ACNE VULGARIS

and
ACNEFORMIS ERUPTION
David Sudarto Oeiria
Dep. Dermatology and Venereology
Medical School, Wijaya Kusuma University

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 Acne Vulgaris : common disorder of the pilosebaceous unit
 Location: Face, Chest and Back
 Four Key elements of pathogenesis :
1. Follicular epidermal hyperproliferation
2. Sebum production increase
3. Propionibacterium acnes increase
4. Inflammation and Immune response
 Clinical features: 1.comedones, 2.papules, 3.pustules 4.nodules
 Treatment:
1. Topical agents
2. Combination of topical and oral agents
 Sequelae: Acne Scars
 Early treatment and life style changes
 Longterm treatment and skin care

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 Although the course of ACNE may be
limited in the majority of patients, but
the sequelae: SCAR FORMATION
is lifelong

Psychological impairment as a
Psychologic Scars

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 Epidemiology
• One of the top most common skin diseases of
adolescents and young adult

• It is world wide/global problem

• Acne can occur at any age, starting at first few

weeks of life as Neonatal Acne and also in infant of
1-12 months as Infantil Acne

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 ACNE Mostly adolescents and young adult
Acne may persist from adolescence into
adulthood.
Acne can have its onset after the adolescent
period

Prevalence of acne in adult is higher in female

The onset of acne has become earlier, as

the adrenarche appears to be dropping
over the years. Bhate K, Williams HC,
Epidemiology of Acne vulgaris. Br J Dermatol.
2013; 168:474-485

Family history of ACNE VULGARIS has

been reported in 62.9% to 78% of
patients

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 Males tend to have more
severe acne but female tend
to persist to adulthood

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 Clinical Features
HISTORY Taking is important
• Onset is GRADUAL, around the puberty and
polymorphic
• Abrupt onset and monomorphic: underlying
aetilogy such as medication or an Androgen-
secreting tumor
• Premenstrual flare is common (56%)
Khunger N, Kumar C. A clinic-epidemiological study of acne: is it different from
adolescent acne? Indian J Dermatolo Venereol Leprol. 2012;78:335-341

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 COMPLETE MEDICATION HISTORY

Abrupt onset :

1. Anabolic Steroids
2. Corticosteroids
3. Phenytoin, Lithium, INH, Vitamin B complexes,
Halogenated compounds
4. Epidermal Growth Factor Receptor ( EGFR )
5. Hormonal Therapy
6. Progestin-only Contraceptives: Injectable
contracepives, IUD with Progestin
7. Testosteron replacement Therapy

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 Clinical Finding

ACNE VULGARIS
Although one type of lesion may
predominate, close inspection usually reveals
the presence of several types of lesions

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 Opened Comedones
• Closed Comedones
Inflammatory papules
Nodules
Klinis Acne vulgaris (3)

• acne conglobata :
• sebagian besar lesi
berupa nodus dan
kista yang meradang,
kadang2 terbentuk
sinus
• Cysts pada acne
adalah PseudoCyst
krn tidak mempunyai
capsul ( epithelial
Lining)
Klinis Acne vulgaris (3)

• Acne conglobata is a
severe form of
nodulocystic acne
that may have an
eruptive onset but
without systemic
manifestations
• Nodules is the
predominant lesions
Jenis akne lain (1)

Acne infantile
 ACNE Comedonal
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 Papulopustules
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Jenis akne lain (2)
Cosmetic ACNE
Jenis akne lain (3)

• acne ekskoriae
Jenis akne lain (5)

Mechanical ACNE
 open and closed comedones as well as
postinflammatory hyperpigmentation (A)

Comedonal acne vulgaris. On the cheek (A) and

forehead (B),

B, Courtesy, Kalman Watsky, MD. and open and closed comedones as well as
inflammatory papules (B).

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 SEVERE ACNE

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 SEVERE ACNE

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Klinis Acne vulgaris (4)

Severe ACNE
 Acne fulminans
Acne fulminans is the most severe form of acne and is characterized
by the abrupt development of nodular and suppurative acne lesions
in association with systemic manifestations

Patients typically have mild to moderate acne

prior to the onset of acne fulminans, when
numerous microcomedones suddenly erupt
and become markedly inflamed

Acne fulminans has also been associated with

late-onset congenital adrenal hyperplasia and
anabolic steroid use, including therapeutic
testosterone

Systemic manifestations include fever,

arthralgias, myalgias, hepatosplenomegaly, and
severe malaise. Erythema nodosum may also
Acne fulminans. Eruptive, friable papulopustules with
erosions, oozing and formation of granulation tissue arise in association with acne fulminans

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 COMPLICATION

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 Honeycomb scarring due to
moderate inflammatory ACNE
VULGARIS
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 Rolling scars

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 Several types of atrophic acne scars

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 KELOIDAL SCARS

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 Pathogenesis of ACNE VULGARIS

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 Etiology

Current understanding of acne is that it is a

complex and multifactorial inflammatory disease

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 4 key elements are
(1) follicular epidermal hyperproliferation,
(2) sebum production,
(3) Propionibacterium acnes,
(4) inflammation and immune response

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 All clinical lesions begin with the
microcomedo and develop into
clinical lesions— comedones,
inflammatory lesions, and scarring
The microcomedo is thought to be the
precursor of all clinically apparent acne lesions

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 Fitzpatrick’s Dermatology 9th Ed, 2019
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 Jean Bolognia, 4th
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Ed Dermatology,
 Follicular epidermal hyperproliferation

Several proposed factors in keratinocyte

hyperproliferation include:
1. androgen stimulation,
2. decreased linoleic acid,
3. increased IL-1-α activity,
4. effects of P. acnes.

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 5-α Reductase, the enzyme responsible
for converting testosterone to the potent DHT,
has greatest activity in areas of skin prone to
acne, face, chest, and back.

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 DIHYDROTESTOSTERONE (DHT)
may stimulate
follicular keratinocyte proliferation

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 Increase sebum production
Sebum is a light yellow viscous fluid, composed
of triglycerides, free fatty acids, squalene, wax
and sterol esters, and free sterols

The main component of sebum, triglycerides,

is important in acne pathogenesis.
Triglycerides are broken down into free fatty
acids by P. acnes. In return these FFA promote
P. acnes colonization and Induction of
Inflammation

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 The microcomedo continue to expand with densely
packed keratin, sebum, and bacteria. Eventually, this
distension causes follicular wall rupture.

The extrusion of the keratin, sebum, and bacteria

into the dermis results in a brisk inflammatory
response

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 P. acnes is one of the key
factors involved in
acne pathogenesis
P. acnes is a gram-positive, anaerobic,
microaerophilic bacterium found in the
sebaceous follicle and is the dominant
bacterial inhabitant of the human sebaceous
gland

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 P. acnes directly induces inflammation
through various mechanisms

1.Antipropionobacterium antibody: The cell wall of P. acnes

contains a carbohydrate antigen that stimulates antibody
development. Patients with the most severe acne have been
shown to have the highest titers of antibodies.
2.Delayed type hypersensitivity:P. acnes also facilitates
inflammation by eliciting a delayed-type hypersensitivity
response and by producing lipases, proteases, hyaluronidases,
and chemotactic factors.
Reactive oxygen species (ROS) and lysosomal enzymes are
released by neutrophils and levels may correlate with severity.
3.Host Innate responses: P. acnes stimulates host innate
responses via secretion of proinflammatory cytokines and
chemokines from peripheral blood mononuclear cells
(PBMCs) and monocytes

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 DIAGNOSIS

The diagnosis of acne vulgaris is

typically made by clinical history
and physical examination

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 Laboratory testing

Laboratory workup may be indicated in

patients with acne if hyperandrogenism is
suspected
The laboratory workup should include
measurement of serum DHEAS, total
testosterone, and free testosterone, with free
testosterone considered the most sensitive
test for PCOS

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 CLINICAL COURSE AND PROGNOSIS

The typical age of onset of acne vulgaris varies

considerably.

Because the age of adrenarche

appears to be dropping over the years,
patients may be presenting with acne at an
earlier age

It may start as early as 8 years of age or it may

not appear until the age of 20 years or even later

In women, there is often variation in relation

to the menstrual cycle, with a flare just before
the onset of menstruation, especially in those
older than 30 years of age.

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Family history, body mass index, and diet

May predict risk for development of moderate to severe acne

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 MANAGEMENT

Treatment regimens should be initiated early

and be sufficiently aggressive to prevent
permanent sequelae.

Often multiple treatments are used in

combination so as to combat the various
factors in the pathogenesis of acne

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 The mechanism of action of the most common
treatments for acne can be divided in the
following categories as they relate to the
pathophysiology:

1. Correct the altered pattern of follicular

keratinization.

2. Decrease sebaceous gland activity.

3. Decrease the follicular bacterial

population, particularly P. acnes.

4. Exert an anti-inflammatory effect

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 TOPICAL Treatment

Topical antibiotic: Clindamycin, Erythromycin

Topical antimicrobial: Benzoyl Peroxide, Azelaic acid

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 SYSTEMIC TREATMENT
Antibiotic

Doxycycline and minocycline are the most

commonly used tetracycline derivatives for the
treatment of acne
Recent guidelines recommend limiting the
duration of oral antibiotic therapy in acne to 3
to 6 months to reduce risk of resistance
Hormonal
The goal of hormonal therapy is to counteract
the effects of androgens on the sebaceous
gland. This can be accomplished with
antiandrogens, or agents designed to decrease
the endogenous production of androgens by
the ovary or adrenal gland, including oral
contraceptives, glucocorticoids, or
gonadotropinreleasing hormone (GnRH)
agonists
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 DIET
There may be some link between milk and
acne as well as between high-glycemic index
foods and acne.
1.Milk, especially skim milk, is positively associated with acne
prevalence and severity.

2.Whey protein supplements for body building

3.High glycemic-load diet.

4.Vitamin B12 supplementation can potentially trigger the

development of acne by altering the transcriptome of skin microbiota,
leading to increased production of proinflammatory porphyrins by
Propionibacterium acnes. (Jean Bolognia, 4th Ed, Dermatology 2017)

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 Differential Diagnosis of Acne

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 Acneiform Eruptions
Acne or acneiform eruptions (e.g. folliculitis) can be seen as a side
effect of a number of medications .

An abrupt, monomorphous eruption of inflammatory papules and

pustules is often observed in drug-induced acne , in contrast to the
heterogeneous morphology of lesions seen in acne vulgaris.

When a history of prescription medication use is not elicited, a

comprehensive review of all over-the-counter medications and
supplements, as well as recent medical procedures, may reveal the
responsible agent.

Bodybuilders and athletes should be questioned about anabolic

steroid use.

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 Drug induced acne due to isoniazid. Courtesy,
Kalman Watsky, MD.

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 Follicular mycosis fungoides that presented as numerous lesions
with a comedonal appearance on the chest, abdomen, and
back. Courtesy, Julie V Schaffer, MD; B, Courtesy, Lorenzo Cerroni, MD
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