Acne vulgaris: overview

Introduction:
Definition:
Multi-factorial disease characterized by
abnormalities in sebum
production, follicular desquamation, bacterial
proliferation and
inflammation.
Prevalence:
85% adolescents experience it
Prevalence of comedones (lesions) in adolescents
approaches 100%

Overview
Acne vulgaris is the most common cutaneous disorder in
the many countries.
It affects more than 17 million Americans.
10 percent of all patient encounters with primary care
physicians.
Pts can experience significant psychological morbidity
and, rarely, mortality due to suicide.
Important that physicians are familiar with Acne Vulgaris
and its treatment.

Pathogenesis:
Acne vulgaris is a disease of
pilosebaceous follicles.
Factors:
Retention hyperkeratosis.

Increased sebum production.

Propionibacterium acnes
within the follicle.

Inflammation

Etiology, signs and symptoms

Acne vulgaris commences in the pilosebaceous
units in the dermis. These units consist of hair
follicle and the associated sebaceous glands.
They are connected to the skin by a
duct(infundibulum) through which the hair shaft
passes.
Non inflamatory acne; ( acne that characterized
by closed and open comedones )
The cause of acne is an increase in the activity
of the sebaceous glands and the epithelial tissue
lining the infundibulum.

Etiology, signs and symptoms

The glands produce more sebum causing
increased oiliness of the skin.
The epithelial cells become more distinct
,durable and stick together to form a coherent
horny layer which blocks the follicular channel.
This impaction plugs distends the follicle to form
a microcomedo
NB, normally epidermal cells continually
sloughs off and moves to the surface of the
skin with the sebum.

continue
As more cells and sebum are added, the
comedo becomes visible (whitehead) and is
called a closed comedo, is., its content do not
reach the surface of the skin. If plug enlarges
and protrudes from the orifice of the follicular
canal, it is called an Open comedo, its contents
open to the surface of the skin. The tip may
darken (blackhead) because of the accumulation
of melanin that is produced by the epithelial cells
of the follicular lining.

Initial pathogenesis (reason unknown):

follicular hyperkeratinization
proliferation +
decreased desquamation of keratinocytes
hyperkeratotic plug
(microcomedone)

Pathogenesis
Sebaceous glands enlarge
Sebum production increases
Growth medium for P. Acnes
plugs provide anaerobic
Lipid-rich environment

Pathogenesis
Bacteria thrive
Inflammation results
Chemotactic factors attract neutrophils
Depending on conditions
Non-inflammatory
open/closed comedones

Inflammatory papule/
pustule/nodule

Terms/Definitions
Microcomedone:

hyperkeratotic plug made of sebum and keratin in follicular canal

Closed comedones (whiteheads)

closed comedo
(a whitehead):
Accumulation of sebum
converts a
microcomedo into this.

Closed comedones (whiteheads)

Open comedo (blackhead)

open comedo
(a blackhead):
when follicular orifice is
opened + distended.
Melanin + packed
keratinocytes + oxidized
lipids dark colour

Open comedo (blackhead)

Whitehead and blackheads

Inflammatory acne
Acne characterized by inflammation surrounding the
comedones, papules, pustules, and nodulocystic lesions. it
may cause permanent scarring.
Inflammatory acne begins in closed comedones, rarely in
open ones. As the micro comedo develops, it .distends the
follicle, which cause thinning of the walls. primary
inflammation of the follicle wall develops with the disruption
of the epithelium and infiltration of lymphocytes in to the
adjacent area of the dermis.
Normal sebum does not contain free fatty acids and is
nonirritating, however, in the presence of biolytic enzymes
produced by C.acne) , triglycerides of the sebum are split
and release fatty acids which are irritating to the tissue. Thus
sebum contribute to inflammation of the surrounding tissue.
The inflamed follicle or pustules either heal in about a week
or develop in to cyst or sterile abscesses, which can lead to
scaring.

Cysts
Cysts:
when follicles rupture into
surrounding tissues,
resulting in
papule/pustule/nodule.

Cysts

Aggravating factors
Change in sebaceous activity and hormonal
level (e.g. before or during premenstrual cycle)
High humidity conditions
Local irritation or friction
Rough or occlusive clothing
Cosmetics( having greasy base)
Diet; chocolate, nuts, fats colas, or
carbohydrates.?
Oils greases , or dyes in hair product.

Medications that can cause acne

ACTH
Azathioprine
Barbiturates
Isoniazid
Lithium
phenytoin

Disulfiram
Halogens
Iodides
Steroids
Cyclosporine
Vitamins B2,6,12

Strategy for treatment of acne

Treatment must be long term however symptoms can
be reduced and permanent scaring can be
minimized.) it involves:
* Removal of excess sebum by washing the affected areas
three times a day with warm water and soap.
*Topically applied oils and fats e.g. in cosmetics should be
eliminated.
* Prevention of pilosebaceous orifice closure by use of mild
irritants. the irritant effect causes an increased rate of
turnover of the epithelial cells lining the follicular duct.
Peeling agents also cause keratolysis, which reduces
the cohesiveness of the follicular lining.

Treatment of Acne Vulgaris

depends on type of clinical lesions
Choose vehicle for topical drug according to pts skin
type. (gel for oily, cream for dry skin).
Microcomedone matures in 8 weeks
Therapy must continue beyond this time frame

How Treatment Works

Mild to moderate acne

Comedonal acne
Topical retinoids
Other topical agents:
Useful when topical retinoids not tolerated

Salicylic acid (promotes desquamation)

Azelaic acid (antimicrobial, reduces hyperpigminetation)
Glycolic acid
Sulfur in OTC rx (keratolytic)

Mild to moderate inflammatory acne

Benzoyl peroxide: (antimicrobial, anticomedonal,
pregnancy risk C)
Topical antibiotic
Combination of both
Combination rx more effective than mono in increased
inflammatory lesions.

Mild to moderate inflammatory acne

Topical antibiotics
Eliminate P. Acne
Reduce inflammation

Clindamycin
Erythromycin
Tetracycline
Metronidazole
Azelaic acid

Moderate to severe acne:

If topical Rx not effective oral isotretinoin

oral antibiotics
hormonal rx

Oral isotretinoin
Reduces sebaceous gland size/sebum production
regulates cell proliferation and differentiation
Effect last 1 yr after cessation
Only med altering course of A. Vulgaris

Moderate to severe acne:

oral isotretinoin
Adverse effects can be severe:
Inc TG, teratogenic, bone marrow suppression,
hepatotoxicity, top 10 drugs for suicide/depression
reports.
FDA practice rules:
2 negative pregnancy tests before rx
Pregnancy test each month (bring pt in)
physicians need authorization before prescribing
Pregnancy risk pts must use 2 contraceptive for at least
1 mo prior to rx. (manufacturermust commit to 2 contracept.)

Moderate to severe acne:

Oral antibiotics
-Tetracycline
- minocycline
- doxycycline

- erythromycin
- TMP-SMX
- clindamycin

Given daily over 4-6 mo, with taper.

Patient FAQs
Soaps, detergents
remove sebum but do
not alter production
Avoid occlusive
clothing
Water based cosmetic
better than oil based
Diet modification no
role in rx

Acne conglobata
Unpleasant form of nodulocystic acne
Interconnecting abscesses and sinuses,
which result in unsightly hypertrophic (thick)
and atrophic (thin) scars.
There are groups of large macrocomedones
and cysts that are filled with smelly pus.
It is occasionally associated with hidradenitis
suppurativa,

Acne fulminans
Allergic reaction to P. acne
Abrupt onset
Inflammatory and ulcerated nodular acne
on chest and back
Severe acne scarring
Fluctuating fever
Painful joints
Malaise (ie. the patient feels unwell)
Loss of appetite and weight loss
Raised white blood cell count.

Treatment severe acne

Oral isotretinoin
Oral steroids