Acne Vulgaris & Rosacea

[Link] Al-Tarawneh ,MD

Consultant Dermatologist and
Dermatopathologist
Associate professor , Mu`tah
University

Edited By : Mohammad Abu-Karaki

Edited and presented By :
Noor Al-Huda Esam Al-Karaki
 Our Lecture talks about :
A. Acne vulgaris
1- Pathogenesis
2- Acne variants
3- Differential diagnosis of Acne
4- Treatment
B. Rosacea
C . Acneform skin rash
lump underneath
the skin that's at
least 1 centimeter
in size
 A. Acne vulgaris ,Pathogenesis

 Family history – predisposition leads to interaction between :

1. Hormonal role , androgens , Testosterone , DHEAS (dehydroepiandrosterone
sulfate) .
2. Increased sebum production.
3. Hypercornification ( increase in keratin formation , keratinocytes in hair follicles )
of the pilosebaceous duct (infundibulum) , block the duct  distention  rupture
and inflammation .
4. Role of propionibacterium acne - enzyme production (lipase).
 Formation of comedones papule pustule cyst healed with
scar. Vulgaris means  MOST COMMON .

is a gram-positive human skin commensal that prefers anaerobic growth conditions and is
involved in the pathogenesis of acne
 Propionibacterium
Acne
Increased sebum production (lipase)

Comedone inflammatory
formation response
follicular hypercornification (lesions)
Comedones : Comedones are small, flesh-colored, white, or dark bumps that give
skin a rough texture
 are essential and characteristic for acne diagnosis
The infundibulum segment is
the upper portion of the
follicle
 Usually in teenagers and asymptomatic , in the face ( most common) , arms ,back and
upper chest .
 Non inflammatory lesions (acne) :
Comedones are the characteristic primary skin lesions for acne .
 White head comedon (closed comedon) , better appreciated by palpation , will develop
into inflammatory lesions .
 Black head comedon (open comedon) , will not develop into inflammatory lesions
because they are open.
Melanin deposition or oxidation of lipids are responsible for black coloration  +VE
lipase  consume the glycosaccharide inside the Comedones.

 Inflammatory lesions (acne) :  Sequelae :

 Papules.  Scars.
 Pustules.  Hyperpigmentation .
 Nodules.  Erythema.
 Cysts .  So acne must be treated in its early stage
to avoid those Sequelae.
  White comedones , and
Erythema and
inflammatory papules and pustules.
hyperpigmentation.
  Inflammatory lesions : papules and
 White Comedonal acne. nodules.
 Some scars.
 Scarring acne.
Indication for Vitamin A derivatives use.
 Acne variants
1. Acne vulgaris.
2. Acne conglobata ( Nodulocystic).
3. Acne fulminans.
4. Acne mechanica.
5. Acne excoriee.
6. Drug induced acne.
7. Occupational acne.
8. Neonatal acne.
9. Infantile acne.
1-Acne conglobata-Nodulocystic acne

Nodulocystic lesions.
Severe form of acne.
 2-Acne Fulminans
 Severe form with cystic lesions and systemic symptoms.
 Rare form.
 Young men 13-16 yr.
 Osteolytic bone lesions.
 Fever , arthralgia , Hepatosplenomegaly.
 Increased ESR , leukocytosis.
 Treatment : Isotritinoin with systemic steroid ( the only type of
acne that is treated with steroids).
 Acne Fulminans

 Young man with inflammed Inflammed cystic lesions

cystic lesions. on the back.
Crusted lesions on the back and face.
 3-Acne Mechanica
Repeated mechanical and frictional
obstruction.

Rubbing by helmets , chin straps ,

masks.

Treatment by eliminating these factors.

Acne Mechanica
 Pustules and papules
at the site of contact.
 Yellowish
discoloration
indicates secondary
infections.
 4-Acne Excoriee
 Young women.

 Underlying psychiatric components.

 Antidepressants or psychotherapy may

be indicated.
 Acne Excoriee

Excoriations only.
No comedones , papules or pustules.
 5-Drug Induced Acne
 Anabolic steroids – Danazole , Stanazole.
 Corticosteroids.
 phenytoin .
 Lithium.
 Iodides , bromides , Vit. Supplements , cough
compounds and sedatives .
 Azathioprine ,Vit.B12, cyclosporine.
 Monomorphic eruption of papules and pustules
 Steroid induced acne ( in spring) : after oral or topical
use of steroids.
 Drug Induced Acne

Monomorphic papules and pustules due to steroids.

 6-Occupational Acne
 Exposure to insoluble , follicle – occlusive substances in the workplace.
 Cutting oils , petrolatum – based products (Vaseline) , coal tar.
 Comedones dominate usually.
 Chloracne:
 Kinds of occupational acne due to Exposure to chlorinated aromatic
hydrocarbons.
 Malar , retro-auricular , mandibular areas , axillae , sacrum , buttock are
involved.
 The causative agents found in :
electrical conductors , insulators , insecticides , fungicides and wood
preservatives (poly chlor naphthalenes tetra chlorobenzene and others).
 Old age ( not typical age for acne .
 Occupational Acne

 Comedone predominant, some  Inflammatory lesions on the

papules. malar area and cheeks.
 7-Neonatal Acne
 Hormonal factors from mother and malasezia

 20% of healthy newborn

 Appears at the ages of 2 weeks and resolves at

the age of 3 months.
 Small papules on cheeks .
 Treatment : 2% ketoconazole , Benzoyl Peroxide.
 Neonatal Acne

Papules and few comedones on the cheeks.

 8-Infantile Acne

 Hormonal factors DHEA.

 If acne present at 3-6months of age: infantile
acne.
 Resolves within 1-2 years.
 More comedones than in neonatal.
 Treatment : Tretinoin , Benzoyl Peroxide .
 Infantile Acne

 Comedones , papules , erythema Comedones and papules.

and hyperpigmentation.
 9-Late onset Acne ( Adult acne)

 Papules , erythema and Hyperpigmentations.

 Must do investigations to rule out causes of androgen excess.
 Usually affect the jaw area and the neck.
 10-Endocrinologic abnormalities
 Most patients do not have acne , investigations for late onset acne include :
1. Hyperandrogenism should be suspected in female with ; Hirsutism , irregular
cycles , severe acne , abrupt onset , coarse voice.
2. AM serum cortisol level if hypercortisolism is suspected.
3. Androgenetic alopecia :Free testosterone , DHEAS , 17-hydroxyprogesterone.
4. Elevated DHEAS and 17-OH-progesterone suggest adrenal source of excess
androgen.
5. DHEAS 4000-8000g\ml or 17-OH progesterone level > 3ng\ml congenital
adrenal hyperplasia.
6. Increased LH /FSH ratio to > 2-3 in polycystic ovary syndrome.
7. Elevated testosterone suggest ovarian source.
8. Serum testosterone >200ngIdl indicates ovarian tumor.
9. Ovarian US : Ovarian cysts.
 DD Of Acne
1. Milia ( small facial cysts).

2. Sebaceous hyperplasia ( appear as papules).

1
3. Folliculitis. benign adnexal
neoplasm
4. Pseudofolliculitis. originating from
basal cells of hair 2
5. Trichoepithelioma, syringoma . follicles

6. Seborrheic dermatitis. syringoma

7. Rosacea.

8. Perioral dermatitis.
Trichoepithelioma
 Treatment of Acne
 Topical: 1st line of treatment
 Retinoids ( the best choice) , Benzoyl peroxide.
 Antibiotic ( Erythromycin , Clindamycin).
 Keratolytic : Salicylic acid.

 Systemic :
 Antibiotics ( Antibacterial + Anti inflammatory) : 1st line.
 Doxycycline, Tetracycline, Erythromycin, Azithromycin. (DETA)
 Retinoids : 2nd line
 Isotritinoin ( the best treatment but last choice).

 Lesions may flare in the first 2 weeks of treatment.

 Isotritinoin ( Roaccutane )
 For severe cases :
1. Nodulocystic acne not responding to first line measurements
2. Scarring acne
3. Dysmorphophobic acne.
4. Gram negative folliculitis
5. Acne Fulminans

 Effective but toxic.

 Teratogenic – cause fetal anomaly in > 95% of cases ( abortion or fetal anomalies).
 Needs close follow up ( liver enzymes , serum lipids , bleeding , papilledema).
 Dose 0,5-1mg\kg , used alone without any combination with other drugs.
 Duration 5-6 months or total accumulative dose 120mg\kg\course.
 With white comedone don’t give vit A becauce the risk of keloid
formation , so use keratolytics first .
 B-Rosacea
 Chronic inflammatory skin disease with characteristic Lesions on the face affecting mostly
middle aged women
 There are eye manifestations too ( Conjunctivitis , Blepharitis ( inflammation of eyelids ).
 Female to male ratio is 9:1
 Characteristic skin lesions: Telangiectasia , erythema ,papules, pustules on cheeks,
forehead , nose and chin.
 Rhinophyma and Otophyma (enlargement of the nose and earlobe) is a feature in -some
cases due to repeated inflammation and edema.
 No comedones.
 Female + Fertile + Fair skin + Fatty , 40-50Y/O.
 Provoked by spicy food , hot drinks , hotness and coldness , sun exposure , stress , alcohol.
 Ttt : topical antibiotics ( doxycycline ) sometimes Roaccutane . Avoid exacerbating factors
 Rosacea

Bilateral pink papules on the  Pink papules with

cheeks , nose and chin. Telengectasia on the cheeks.
 Rosacea

Rhinophyma
Erythematous papules on
( complicated
the cheeks.
 Rosacea

Rhinophyma before and after the Rhinophyma and

surgical treatment. Otophyma.
 C . Acneform skin rash
1. Pseudofolliculitis Barbae ; Skin reaction to
hair as foreign –Body. in skin areas prone to
shaving
2. Pityrosporum folliculitis.

3. Acne keloidalis nuchae : inflammatory

keloidal lesions on the nape of the neck.
 Pseudofolliculitis barbae

 Not a true folliculitis ( not due to infection) but due to a reaction against the
hair itself when its plugged inside ( foreign body reaction).
 Occurs in Negroid people , Curley hair.
 Pityrosporum folliculitis

Acne form rash due to fungal infection.

Acne keloidalis nuchae Keloid :type of raised scar

 Acne form rash with scarring on the nape of the neck , could lead to permanent hair loss .