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U N I T 1 3
Integumentary Function
overall the incidence and severity are greater in males.
The disorder is very common, affecting more than 85%
of teenagers, and a large percentage of young adults
continue to show signs of the disorder.
20
Acne vulgaris is characterized by both noninflamma-
tory and inflammatory lesions. The lesions are typically
located on the face and neck and, to a lesser extent, on
the back, chest, and shoulders. Noninflammatory lesions
consist of
comedones
(whiteheads and blackheads).
Blackheads
are plugs of material that accumulate in
sebaceous glands that open to the skin surface. The color
of blackheads results from melanin that has moved into
the sebaceous glands from adjoining epidermal cells.
Whiteheads
are pale, slightly elevated papules with no
visible orifice. Inflammatory lesions consist of papules,
pustules, nodules, and, in severe cases, cysts.
Papules
are
raised areas less than 5 mm in diameter.
Pustules
have
a central core of purulent material.
Nodules
are larger
than 5 mm in diameter and may become suppurative or
hemorrhagic. Suppurative nodules often are referred to
as
cysts
because of their resemblance to inflamed epi-
dermal cysts. The inflammatory lesions are believed to
develop from the escape of sebum into the dermis and
the irritating effects of the fatty acids contained in the
sebum.
The cause of acne vulgaris is largely unknown. There
is a hereditary factor, multiple generations of family
members being affected. Several factors are believed to
contribute to acne, including (1) the influence of andro-
gens on sebaceous gland activity; (2) increased prolif-
eration of the keratinizing epidermal cells that form the
sebaceous cells; (3) increased sebum production in rela-
tion to the severity of the disease; and (4) the presence
of
Propionibacterium acnes,
the microorganism respon-
sible for the inflammatory stage of the disorder. These
factors are probably interrelated. Increased androgen
production results in increased sebaceous cell activity,
with resultant plugging of the pilosebaceous ducts. The
excessive sebum provides a medium for
P. acnes
growth,
and the organism contains lipases that break down the
free fatty acids that produce the acne inflammation.
P. acnes
is also thought to form a biofilm (an extracellular
polysaccharide lining in which the bacteria are encased)
that acts as a protective barrier to antibiotic treatment
(see Chapter 14), explaining why prolonged antibiotic
treatments are necessary.
21
The sebaceous glands also
may serve as sites for immune reactions.
22
Acne may
be triggered or worsened by external factors such as
obstructions (e.g., head bands, collars), manipulation of
the lesions, cosmetics, and occupational exposures.
The diagnosis of acne is based on history and physi-
cal examination. The severity of the acne is gener-
ally assessed by the number, type, and distribution of
lesions.
17
Mild acne is usually characterized by the pres-
ence of a small number (generally <10) of open and closed
comedones, with a few inflammatory papules; moderate
acne by the presence of a moderate number (10 to 40) of
erythematous papules and pustules (Fig. 46-11), usually
limited to the face; and moderately severe acne by the
presence of numerous papules and pustules (40 to 100)
and occasionally larger, deeper, nodular inflamed lesions
involving the face, chest, and back. Treatment of acne
focuses on clearing up existing lesions, preventing new
lesions, and limiting scar formation.
17–20
Treatment measures include the use of topical antimi-
crobials, oral antibiotics, topical retinoids, and isotreti-
noin. Soaps are usually not effective in treating acne,
and unless the skin is exceptionally oily, a mild soap
should be used to avoid additional irritation that will
limit the effectiveness of other topical treatments. Mild
acne is usually treated with a topical preparation con-
taining a combination of erythromycin or clindamycin
and benzoyl peroxide. Topical antibiotics do not affect
existing lesions but decrease the
P. acnes
on the skin,
thereby reducing subsequent inflammation resulting
from free fatty acid release and breakdown. Benzoyl
peroxide, which is a bactericide, does not induce resis-
tance, and when used with topical and oral antibiotics
it protects against the development of lesions. Azelaic
acid, products containing sodium sulfacetamide and
sulfur, and salicylic acid preparations are also available.
These agents are usually not considered as first-line ther-
apies, but may be used in persons who cannot tolerate
other topical agents.
Moderate to severe cases of acne may be managed
with systemic antibiotics (e.g., tetracycline), topi-
cal vitamin A derivatives (retinoids), or oral retinoids
(isotretinoin). Systemic antibiotics decrease
P. acnes
col-
onization and have intrinsic anti-inflammatory effects.
The action of topical vitamin A (e.g., tretinoin) has been
attributed to decreased cohesiveness of epidermal cells
and increased epidermal cell turnover. This is thought
to result in increased extrusion of open comedones and
transformation of closed comedones into open ones.
Isotretinoin is approved for treatment of recalcitrant
cases of acne and cystic acnes. Although the exact mode
of action is unknown, isotretinoin decreases sebaceous
gland activity, prevents new comedones from forming,
reduces the
P. acnes
count through sebum reduction,
and has an anti-inflammatory effect. Because of its many
side effects, it is used only in persons with severe acne.
The oral retinoids are known teratogens and must not
FIGURE 46-11.
Moderate acne. Erythematous papules and
pustules are the predominant lesions, and lesions are limited to
the face. (From JamesWD. Acne. N Engl J Med. 2005;352:1464.
Copyright © 2005. Massachusetts Medical Society.)
