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Acne Vulgaris: Audi Adibah - Affan Syafiqi - Amanina Nasir - Nurul Hidayu - Nik Nor Liyana - Sathishwaran
Acne Vulgaris: Audi Adibah - Affan Syafiqi - Amanina Nasir - Nurul Hidayu - Nik Nor Liyana - Sathishwaran
VULGARIS
AUDI ADIBAH | AFFAN SYAFIQI | AMANINA NASIR | NURUL HIDAYU | NIK NOR LIYANA | SATHISHWARAN
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.
AGGRAVATING FACTORS
1. Smoking
2. Stress
3. 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
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
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.
TYPES OF ACNE
COSMETIC ACNE
Eruption seen in women using cosmetics, especially oil-
based ones.
Almost always comedones.
Lesion frequently on the chin.
DRUG-INDUCED ACNE
ACNE FULMINANS
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
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 PILIARIS
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.
DIFFERENTIAL DIAGNOSIS
PRINCIPLE MANAGEMENT
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.
Mild disease
First-line therapies include a topical retinoid + a topical antibioticBenzoyl
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, 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.
PHARMACOLOGICAL TX
3. NODULAR ACNE
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