acne treatment.
2. Advice the patient to control his/her diet.
3. Advice patient to compliant to the medications given.
4. Counselling is needed because some of patient will have depression, low
self-esteem and anxiety when they have acnes.
THANK YOU!!

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Acne vulgaris dermatology ppt

  • 2. ACNE VULGARIS •THE PREVALENCE OF ACNE IN ADOLESCENTS HAS BEEN REPORTED TO BE AS HIGH AS 95% WITH A 20% TO 35% PREVALENCE OF MODERATE TO SEVERE ACNE. •ACNE MAY PERSIST INTO ADULTHOOD IN UP TO 50% OF AFFECTED INDIVIDUALS. •ACNE RARELY CAUSE SERIOUS SYSTEMIC PROBLEMS, BUT QUALITY OF LIFE ISSUES ARE A VERY IMPORTANT CONCERN FOR INDIVIDUALS (ESPECIALLY TEENAGERS) WITH ACNE. • DEPRESSION, ANXIETY, AND LOW SELF-ESTEEM ARE MORE COMMON IN PATIENTS WITH ACNE.
  • 3. RISK FACTORS •GENETIC •OBESITY: HYPERANDROGENISM • A SIGNIFICANT POSITIVE FAMILY HISTORY OF ACNE HAS BEEN DEMONSTRATED ESPECIALLY WHEN ACNE IS FOUND IN: TWINS ,MOTHER , FIRST DEGREE RELATIVE , MULTIPLE FAMILY MEMBERS • A SIGNIFICANT ASSOCIATION BETWEEN OBESITY AND ACNE IN CHILDREN AGGRAVATING FACTORS • SMOKING • STRESS • FACIAL THERAPY OR SALON FACIAL MASSAGE
  • 4. DIET AND SUPPLEMENTS A. DIETARY FACTORS THAT MAY EXACERBATE ACNE 1. HIGH GLYCEMIC LOADS DIET 2. MILK AND MILK PRODUCTS RISK OF ACNE INCREASED BY: FOUR-FOLD WHEN MILK INTAKE FREQUENCY INCREASED FROM LESS THAN ONCE A WEEK TO DAILY CONSUMPTION SEVEN-FOLD WHEN ICE CREAM INTAKE FREQUENCY IS BETWEEN LESS THAN ONCE A WEEK TO DAILY CONSUMPTION COMPARED TO NO CONSUMPTION LOW FIBRE AND HIGH FAT DIET B. DIETARY SUPPLEMENTS 1.THERE IS NO CONCLUSIVE STATEMENT ON THE EFFECTIVENESS OF ZINC SUPPLEMENT IN ACNE 2.THERE IS NO RETRIEVABLE EVIDENCE ON THE EFFICACY OF VITAMIN A, VITAMIN C, VITAMIN E AND OMEGA-3 FATTY ACIDS IN THE MANAGEMENT OF ACNE
  • 5. FEATURES OF ACNE 1.COMEDONAL ACNE • OPEN COMEDONES (BLACKHEADS) WITH A CENTRAL DARK KERATIN PLUGS. • CLOSED COMEDONES (WHITEHEADS) WITH NO VISIBLE KERATIN PLUG. 2.PAPULAR/PUSTULAR ACNE •PATIENTS PRESENTED WITH INFLAMMED •2 TO 5 MM PAPULES/PUSTULES
  • 6. 3.NODULAR ACNE PATIENTS PRESENT WITH RED, FIRM, OR FLUCTUANT NODULES (CYST LIKE) THAT MAY DRAIN OR FORM SINUS TRACTS. THESE LESIONS MAY LEAVE PERMANENT SCARS.
  • 7. PATHOGENESIS HE PATHOGENESIS OF ACNE IS MULTIFACTORIAL. ACNE VULGARIS CAN BE DIVIDED INTO NON- INFLAMMATORY (OPEN AND CLOSED COMEDONES) AND INFLAMMATORY (PAPULES, PUSTULES AND NODULES) LESIONS. THE MOST IMPORTANT FACTORS INVOLVED ARE: 1. INCREASED SEBUM PRODUCTION 2. BACTERIA – PROPIONIBACTERIUM ACNES 3. ALTERED FOLLICULAR KERATINIZATION 4. INFLAMMATION
  • 8. INCREASE SEBUM PRODUCTION WHAT TRIGGERS EXCESS SEBUM? IN MEN, TESTOSTERONE IS SECRETED BY THE MALE SEXUAL ORGANS, AND IN WOMEN IT ORIGINATES FROM THE OVARIES AND ADRENAL GLANDS. IN BOTH SEXES, TESTOSTERONE IS SECRETED INTO THE BODY AND ENTERS INTO THE SEBACEOUS GLAND, WHERE THE ENZYME 5- ALPHA REDUCTASE CONVERTS THE TESTOSTERONE INTO DI-HYDROTESTOSTERONE; THIS IN TURN STIMULATES SEBUM FORMATION IN THE SEBACEOUS GLANDS. BECAUSE 5-ALPHA REDUCTASE IS SENSITIVE TO HORMONE LEVELS, IT GOES INTO OVERDRIVE, CAUSING AN EXCESS PRODUCTION OF SEBUM WHEN TESTOSTERONE LEVELS ESCALATE. THIS IS VERY NOTICEABLE DURING PUBERTY. HOWEVER, RECENT STUDIES HAVE SHOWN THAT HORMONE LEVELS ALONE ARE NOT SOLELY RESPONSIBLE FOR SEBUM PRODUCTION. 5-ALPHA REDUCTASE MAY INCREASE ITS SENSITIVITY TO TESTOSTERONE, TRIGGERING EXCESS SEBUM PRODUCTION EVEN WHEN LOWER LEVELS OF THE HORMONE ARE PRESENT. UNFORTUNATELY, THE CAUSE OF THIS PHENOMENON IS UNKNOWN.
  • 9. ALTERED FOLLICULAR KERATINIZATION IN PATIENTS WITH ACNE, THE RATE OF KERATINOCYTE DESQUAMATION AT THE FOLLICULAR INFUNDIBULUM IS ALTERED. THE KERATINOCYTES ACCUMULATE AND BECOME INTERWOVEN WITH MONOFILAMENTS AND LIPID DROPLETS. THIS ACCUMULATION OF CELLS AND SEBUM RESULTS IN THE FORMATION OF MICRO-COMEDONES, THE MICROSCOPIC PRECURSOR TO ALL ACNE LESIONS.THERE IS ALSO THE PRESENCE OF 5Α-REDUCTASE ACTIVITY IN THE INFRAINFUNDIBULAR SEGMENTS OF SEBACEOUS FOLLICLES WHICH INCREASES ANDROGEN PRODUCTION AND SUBSEQUENT FOLLICULAR HYPERKERATOSIS.
  • 10. PROPIONIBACTERIUM ACNES THE PROLIFERATION OF PROPIONIBACTERIUM ACNES IS RESPONSIBLE FOR THE INITIATION OF INFLAMMATION. PROPIONIBACTERIUM ACNES RELEASES MANY ENZYMES SUCH AS PROTEINASES, LIPASES AND HYALURONIDASES. BACTERIA IN THE FOLLICLE EXCRETE A LIPASE ENZYME TO BREAK DOWN THE SEBUM TRIGLYCERIDES INTO FATTY ACIDS AND GLYCEROL. THE SEBUM IS USED AS A FOOD SOURCE AND THE FREE FATTY ACIDS ARE MERELY WASTE PRODUCTS THAT IRRITATE THE LINING OF THE FOLLICLE. AT THIS POINT, THE DISEASE MAY RESULT IN NON-INFLAMMATORY LESIONS AND SIMPLY PRODUCE CLOSED COMEDONES (WHITEHEADS – IMAGE B), WHICH MAY TURN INTO OPEN COMEDONES (BLACKHEADS – IMAGE C) AND EXPEL THEIR CONTENTS.
  • 11. INFLAMMATION CELLULAR PRODUCTS FROM P. ACNES STIMULATE THE RECRUITMENT OF CD4 LYMPHOCYTES AND SUBSEQUENTLY NEUTROPHILS. THESE INFLAMMATORY CELLS PENETRATE THE FOLLICULAR WALL, CAUSING DISRUPTION OF THE FOLLICULAR BARRIER. THIS LEADS TO THE RELEASE OF LIPIDS, SHED KERATINOCYTES AND P. ACNES INTO THE SURROUNDING DERMIS, INCITING FURTHER RECRUITMENT OF INFLAMMATORY CYTOKINES AND NEUROPEPTIDES INCLUDING SUBSTANCE P. LINOLEIC ACID HAS ALSO BEEN FOUND TO REGULATE IL-8 SECRETION AND REDUCE THE INFLAMMATORY REACTION. HENCE, DEFICIENCY OF LINOLEIC ACID MAY INCREASE HYPER- KERATINISATION OF THE EPIDERMIS. TWO MAIN FATTY ACIDS ESSENTIAL IN THE DIET ARE LINOLEIC (OR OMEGA-6) FATTY ACID AND ALPHA-LINOLENIC (OR OMEGA-3) ACID. LINOLEIC ACID KEEPS THE SKIN IMPERMEABLE TO WATER, BUT TO EXERT OTHER EFFECTS THE COMPOUND MUST UNDERGO SPECIFIC METABOLISM.
  • 12. TYPES OF ACNE • ACNE CONGLOBATA • OCCUPATIONAL ACNE •COSMETIC ACNE • DRUG-INDUCED ACNE • INFANTILE ACNE •LATE ONSET ACNE • ACNE EXCORIEE • ACNE FULMINANS • POST-FACIAL MASSAGE ACNE
  • 13. ACNE CONGLOBATA •SEVERE FORM. • CHARACTERIZED BY INTERCOMMUNICATING ABSCESSES, CYSTS AND SINUSES LOADED WITH SEROSANGUINOUS FLUID OR PUS. • COMEDONES – MULTIPAROUS. •LESIONS TAKE MONTHS TO HEAL AND ON HEALING LEAVE BEHIND DEEP PITTED OR HYPERTROPHIC SCARS, JOINED BY KELOIDAL BRIDGES. • MAY BE A/W FOLLICULAR • OCCLUSION SYNDROME OCCUPATIONAL ACNE • CAUSED BY EXPOSURE TO INDUSTRIAL CHEMICALS. •PREDOMINANTLY COMEDONES. •SUSPECTED IN : A. UNUSUAL SITES OF INVOLVEMENT E.G. FOREARMS. B. UNUSUAL AGE E.G. MIDDLE AGE MALES.
  • 14. COSMETIC ACNE •ERUPTION SEEN IN WOMEN USING COSMETICS, ESPECIALLY OIL- BASED ONES. •ALMOST ALWAYS COMEDONES. •LESION FREQUENTLY ON THE CHIN. DRUG-INDUCED ACNE •STEROIDS, ANDROGENS, ANABOLIC STEROIDS, OCPS, ANTI-TB DRUGS, IODIDES, BROMIDES AND ANTICONVULSANT CAN CAUSE ACNEIFORM ERUPTION. • LESIONS – MONOMORPHIC, CONSISTING OF PAPULES AND PUSTULES. • TRUNK ESPECIALLY BACK AND FACE MAY BE INVOLVED.
  • 15. INFANTILE ACNE • DUE TO PRESENCE OF MATERNAL HORMONES IN THE CHILD. • HIGHER IN MALES. • MAY PRESENT AT BIRTH AND MAY LAST FOR UP TO 3 YEARS. • LESIONS SIMILAR TO THOSE OF ADOLESCENT ACNE. LATE ONSET ACNE •ACNE WITH ONSET AFTER 25 YEARS OLD. •PREDOMINANTLY WOMEN. • PRESENTS AS DEEP SEATED, PERSISTENT LESIONS ON LOWER HALF OF FACE. ACNE EXCORIEE •SEEN IN YOUNG GIRLS, WHO EXCESSIVELY PICK THEIR OTHERWISE MILD ACNE. •RESULTS IN DISCRETE EXCORIATIONS ON THE FACE, WHILE COMODONES AND PAPULES (PRIMARY LESIONS OF ACNE) ARE FEW AND FAR IN BETWEEN
  • 16. ACNE FULMINANS •ACUTE ONSET • PRESENTS AS CRUSTED, ULCERATED LESIONS. •ASSOCIATED WITH FEVER, MYALGIA AND ARTHRALGIA POST-FACIAL MASSAGE ACNE • FACIAL MASSAGE MAY BE FOLLOWED (3-6 WEEKS LATER) BY AN ACNEIFORM ERUPTION IN ABOUT 30% PATIENT. • INDOLENT DEEP SEATED NODULES WITH VERY FEW (OR NO) COMEDONES. • HEAL WITH HYPERPIGMENTATION AFTER SEVERAL WEEKS. • PREDOMINANTLY ON CHEEKS, ALONG THE MANIBLE
  • 17. DIFFERENTIAL DIAGNOSIS MILIA. • RESEMBLE CLOSED COMEDONES AND HAVE THE APPEARANCE OF A TINY, WHITE, FIRM BEAD. THEY ARE MORE COMMON IN YOUNG CHILDREN AND OLDER ADULTS. KERATOSIS PILARIS. • VERY COMMON FINDING IN PRE-PUBESCENT CHILDREN AND MAY PERSIST INTO ADULTHOOD. IT PRESENTS WITH 1- TO 2- MM KERATOTIC PAPULES TYPICALLY ON THE CHEEKS AND UPPER ARMS. INFLAMMATORY PAPULES AND PUSTULES ARE USUALLY NOT SEEN
  • 18. PRINCIPAL MANAGEMENT PRINCIPLE MANAGEMENT THE AIMS OF ACNE MANAGEMENT ARE: •TO INDUCE CLEARANCE OF LESIONS • TO MAINTAIN REMISSION AND PREVENT RELAPSE • TO PREVENT PHYSICAL AND PSYCHOLOGICAL COMPLICATIONS
  • 19. ASSESSEMENT A NEW GRADING SYSTEM NAMED COMPREHENSIVE ACNE SEVERITY SCALE – CASS (MODIFICATION OF AN INVESTIGATOR GLOBAL ASSESSMENT [IGA] OF ACNE SEVERITY) IS A VALIDATED TOOL WHICH SIGNIFICANTLY CORRELATES WITH THE LEEDS TECHNIQUE FOR FACE, CHEST AND BACK.IT IS SIMPLER TO USE IN CLINICAL PRACTICE. INSPECTION IS DONE AT A DISTANCE OF 2.5 METERS AWAY FOR ACNE ON FACE, CHEST AND BACK. • CHEST AREA DEFINED AS: ANTERIOR TORSO SUPERIORLY DEFINED BY SUPRASTERNAL NOTCH EXTENDING LATERALLY TO SHOULDERS AND INFERIORLY BY A HORIZONTAL LINE DEFINED BY THE XIPHOID PROCESS. •BACK AREA DEFINED AS: (IS DEMARCATED BY THE) SUPERIOR ASPECTS OF THE SHOULDERS EXTENDING TO THE NECK AND INFERIORLY BY THE COSTAL MARGINS.
  • 20.
  • 21. TREATMENT AS ACNE IS A CHRONIC DISEASE, PHARMACOLOGICAL TREATMENT CAN BE DIVIDED INTO TWO PHASES: 1. INDUCTION THERAPY THIS PHASE OF TREATMENT AIMS TO INDUCE ACNE REMISSION WHICH CAN BE ACHIEVED USING TOPICAL OR SYSTEMIC AGENTS 2. MAINTENANCE THERAPY RECURRENCE OF ACNE LESIONS AFTER SUCCESSFUL TREATMENT IS COMMON. HENCE, MAINTENANCE THERAPY IS AN IMPORTANT MODALITY AS PART OF A COMPREHENSIVE MANAGEMENT OF ACNE. THE MAINSTAY OF MAINTENANCE TREATMENT IS TOPICAL THERAPY. NON-PHARMACOLOGICAL TREATMENT INCLUDES PHYSICAL THERAPY SUCH AS LASER, PHOTOTHERAPY, CHEMICAL PEELS AND COMEDONE EXTRACTION. HOWEVER, THESE ARE NOT THE MAINSTAY OF ACNE TREATMENT.
  • 22. PHARMACOLOGICAL TREATMENT 1.COMEDONAL ACNE • TOPICAL RETINOID ARE THE FIRST-LINE TREATMENT FOR COMEDONAL ACNE. • THERAPY IS USUALLY INITIATED WITH THE LOWEST STRENGTH RETINOID TO MINIMIZE REDNESS AND DRYNESS. THE STRENGTH OF THE RETINOID MAY BE INCREASED IF NEEDED. • ALTERNATIVE THERAPIES INCLUDE BENZOYL PEROXIDE, AZELAIC ACID, OR SALICYLIC ACID. 2.PAPULAR/PUSTULAR ACNE • MILD DISEASE FIRST LINE THERAPIES INCLUDE A TOPICAL RETINOID + A TOPICAL ANTIBIOTIC BEZOYL PEROXIDE MAYBE ADDED AZELAIC ACID IS THE ALTERNATIVE THERAPY • MODERATE TO SEVERE DISEASE MODERATE DISEASE CAN BE TREATED WITH THE SAME FIRST-LINE THERAPY AS MILD DISEASE. IF THE PATIENT DOES NOT RESPOND OR IF THE PATIENT HAS SEVERE DISEASE, ORAL ANTIBIOTICS+ A TOPICAL RETINOID+BENZOYL PEROXIDE GEL OR WASH ARE FIRST-LINE THERAPIES. ALTERNATIVE THERAPIES INCLUDE SWITCHING TO ANOTHER TYPE OF TOPICAL RETINOID PLUS ANOTHER TYPE OF ANTIBIOTIC PLUS BENZOYL PEROXIDE.
  • 23. 3.NODULAR ACNE •THE FIRST-LINE THERAPY FOR NODULAR ACNE INCLUDES AN ORAL ANTIBIOTICS+ A TOPICAL RETINOID+BENZOYL PEROXIDE • PATIENTS WHO DO NOT RESPOND TO THERAPY COULD BE SWITCHED TO ANOTHER ORAL ANTIBIOTIC OR ANOTHER TYPE OF TOPICAL RETINOID. • IF THE PATIENT STILL HAS PERSISTENT NODULAR ACNE, THEY MAY NEED A REFERRAL TO DERMATOLOGY FOR MANAGEMENT THAT MIGHT INCLUDE THE USE OF ORAL ISOTRERINOIN THERAPY.
  • 26. NON- PHARMACOLOGICAL 1. Laser, phototherapy, chemical peels and comedone extraction. However, these are not the mainstay of acne treatment. 2. Advice the patient to control his/her diet. 3. Advice patient to compliant to the medications given. 4. Counselling is needed because some of patient will have depression, low self-esteem and anxiety when they have acnes.
  • 27.
  • 28.