Acne Vulgaris

INTRODUCTION
 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
1. Genetic
2. Obesity: hyperandrogenism
3. A significant positive family history of acne has been demonstrated
especially when acne is found in:
 Twins
 Mother
 First degree relative
 Multiple family members
4. A significant association between obesity and acne in children
1. Smoking
2. Stress
3. Facial therapy or salon facial massage
AGGRAVATING FACTORS

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
 There is no conclusive statement on the effectiveness of zinc supplement
in acne
 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.

FEATURES OF ACNE
2. PAPULAR / PUSTULAR ACNE
 Patients present with inflamed, 2- to 5-mm papules/pustules.

FEATURES OF ACNE
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
The 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

PATHOGENESIS
Pillosebaceous unit

INCREASED 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.

INCREASED SEBUM PRODUCTION
WHAT TRIGGERS EXCESS SEBUM?

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

TYPES OF ACNE
ACNE CONGLOBATA
OCCUPATIONAL ACNE
 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.
 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.

TYPES OF ACNE
COSMETIC ACNE
DRUG-INDUCED ACNE
 Eruption seen in women using cosmetics, especially oil-
based ones.
 Almost always comedones.
 Lesion frequently on the chin.
 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.

TYPES OF ACNE
INFANTILE ACNE
LATE ONSET 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.
 Acne with onset after 25 years old.
 Predominantly women.
 Presents as deep seated, persistent lesions on
lower half of face.
 Exclude underlying androgen secreting
pathology, especially polycystic ovarian
syndrome.

TYPES OF ACNE
ACNE EXCORIEE
ACNE FULMINANS
 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.
 Acute onset
 Presents as crusted, ulcerated lesions.
 Associated with fever, myalgia and arthralgia.

TYPES OF ACNE
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
KERATOSIS PILIARIS
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.

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

ASSESSMENT
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.
ASSESSING SEVERITY OF ACNE
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 TX
 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.
1. COMEDONAL ACNE
Topical retinoid

PHARMACOLOGICAL TX
 Mild disease
First-line therapies include Benzoyl
peroxide may be added. Azelaic acid is an 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, 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.
2. PAPULAR / PUSTULAR ACNE
oral antibiotics + a topical retinoid + benzoyl peroxide
a topical retinoid + a topical antibiotic

PHARMACOLOGICAL TX
 The first-line therapy for nodular acne includes an
 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
therapy.
3. NODULAR ACNE
oral antibiotics
+ a topical retinoid + benzoyl peroxide
oral isotrerinoin

PHARMACOLOGICAL TX
COMMON SIDE EFFECTS OF ACNE MEDICATIONS:
Skin irritation, dryness, or peeling.

NON- PHARMACOLOGICAL TX
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.

Acne Vulgaris

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Acne Vulgaris

Similar to Acne Vulgaris (20)

More from yuyuricci

More from yuyuricci (20)

Recently uploaded

Recently uploaded (20)

Acne Vulgaris