CHAPTER

Disorders of Sebaceous
and Sweat Glands 20
DISORDERS OF SEBACEOUS GLANDS

Acne Vulgaris
Acne vulgaris is a self-limited multifactorial disease involving the sebaceous
follicles. A prerequisite for the development of acne is active sebaceous glands,
the level of their sebum secretion correlates with the severity of the acne. Sebum
consists of a mixture of squalene, wax and sterol esters, cholesterol, polar lipids,
and triglycerides all of which play a key role in the genesis of this disorder.
Sebum and its breakdown products may be involved in ductal hypercornification
and growth of the bacteria, Propionibacterium acnes. Increased production of
sebum occurs at puberty under the influence of androgen hormone. This ductal
hypercornification ultimately results in impacted tightly packed horny cells—the
comedone. This may lead to a disruption of the follicular epithelium, permit-
ting discharge of the follicular contents into the dermis. This, in turn, causes
the formation of inflammatory papules, pustules, and nodulocystic lesions. To
sum up, three pathophysiologic processes are involved.
1. Increased sebum production
2. Pilosebaceous duct hyperkeratosis
3. Increased colonization of pilosebaceous apparatus with P. acnes.
Acne vulgaris occurs predominantly during adolescence and in early adulthood.
It affects mainly the face, upper back, and upper chest. Clinically, two types of
lesions occur: noninflammatory and inflammatory lesions. Noninflammatory lesion
is a comedo, which can be located either in an open follicle as blackhead (open
comedone) (Fig. 20.1) or in a closed follicle as a white head (closed comedone).
Inflammatory lesions only rarely develop at sites of open comedones. They tend
to arise either in a closed comedo or a microcomedo that is only visible in his-
tologic sections. An inflammatory lesion begins either as a follicular papule that
may evolve into a pustule or as a nodule that evolves into a cyst. Severe acne is
characterized by many cysts and is often referred to as cystic acne.
Acne usually persists until the early 20s, although in a few patients particu-
larly women, the disease continues. Scars may follow healing, especially of cysts
or abscesses. Scars may be “ice pick,” atrophic or keloidal.
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Fig. 20.1 Papular comedonal lesions over the face—acne vulgaris

Diagnosis
The combination of comedones, papules, pustules, nodules, and cysts in a
characteristic distribution is diagnostic.

Differential diagnosis
Diagnosis is usually easy but acne may be confused with folliculitis, rosacea (Table
20.1), or perioral dermatitis. These do not have comedones.

Treatment
Four principles in treating acne are:
1. To reverse the hypercornification of pilosebaceous duct.
2. To decrease the population of P. acnes.
3. To decrease sebaceous gland activity.
4. To decrease inflammation.
Local treatment is adequate for mild acne and is used with systemic drugs
for more severe cases.
Local/Topical therapy
1. Benzoyl peroxide 2.5 to 5% is antibacterial and comedolytic, applied once daily.
It should be a mainstay of every acne program, if tolerated. It decreases the
likelihood of bacterial resistance and can bleach the color out of clothing.
 DISORDERS OF SEBACEOUS AND SWEAT GLANDS 227

Table 20.1 Acne vulgaris vs rosacea

Clinical Acne vulgaris Rosacea
parameters
Etiopathogen- Four pathogenetic mechanisms Patients have vasomotor instability
esis involved are increased sebum and exacerbations by hot beverages,
production, comedogenesis, spicy food, alcohol, Demodex, Heli-
Propionibacterium acnes, and cobacter pylori, and HIV
inflammation
Age group Female: 14–17 years 30–50 years; F>M; severe forms in
Male: 16–19 years male
100% in mid-teens
Site Face, neck, and trunk Mid-face (nose, forehead, cheeks,
chin) and eyes, extrafacial—rare
Morphology Polymorphic comedones are the In early stages, presents as erythe-
hallmark of acne. Seborrhea, matotelangiectatic (redness, flush-
inflammatory papules, pustules, ing, telangiectasia) or papulopustular
nodulocystic lesions, and scar- (papules and pustules without come-
ring may occur dones). In late stages, lead to chronic
peau d’orange appearance and rhi-
nophyma. Ocular rosacea presents
as iritis, keratitis, and episcleritis

2. Antibiotics, e.g., clindamycin (1%), erythromycin (2–3%), sodium sulfac-

etamide, and tetracycline.
3. Sulfur and resorcinol, e.g., sulfur calamine lotion.
4. Tretinoin (0.025–0.1% cream or gel)/adapalene (0.1% cream, gel, or solu-
tion)/tazarotene (0.05–0.1% cream or gel) are potent comedolytic agents.
Adapalene is a good first-line therapy in colder climates and in patients
with sensitive skin. Tazarotene can be irritating and should be avoided in
patients with sensitive skin or seborrheic dermatitis. The cream base is
preferred for dry skin and the gels are preferred for oily skin. Instruct the
patients to apply it sparingly at night to the entire face except around the
eyes, lips, and nares and leave it over the face for 20–30 minutes. Wash
it off with a mild gentle soap. Flare up of acne may occur in the first 2–4
weeks which is due to surfacing of the lesions on to the skin. Clearing
requires approximately 3 months. Maintenance therapy with the retinoids
is essential.
5. Salicylic acid is a beta hydroxyl acid that penetrates into the sebaceous
gland and has comedolytic and anti-inflammatory properties. It can be used
as an adjunctive therapy and is found in cleansers, toners, and peels.
6. Azelaic acid (20% cream) is a dicarboxylic acid that has antimicrobial,
anti-inflammatory, and comedolytic activity. It may help lighten postinflam-
matory hyperpigmentation in acne patients.
Systemic therapy
1. Antibiotics (tetracycline, doxycycline, minocycline, erythromycin, azithro-
mycin, and clarithromycin): Tetracycline (250 mg four times daily or 500
228 TEXTBOOK OF DERMATOLOGY, VENEREOLOGY, AND LEPROLOGY

mg twice daily taken on an empty stomach) or doxycycline (100 mg twice

daily) is often the first antibiotic prescribed. The duration of treatment
can be from 2 weeks to 10 months. Minocycline is a useful but expensive
antibiotic. It is overall the most effective antibiotic to treat acne but it can
have serious side effects. Erythromycin is an option for those who cannot
take tetracyclines because of side effects or in pregnant women requiring
oral antibiotic therapy. Pulse therapy with azithromycin and clarithromycin
is in vogue for increasing the patient’s compliance.
2. Dapsone has been used in severe acne conglobata (characterized by nodu-
locystic lesions, intercommunicating sinuses), but is rarely used today.
3. Corticosteroids: Prednisolone 2.5–7.5 mg administered at night or dex-
amethasone 0.25–0.75 mg are useful in female patients with severe acne
unresponsive to conventional therapy, who suffer from adrenal gland over
production of androgens such as congenital adrenal hyperplasia.
4. Oral retinoids: Isotretinoin (0.5–1 mg/kg/day) is the drug of choice for
severe nodulocystic acne unresponsive to other treatment regimens. Most
physicians plan a course of therapy that reaches a total dose of 100–120
mg/kg which may take up to 6 months to achieve. Any women who fail
to respond to isotretinoin should be evaluated for hyperandrogenism. Isot-
retinoin is teratogenic in humans and a pregnancy prevention program may
be initiated before the start of therapy. Men may take isotretinoin without
concern for its teratogenic effects.
5. Oral contraceptives, spironolactone, cyproterone acetate, flutamide, and
gonadotropin releasing hormone agonist may be of use in unresponsive
cases in young women after more conventional regimens have failed.
Adjunctive therapy like intralesional steroids for nodulocystic lesions may be
given. Some cases may require comedone extraction, chemical peels, dermabra-
sion, laser and light therapies, fillers, and other modalities of acne surgeries.

Rosacea
Rosacea is a chronic inflammatory condition of the centrofacial part of the face
(the flush area of the face-nose, cheek, chin, forehead, glabella) characterized
by a prior history of idiopathic facial burning/flushing over a prolonged period,
followed by polymorphic picture of persistent erythema, papules, pustules, te-
langiectasia, thickening and coarsening of the skin, and eventual development
of gross enlargement and deformity of the nose (rhinophyma-phyma, a Greek
word for “swelling, mass, or bulb”). It typically involves fair skinned individuals
in 30–50 years of age, more commonly females.

Treatment
Patients who flush easily should avoid hot food and drinks and activities that
induce this change. These may include tea, coffee, sunlight, extremes of heat
and cold, and emotional stress. Rosacea is difficult to treat, cure often not pos-
sible. Topical therapy with antibiotics (clindamycin 0.5%, erythromycin 2.0%),
metronidazole (0.75%), ketoconazole, or tretinoin (0.025%) and broad-spectrum
 DISORDERS OF SEBACEOUS AND SWEAT GLANDS 229

sunscreens (always recommended to rosacea patients) with or without systemic

therapy may be effective. Generally, systemic therapy with tetracycline, doxycy-
cline, minocycline, or erythromycin is required when papulopustular lesions are
predominant in rosacea. Other drugs used in rosacea are isotretinoin (0.5 mg/
kg body weight), metronidazole (500 mg twice daily), or spironolactone may
be useful. Surgery is required in the successful management of rhinophyma.

Perioral Dermatitis
Perioral dermatitis is basically not dermatitis, but a persistent erythematous
eruption of unknown cause consisting of tiny monomorphous papules and
papulopustules with a distribution primarily around the mouth and not re-
sponsive to topical treatments. Pruritus, burning, and soreness are prominent
symptoms. This condition occurs in young individuals (16–45 years of age).
Exact etiopathogenesis of this disorder is unknown. Topical fluorinated corti-
costeroids exacerbate the condition.

Treatment
All existing topical preparations should be discontinued. A 4-week course of
oral tetracycline (500 mg qid) is usually sufficient to clear the eruption. Recur-
rence after treatment is uncommon.

DISORDERS OF SWEAT GLANDS

Miliaria
Miliaria occurs due to the obstruction of free flow of eccrine sweat to the
skin surface, so the sweat is retained within the skin resulting in a variety of
signs and symptoms. Based on clinical and histopathologic findings, miliaria
is subdivided into four groups: (a) miliaria crystallina, (b) miliaria rubra, (c)
miliaria pustulosa, and (d) miliaria profunda.
Miliaria crystallina (sudamina) consists of superficial, subcorneal, noninflam-
matory vesicles that easily rupture when rubbed with a finger. It usually follows
high-grade fever with profuse perspiration.
Miliaria rubra (prickly heat) is the commonest type of miliaria, which results
when obstructed sweat migrates into the living layers of the epidermis as well
as the upper dermis, causing pruritic inflammatory papules around the sweat
pores. This disorder is common in infants and children but also occurs in adults
after repeated episodes of sweating in a hot, humid environment. Some of the
eruptions of miliaria rubra become pustular, resulting in miliaria pustulosa.
Miliaria profunda results when the sweat leaks into the dermis. During ex-
posure to intense heat, the affected skin can be uniformly covered with multiple
discrete, flesh-colored papules.

Fox-Fordyce Disease
Fox-Fordyce disease is a chronic, pruritic, papular eruption, mainly in women,
with localization to areas bearing apocrine glands (axillae, pubic area, labia,
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perineum, areola, presternal skin, umbilicus, and medial thighs). The eruption
is usually worse in the summer, and it improves with the use of oral contra-
ceptives.

Hidradenitis Suppurativa
Hidradenitis suppurativa is a chronic, inflammatory, scarring disease of the
apocrine sweat gland–bearing skin, characterized by the presence of multiple
abscesses, fibrosis, and sinus tracts.

Follicular Occlusion Tetrad

The concept of follicular occlusion tetrad stems from the concept that hidradeni-
tis suppurativa, acne conglobata, pilonidal sinus, and dissecting cellulitis of the
scalp all share follicular occlusion as an inciting event that eventually leads to
disease expression.