Download Clinical Overview of Acne Vulgaris

Clinical Overview of Acne
Vulgaris
Rich Callahan MSPA, PA-C
ICM I – Summer 2009
A disease of the pilosebaceous
unit
• Anatomy of this structure is key to full
understanding of the disease.
• Each PS unit built around a long, narrow tube
(a.k.a. – “pore”) vertically oriented in the skin,
which houses a single hair follicle.
• Epithelial lining at entrance of pore is stratum
corneum, prone to overkeratinization (“clogging”)
if the right etiological factors are present.
• Sebaceous gland activity is the biggest player in
instigating the disease.
Sebaceous Glands
• Distributed most densely on face, chest, back, upper arms.
• Positioned around the infundibulum (main tube) of the
pore, each having a single duct communicating with it.
• Secrete sebum (oil) into the duct. Sebum is rich in
triglycerides.
• Highly sensitive to hormonal stimulation by androgens.
• Circulating testosterone reaches the skin, where it is
changed into dihydrotestosterone (DHT.)
• DHT acts on the sebaceous glands causing increase in size
and oil production.
Hormonal aspect will become much more relevant later
when we talk about treatment of acne
• We know that hormonal influences during puberty cause
increased sebum production/keratinization in both men and
women. Majority of these cases resolve post-puberty.
• Some research suggests that increased cortisol production
secondary to prolonged stress can lead to androgen overproduction and acne.
• Middle aged women with recurrent pre-menstrual acne are
often showing a sensitivity to the brief surge of
testosterone produced by the ovaries prior to initiation of
menses.
Other structures in the pilosebaceous unit
• Apocrine sweat glands – have a duct communicating with
infundibulum of PS unit which secretes apocrine sweat
(clear sweat mixed with cytoplasmic components of the
gland which add odor, phermones, etc.)
• Eccrine sweat glands – positioned alongside the PS unit in
the skin, but has its own vertically-oriented duct
communicating directly with the skin surface. As you
might expect, they secrete eccrine (clear) sweat.
• Arrector pili muscle – tiny muscle connecting
infundibulum with skin surface. Cause of “goose bumps”
Pathogenesis of Acne Starts with formation of
microcomedos
• In predisposed individuals, starts with increased sebum
production from sebaceous glands and overgrowth of
keratin-producing cells lining the pore walls. Excess
keratinization leads to the formation of a sticky plug which
blocks the superficial aspect of the pore.
• This is a microcomedo – the precursor lesion to acne.
• At this stage the sebaceous glands are still producing
sebum, which is now unable to drain out to the skin
surface, causing the formation of a comedo.
A comedo is the basic lesion of acne vulgaris. It has
two subtypes:
• Open comedone – a “blackhead.” Forms when the pore
wall is able to dilate in response to the increased pressure
created by the trapped sebum, creating a non-inflamed
lesion.
• Closed comedone – a “whitehead.” A semi-firm, white,
dome-shaped papule, which is also non-inflamed. Forms
when trapped sebum pushes up against the non-dilated
opening of the pore.
• All the acne you see starts with one or both of these
lesions.
Pathogenesis of Acne – What Happens Next?
Inflammation and bacterial overgrowth
• Propionibacterium Acnes: Anaerobic bacteria which is normal flora
within PS unit. Has ability to digest sebum.
• Large plug of sebum stimulates p. acnes to produce lipase, which
breaks down (hydrolyzes) the triglycerides in the sebum to free fatty
acids.
• Free fatty acids highly irritating to PS unit and surrounding tissues,
causing inflammation and further comedo formation.
• Neutrophils are attracted to inflamed site, attach to follicular wall, and
release hydrolases which further weaken it. Wall eventually ruptures,
spilling out highly irritating FFA’s into surrounding tissue.
Now we are ready to talk about what happens after
comedogenesis
• Pustule formation – Inflamed comedo starts to fill with
purulent material which pools at the surface.
• Papule formation – Inflamed comedo enlarges into a red
papule without pooling of purulent material at top.
• Nodule formation – Follicular walls of papules/pustules
rupture and spill inflamed contents into surrounding tissue.
Lesion increases in size and becomes a nodule (>5mm
diameter.) At this point level of skin involvement creates
risk for later scarring. Nodules can become hemhorragic,
secondarily infected, or form communications between
multiple draining lesions (sinus tracks.)
How Severity of Acne is graded:
• Overall severity of acne classified as Grades 1-4, with
higher grades having a higher overall lesion count, more
inflammation, larger lesions, etc.
• Further characterized as comedonal, pustular,
papularpustular, nodular and nodulocystic.
• (Important to remember that by definition, comedonal acne
is the only subtype which is non-inflamed.)
• For Example: A mild case would be Grade I comedonal.
You see scattered open comedones on forehead and face.
• A severe case could be Grade 3 nodulocystic acne
characterized by presence of many inflamed, tender
nodules and cysts.
Clinical Presentation
• Acne presents as solitary or grouped comedones, papules,
pustules, nodules and cysts. Mild to severe inflammation
will accompany all with the exception of comedones.
• Generally distributed on forehead, face, neck, chest and
back. Rarely appears on scalp. Corresponds with areas of
highest sebaceous gland density.
• Patients are usually, although not always anxious and selfconscious about their condition, which can lend the disease
a strong emotional component.
• Many patients previously diagnosed and frustrated with
treatment.
Diagnosis
• Almost always a straightforward, visual diagnosis.
• Vast majority of cases are pre-pubescent and pubescent
males and females. Significant number of cases middleaged women; rare in post-pubescent males.
• I have seen a few cases of acne suddenly appearing in
patients with no prior history and who don’t fit into the
above categories
• When you see this look for occupational acne: Workplace
exposure to light oils (machine oil, cosmetics) which
occludes pores leading to comedogenesis and acne. This is
the only type of acne I have needed to biopsy for
diagnosis.
Speaking of Oil, let’s not forget about Pomade Acne
• Unique form of acne secondary to chronic use of oily hair
mousses, gels, tonics by susceptible individuals.
• Always distributed on upper forehead/hairline/anterior
scalp with a fairly clear border. Lower face unaffected.
• Patient will usually present with offending substance in
their hair which helps the diagnosis
• Usually an easy problem to fix: They stop using the
product, the acne clears in 2-6 weeks!
Treatment of Acne – Guided by the
Severity of Disease
• Topical retinoids are first-line: adapelene (differin,)
tretinoin (Retin-A) and tazarotene (Tazorac)
• Benzoyl peroxide creams, gels and washes.
• Topical antibiotics (clindamycin, erythromycin, dapsone)
• Azeleic acid (Azelex, Finacea): Unique plant-derived
compound that has anti-bacterial and anti-comedogenic
properties (and Pregnancy Category B)
• Salycylic and Glycolic Acid gels and washes (Two of the
active ingredients of ProActiv, as endorsed by Shawn
“Puffy” Combs!)
Treatment of Acne – Guided by the Severity
of Disease
• Oral antibiotics – minocycline, tetracycline, doxycycline.
Also to a lesser degree trimethoprim-sulfamethoxasole
(Bactrim) and beta-lactams/derivatives like PCN,
amoxicillin and cephalexin.
• Isotretinoin (Accutane) – The big gun of acne
medications. Drastically attenuates activity of sebaceous
glands and rate of keratinization in epidermis. Many
potential side effects. Teratogenic. Photosensitizing. Can
be a permanent cure for approximately 85% of patients on
6 month course.
• Now subject to a massive federal regulatory apparatus
called I-Pledge.