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Page 1
Disorders Of SebaceousDisorders Of Sebaceous
And Apocrine GlandsAnd Apocrine Glands
(Acne Vulgaris)
Page 2
Acne Vulgaris And Cystic Acne
 An inflammation of pilosebaceous units, very
common
 Appears in certain body areas (face, trunk,
rarely buttocks)
 Most frequently in adolescents
 Manifests as comedones, papulopustules,
nodules, and cysts
 Results in pitted, depressed, or hypertrophic
scars
Page 3
EpidemiologyEpidemiology
• Age of Onset :
Puberty—10 to 17 years in females.
14 to 19 in males; however, may appear first
at 25 years or older.
• Sex : more sever in Males > females.
(why???)
Page 4
Genetic Aspects
• Multifactorial genetic background.
• Familial predisposition: majority of
individuals with cystic acne have parent(s)
with a history of severe acne. Severe acne
may be associated with XYY syndrome.
Page 5
PATHOGENESIS
Hypertrophy --
hyperkeratinization –
obs. Of s. gland –
accumulationof sebum –
comedons formation
Page 6
Microcomedone
• hyperkeratotic
infundibulum
• cohesive
corneocytes
• sebum secretion
Comedone
• accumulation
of
shed
corneocytes
and sebum
• dilation of
follicular
ostium
Inflammatory
papule/
pustule
• further expansion
of follicular unit
• proliferation of
Propionibacterium
acnes
perifollicular
inflammation
Nodule
• rupture of
follicular wall
• marked
perifollicular
inflammation
• scarring
Page 7
Contributory Factors
• Acnegenic mineral oils, rarely dioxin and
others.
Drugs :
Lithium, hydantoin, isoniazid, glucocorticoids, oral
contraceptives, iodides, bromides and
androgens (e.g., testosterone), danazol.
Page 8
Others
Emotional stress can definitely cause
exacerbations.
Occlusion and pressure on the skin,
such as by leaning face on hands, very
important and often unrecognized
exacerbating factor ( acne mechanica ).
Acne is not caused by chocolate or
fatty foods or, in fact, by any kind of
food.
Page 9
Clinical Manifestation
• Duration : Weeks to Months .
• Season: Often worse in fall and winter.
• Skin Symptoms :
 Pain in lesions (especially nodulocystic
type).
Page 10
Skin Lesions
1. Comedones :
open (blackheads) or closed (whiteheads);
comedonal acne
Page 11
2. Papules and papulopustules :
i.e., a papule topped by a pustule;
papulopustular acne
Page 12
3. Nodules or cysts :
1–4 cm in diameter ; nodulocystic acne .
Page 13
Sites of Predilection
Face
Neck
Trunk
Upper Arms
Buttocks.
Page 14
Page 15
Special Forms :
1. Acne Conglobata :
Severe cystic acne with more involvement
of the trunk than the face.
• Coalescing nodules, cysts, abscesses,
and ulceration; occurs also on buttocks .
• Spontaneous remission is long delayed.
• acne conglobata seen in - XYY genotype
- the polycystic ovary syndrome.
Page 16
Acne
Conglobata
In this severe
nodulocystic acne,
There is
postulation, scarring
and lesions are
very painful.
Page 17
Page 18
Acne conglobata Inflammatory nodules and cysts have coalesced,
forming abscesses and even
leading to ulceration. There are multiple comedones and many recent
red scars following resolution of inflammatory
lesions on the upper chest, neck, and arms.
Page 19
 2. Acne Fulminans
• Teenage boys (ages 13 to 17).
• Acute onset , severe cystic acne with
concomitant suppuration and always
ulceration ;
• also present are malaise, fatigue, fever,
generalized arthralgias, leukocytosis, and
elevated erythrocyte sedimentation rate.
Page 20
3. SAPHO Syndrome:
Synovitis, acne, acne fulminans,
palmoplantar pustulosis , hidradenitis
suppurativa, hyperostosis, and osteitis.
Rare.
4. PAPA Syndrome:
Sterile pyogenic arthritis, pyoderma
gangrenosum acne. An inherited
autoinflammatory disorder; very rare.
Page 21
5. Tropical Acne:
Flare of acne, usually with severe folliculitis,
inflammatory nodules, and draining cysts
on trunk and buttocks in tropical climates;
secondary infection with Staphylococcus
aureus .
Page 22
6. Acne with Facial Edema :
Associated with recalcitrant, disfiguring
midline facial edema. Woody induration
with and without erythema.
Page 23
7. Acne in the Adult Woman:
Persistent acne in an (often) hirsute female
with or without irregular menses needs an
evaluation for hypersecretion of adrenal
and ovarian androgens:
• total testosterone, free testosterone,
and/or dehydroepiandrosterone sulfate
(DHEAS) (e.g., in the polycystic ovary
syndrome).
Page 24
8. Recalcitrant Acne:
Can be related to congenital adrenal
hyperplasia (11β- or 21β- hydroxylase
deficiencies).
9. Acne Excoriée:
Mild acne, usually in young women,
associated with extensive excoriations and
scarring due to emotional and
psychological problems (obsessive
compulsive disorder).
Page 25
10. Occupational Acne:
Due to exposure to tar derivatives, cutting
oils, chlorinated hydrocarbons (see
“Chloracne,” below). Large comedones,
inflammatory papules and cysts; not
restricted to predilection sites of acne but
can appear on other (covered) body sites.
Page 26
• 11. Acne Cosmetica :
Due to comedogenic cosmetics.
Page 27
Acne-Like Conditions:
• Steroid Acne: Following systemic or
topical glucocorticoids. Monomorphous
folliculitis small erythematous papules and
pustules without comedones.
• Drug-Induced Acne: Monomorphous
acnelike eruption due to phenytoin,
lithium, isoniazid, high-dose vitamin B
complex, epidermal growth factor
inhibitors
Page 28
• Acne Aestivalis : Papular eruption after
sun exposure (“Mallorca acne”). Usually
on forehead, shoulders, arms, neck, and
chest. No comedones. Pathogenesis
unknown.
• Gram-Negative Folliculitis: Multiple tiny
yellow pustules develop on top of acne
vulgaris as a result of long-term antibiotic
administration.
Page 29
Diagnosis And Differential Diagnosis
• Note : Comedones are required for
diagnosis of any type of acne. Comedones
are not a feature of acne-like conditions
(above) and of the conditions listed below.
• Face S. aureus folliculitis,
pseudofolliculitis barbae, rosacea, perioral
dermatitis.
Page 30
• Trunk: Malassezia folliculitis, “hot-tub”
pseudomonas folliculitis, S. aureus
folliculitis, and acne-like conditions (see
above).
Page 31
Laboratory Examination
No laboratory examinations required.
If there is suspicion of an endocrine
disorder, free testosterone, follicle-
stimulating hormone …etc
Page 32
Course
• Acne most often clears spontaneously by the
early twenties but can persist to the fourth
decade or older. Flares occur in the winter and
with the onset of menses
Page 33
Complications of acne:
1- Scarring.
2-Psychological impact
Page 34
Scarring: can also occur if you pick or
squeeze your spots, so it's important not to do this.
Page 35
There are three main types of acne scars:
1)ice pick scars – small, deep holes in the surface of
your skin that look like the skin has been punctured with a
sharp object
Page 36
2) rolling scars – caused by bands of scar
tissue that form under the skin, giving the surface
of the skin a rolling and uneven appearance.
Page 37
3) boxcar scars : round or oval
depressions, or craters, in the skin .
Page 38
1.General measures:
• Reassurance.
• Education.
• Avoidence of comedogenic factors .
• Avoid squeezing the lesions.
• Gentle cleansing.
• Pillow changes
• Less sun exposure
• Less use makeup
Management
Page 39
2. Mild Acne:
• Topical antibiotics :
(clindamycin and erythromycin)
• Benzoyl peroxide gels: (2%, 5%, or 10%)
• Topical retinoids (tretinoin, adapalene)
Page 40
3. Moderate Acne:
Oral antibiotics are added to the above
regimen. Most effective antibiotic is:
• minocycline, 50 –100 mg twice daily
• or doxycycline, 50 – 100 mg twice daily,
Page 41
• In females, moderate acne can be
controlled with high doses of oral estrogens
combined with progesterone or
antiandrogens, but recurrences are the rule
after cessation of treatment.
Cerebrovascular accidents are a serious
risk.
Page 42
 3. Severe Acne:
• In addition to the topical treatment outlined
above, systemic treatment with isotretinoin
is indicated for cystic or conglobate acne
or for acne refractory to treatment.
**This retinoid inhibits sebaceous gland
function and keratinization and is very
effective
Page 43
Other Systemic Treatments for Severe
Acne :
• Systemic glucocorticoids: may be required in
severe acne conglobata, acne fulminans, and
the SAPHO and PAPA syndromes.
• The TNF-α inhibitor infliximab and anakinra are
investigational drugs in these severe forms and
show promising effects. Note : For inflammatory
cysts and nodules, intralesional triamcinolone
(0.05 mL of a 3 to 5 mg/mL solution) is
indicated.
Page 44
Differential diagnosis of acne:
1- Rosocea.
2-Perioral dermatitis.
3-Pitrosporum folliculitis.
4-Folliculitis barbae and
Psudofolliculitis barbae.
5-Acneform drug eraption
6-Acneform secondary syphilis.
Page 45
Acne Rosacea
Onset Adolescence Thirties To Fifties
Sex Male>.F Females.>Males
Site Face,upper Tunck, Upper
Arms
Face
Flushing&teleangectasia _ +
Comedons + _
Eye Complecations _ +
Rhinophyma _ +
Responce To
Treatment
Slow Rapid
Page 46
• SOURCE: From FITZPATRICK’S COLOR ATLAS
AND SYNOPSIS OF CLINICAL DERMATOLOGY
SIXTH EDITION
Page 47

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Acne vulgaris

  • 1. Page 1 Disorders Of SebaceousDisorders Of Sebaceous And Apocrine GlandsAnd Apocrine Glands (Acne Vulgaris)
  • 2. Page 2 Acne Vulgaris And Cystic Acne  An inflammation of pilosebaceous units, very common  Appears in certain body areas (face, trunk, rarely buttocks)  Most frequently in adolescents  Manifests as comedones, papulopustules, nodules, and cysts  Results in pitted, depressed, or hypertrophic scars
  • 3. Page 3 EpidemiologyEpidemiology • Age of Onset : Puberty—10 to 17 years in females. 14 to 19 in males; however, may appear first at 25 years or older. • Sex : more sever in Males > females. (why???)
  • 4. Page 4 Genetic Aspects • Multifactorial genetic background. • Familial predisposition: majority of individuals with cystic acne have parent(s) with a history of severe acne. Severe acne may be associated with XYY syndrome.
  • 5. Page 5 PATHOGENESIS Hypertrophy -- hyperkeratinization – obs. Of s. gland – accumulationof sebum – comedons formation
  • 6. Page 6 Microcomedone • hyperkeratotic infundibulum • cohesive corneocytes • sebum secretion Comedone • accumulation of shed corneocytes and sebum • dilation of follicular ostium Inflammatory papule/ pustule • further expansion of follicular unit • proliferation of Propionibacterium acnes perifollicular inflammation Nodule • rupture of follicular wall • marked perifollicular inflammation • scarring
  • 7. Page 7 Contributory Factors • Acnegenic mineral oils, rarely dioxin and others. Drugs : Lithium, hydantoin, isoniazid, glucocorticoids, oral contraceptives, iodides, bromides and androgens (e.g., testosterone), danazol.
  • 8. Page 8 Others Emotional stress can definitely cause exacerbations. Occlusion and pressure on the skin, such as by leaning face on hands, very important and often unrecognized exacerbating factor ( acne mechanica ). Acne is not caused by chocolate or fatty foods or, in fact, by any kind of food.
  • 9. Page 9 Clinical Manifestation • Duration : Weeks to Months . • Season: Often worse in fall and winter. • Skin Symptoms :  Pain in lesions (especially nodulocystic type).
  • 10. Page 10 Skin Lesions 1. Comedones : open (blackheads) or closed (whiteheads); comedonal acne
  • 11. Page 11 2. Papules and papulopustules : i.e., a papule topped by a pustule; papulopustular acne
  • 12. Page 12 3. Nodules or cysts : 1–4 cm in diameter ; nodulocystic acne .
  • 13. Page 13 Sites of Predilection Face Neck Trunk Upper Arms Buttocks.
  • 15. Page 15 Special Forms : 1. Acne Conglobata : Severe cystic acne with more involvement of the trunk than the face. • Coalescing nodules, cysts, abscesses, and ulceration; occurs also on buttocks . • Spontaneous remission is long delayed. • acne conglobata seen in - XYY genotype - the polycystic ovary syndrome.
  • 16. Page 16 Acne Conglobata In this severe nodulocystic acne, There is postulation, scarring and lesions are very painful.
  • 18. Page 18 Acne conglobata Inflammatory nodules and cysts have coalesced, forming abscesses and even leading to ulceration. There are multiple comedones and many recent red scars following resolution of inflammatory lesions on the upper chest, neck, and arms.
  • 19. Page 19  2. Acne Fulminans • Teenage boys (ages 13 to 17). • Acute onset , severe cystic acne with concomitant suppuration and always ulceration ; • also present are malaise, fatigue, fever, generalized arthralgias, leukocytosis, and elevated erythrocyte sedimentation rate.
  • 20. Page 20 3. SAPHO Syndrome: Synovitis, acne, acne fulminans, palmoplantar pustulosis , hidradenitis suppurativa, hyperostosis, and osteitis. Rare. 4. PAPA Syndrome: Sterile pyogenic arthritis, pyoderma gangrenosum acne. An inherited autoinflammatory disorder; very rare.
  • 21. Page 21 5. Tropical Acne: Flare of acne, usually with severe folliculitis, inflammatory nodules, and draining cysts on trunk and buttocks in tropical climates; secondary infection with Staphylococcus aureus .
  • 22. Page 22 6. Acne with Facial Edema : Associated with recalcitrant, disfiguring midline facial edema. Woody induration with and without erythema.
  • 23. Page 23 7. Acne in the Adult Woman: Persistent acne in an (often) hirsute female with or without irregular menses needs an evaluation for hypersecretion of adrenal and ovarian androgens: • total testosterone, free testosterone, and/or dehydroepiandrosterone sulfate (DHEAS) (e.g., in the polycystic ovary syndrome).
  • 24. Page 24 8. Recalcitrant Acne: Can be related to congenital adrenal hyperplasia (11β- or 21β- hydroxylase deficiencies). 9. Acne Excoriée: Mild acne, usually in young women, associated with extensive excoriations and scarring due to emotional and psychological problems (obsessive compulsive disorder).
  • 25. Page 25 10. Occupational Acne: Due to exposure to tar derivatives, cutting oils, chlorinated hydrocarbons (see “Chloracne,” below). Large comedones, inflammatory papules and cysts; not restricted to predilection sites of acne but can appear on other (covered) body sites.
  • 26. Page 26 • 11. Acne Cosmetica : Due to comedogenic cosmetics.
  • 27. Page 27 Acne-Like Conditions: • Steroid Acne: Following systemic or topical glucocorticoids. Monomorphous folliculitis small erythematous papules and pustules without comedones. • Drug-Induced Acne: Monomorphous acnelike eruption due to phenytoin, lithium, isoniazid, high-dose vitamin B complex, epidermal growth factor inhibitors
  • 28. Page 28 • Acne Aestivalis : Papular eruption after sun exposure (“Mallorca acne”). Usually on forehead, shoulders, arms, neck, and chest. No comedones. Pathogenesis unknown. • Gram-Negative Folliculitis: Multiple tiny yellow pustules develop on top of acne vulgaris as a result of long-term antibiotic administration.
  • 29. Page 29 Diagnosis And Differential Diagnosis • Note : Comedones are required for diagnosis of any type of acne. Comedones are not a feature of acne-like conditions (above) and of the conditions listed below. • Face S. aureus folliculitis, pseudofolliculitis barbae, rosacea, perioral dermatitis.
  • 30. Page 30 • Trunk: Malassezia folliculitis, “hot-tub” pseudomonas folliculitis, S. aureus folliculitis, and acne-like conditions (see above).
  • 31. Page 31 Laboratory Examination No laboratory examinations required. If there is suspicion of an endocrine disorder, free testosterone, follicle- stimulating hormone …etc
  • 32. Page 32 Course • Acne most often clears spontaneously by the early twenties but can persist to the fourth decade or older. Flares occur in the winter and with the onset of menses
  • 33. Page 33 Complications of acne: 1- Scarring. 2-Psychological impact
  • 34. Page 34 Scarring: can also occur if you pick or squeeze your spots, so it's important not to do this.
  • 35. Page 35 There are three main types of acne scars: 1)ice pick scars – small, deep holes in the surface of your skin that look like the skin has been punctured with a sharp object
  • 36. Page 36 2) rolling scars – caused by bands of scar tissue that form under the skin, giving the surface of the skin a rolling and uneven appearance.
  • 37. Page 37 3) boxcar scars : round or oval depressions, or craters, in the skin .
  • 38. Page 38 1.General measures: • Reassurance. • Education. • Avoidence of comedogenic factors . • Avoid squeezing the lesions. • Gentle cleansing. • Pillow changes • Less sun exposure • Less use makeup Management
  • 39. Page 39 2. Mild Acne: • Topical antibiotics : (clindamycin and erythromycin) • Benzoyl peroxide gels: (2%, 5%, or 10%) • Topical retinoids (tretinoin, adapalene)
  • 40. Page 40 3. Moderate Acne: Oral antibiotics are added to the above regimen. Most effective antibiotic is: • minocycline, 50 –100 mg twice daily • or doxycycline, 50 – 100 mg twice daily,
  • 41. Page 41 • In females, moderate acne can be controlled with high doses of oral estrogens combined with progesterone or antiandrogens, but recurrences are the rule after cessation of treatment. Cerebrovascular accidents are a serious risk.
  • 42. Page 42  3. Severe Acne: • In addition to the topical treatment outlined above, systemic treatment with isotretinoin is indicated for cystic or conglobate acne or for acne refractory to treatment. **This retinoid inhibits sebaceous gland function and keratinization and is very effective
  • 43. Page 43 Other Systemic Treatments for Severe Acne : • Systemic glucocorticoids: may be required in severe acne conglobata, acne fulminans, and the SAPHO and PAPA syndromes. • The TNF-α inhibitor infliximab and anakinra are investigational drugs in these severe forms and show promising effects. Note : For inflammatory cysts and nodules, intralesional triamcinolone (0.05 mL of a 3 to 5 mg/mL solution) is indicated.
  • 44. Page 44 Differential diagnosis of acne: 1- Rosocea. 2-Perioral dermatitis. 3-Pitrosporum folliculitis. 4-Folliculitis barbae and Psudofolliculitis barbae. 5-Acneform drug eraption 6-Acneform secondary syphilis.
  • 45. Page 45 Acne Rosacea Onset Adolescence Thirties To Fifties Sex Male>.F Females.>Males Site Face,upper Tunck, Upper Arms Face Flushing&teleangectasia _ + Comedons + _ Eye Complecations _ + Rhinophyma _ + Responce To Treatment Slow Rapid
  • 46. Page 46 • SOURCE: From FITZPATRICK’S COLOR ATLAS AND SYNOPSIS OF CLINICAL DERMATOLOGY SIXTH EDITION