Chapter 82.Perioral Dermatitis
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Transcript of Chapter 82.Perioral Dermatitis
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7/29/2019 Chapter 82.Perioral Dermatitis
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Chapter 82Perioral Dermatitis
Leslie P. Lawley & Sareeta R.S. Parker
PERIORAL DERMATITIS AT A GLANCE
Inflammatory skin disorder of young women and children. Small papules, vesicles, and pustules in perioral, periorbital, and/or perinasal
distribution.
Treatment: stop topical corticosteroid use; initiate 2- to 3-month course of systemicantibiotics (tetracycline family or erythromycin) and/or topical metronidazole
Perioral dermatitis is characterized by small, discrete papules and pustules in a periorificial
distribution, predominantly around the mouth. Because this condition can involve areas other thanthe perioral region, the term periorificial dermatitis has been proposed for this disorder.1,2 The
classic presentation is an eruption with overlapping features of an eczematous dermatitis and an
acneiform eruption. Although initially described in young women of 1525 years of age, perioral
dermatitis is now recognized to occur in children as well.3 A subset of perioral dermatitis shows
granulomas when lesional skin is examined histologically. Several names have been used to describe
this granulomatous form of perioral dermatitis, including granulomatous perioral dermatitis, facial
Afro-Caribbean childhood eruption, and granulomatous periorificial dermatitis.
HISTORICAL ASPECTS
The first reports describing perioral dermatitis appeared in the 1950s; various names were given to
the condition, however, there was a lack of defining clinical criteria. In 1957, Frumess and Lewis
described a light sensitive seborrheid that is generally accepted as the first account of what was
later termed perioral dermatitis by Mihan and Ayres in 1964.6,7 Later descriptions by Cochran and
Thomson8 and Wilkinson, Kirton, and Wilkinson9 further defined this disorder, and more recently
the term periorificial dermatitis has been proposed.2 The condition was first described in children in
the late 1960s.
EPIDEMIOLOGY
Adult perioral dermatitis predominantly affects women. Pediatric perioral dermatitis may have a
slight female preponderance and is seen equally among those of different races.1,10 The
granulomatous form of perioral dermatitis has been reported mostly in children of prepubertal age.5
Perioral dermatitis can occur as early as 6 months.1 An increased prevalence in African-American
children has been reported, but more recent reviews do not support this finding.2,11
ETIOLOGY AND PATHOGENESIS
A relationship of perioral dermatitis to the misuse of topical corticosteroids (fluorinated or
nonfluorinated) has been well established.12 Patients often reveal a history of an acute steroid-
responsive eruption around the mouth, nose, and/or eyes that worsens when the topicalcorticosteroid is discontinued. Dependency on the use of the topical corticosteroid may develop as
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the patient repeatedly treats the recurrent eruption. In other cases, the condition may worsen with
the application of topical corticosteroids, especially in the granulomatous variant of perioral
dermatitis, which usually occurs in prepubertal children.2 Perioral dermatitis has been reported in
patients using inhaled corticosteroids13 and with inadvertent facial exposure to topical
corticosteroids.14 However, perioral dermatitis is not always linked to topical corticosteroids.9 The
exact cause of perioral dermatitis in these other cases is unclear. Although isolated reports of
affected siblings exist,2,15 no clear genetic predisposition has been noted, nor have specific
environmental exposures been consistently implicated. Of note, the disease is predominant in young
women yet no link to hormonal causes has been found. The initial reports of photosensitivity by
Frumess and Lewis6 were not further substantiated, nor were theories of microbiologic causes such
as infection with Candida, fusiform bacteria, or Demodex folliculorum.16 Cases of allergic contact
with fluorides or other components in toothpaste and dentifrices have also been reported, however,
use of these agents after clearing of the perioral dermatitis without further eruption has also been
described. Patch testing in a small series of patients led to few positive results, and these were not
considered relevant.9
In the past, authors have considered the relationship of perioral dermatitis to acne rosacea,
however, the clinical features are distinct (see Section Differential Diagnosis). In perioral
dermatitis, the histopathologic findings are variable and are dependent on the form of perioral
dermatitis. In a histopathologic review of 26 patients with the nongranulomatous form, follicular
spongiosis and eczematous changes were prominent features, suggesting that perioral dermatitis is
distinct from rosacea.17 A lymphohistiocytic infiltrate and occasional plasma cells were noted in a
perifollicular and perivascular distribution in this series. In granulomatous perioral dermatitis,
histopathology demonstrates follicular hyperkeratosis, edema and vasodilatation in the papillary
dermis, perivascular and parafollicular infiltrates of lymphocytes, histiocytes, andpolymorphonuclear leukocytes with occasional epithelioid granulomas and giant cells, similar to the
histopathologic changes in acne rosacea.5,18
CLINICAL FINDINGS
The primary lesions of perioral dermatitis are discrete and grouped erythematous papules, vesicles,
and pustules (Figs. 82-1 and 82-2). The lesions are often symmetric but may be unilateral and appear
in the perioral, perinasal, and/or periocular regions (Figs. 82-2 and 82-3 and eFigs. 82-3.1 and 82-3.2
in online edition). In a retrospective review of 79 children with perioral dermatitis, isolated perioral
involvement was present in only 39%, and in rare cases nonperioral regions were involved
exclusively.1 Background erythema and/or scale may be present. A distinct 5-mm clear zone at the
vermilion edge is well described (Fig. 82-2). The granulomatous variant of perioral dermatitis
presents with small flesh-colored, erythematous, or yellowbrown papules, some with confluence,
and shares the distribution of perioral dermatitis in adults (Fig. 82-3). In addition, lesions have been
reported to appear on the ears, neck, scalp, trunk, labia majora, and extremities
Occasionally, an associated burning sensation or itching is reported, and intolerance to moisturizers
and other topical products is described.1,9 In a few cases of granulomatous perioral dermatitis, an
associated blepharitis or conjunctivitis has been reported.11 Systemic findings and regional
lymphadenopathy are absent.
DIFFERENTIAL DIAGNOSIS
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The differential diagnosis of nongranulomatous and granulomatous perioral dermatitis is outlined in
Box 82-1.1924 Both forms of perioral dermatitis lack systemic symptoms and a thorough history
and physical examination are generally sufficient to establish the diagnosis. However, in some cases
histopathological evaluation of lesional skin, chest radiography, and/or ophthalmologic examination
may be necessary, particularly with the granulomatous variant.11 Sarcoidosis in young children is
rare and often accompanied by systemic signs and symptoms such as weight loss, fatigue, joint
pains, lymphadenopathy, and uveitis.5,25 At least some of the reported cases of sarcoidosis in young
children represent Blau syndrome with underlying mutations in CARD15/NOD2 (see Chapter 134).
COMPLICATIONS
The majority of cases of perioral dermatitis and granulomatous perioral dermatitis resolve without
sequelae or relapse. However, there are rare reports of scarring
PROGNOSIS AND CLINICAL COURSE
Perioral dermatitis is usually a self-limited disorder that evolves over a few weeks and resolves over
months or rarely years. The condition may take on a waxing and waning course, often with a
tendency to progress (granulomatous form). If treated with topical corticosteroids alone, recurrent
episodes on withdrawal of therapy or with continuing therapy are typical. With appropriate
intervention the condition resolves with rare recurrences.
TREATMENT
If topical corticosteroids are being used, they should be discontinued. If fluorinated corticosteroids
are being applied, initial substitution with a low-potency hydrocortisone cream may minimize a flare
of the dermatitis. Patients should be educated about the link between application of topical
corticosteroids and exacerbation of the dermatitis.
In most cases, effective therapy is oral tetracycline, doxycycline, or minocycline, for a course of 8 to
10 weeks, with a taper over the last 2 to 4 weeks. In children under 8 years of age, nursing mothers,
or tetracycline-allergic patients, oral erythromycin is recommended. Not uncommonly, patients
require continued low-dose systemic antibiotic therapy for months or sometimes years to maintain
control. In recalcitrant cases, isotretinoin may be considered.27
Topical antibiotic therapy, most commonly with topical metronidazole, should be initiated
concurrently with the systemic antibiotic. For milder cases, topical metronidazole alone maysuffice.1,28,29 In a retrospective review of 79 children, best outcomes were associated with the use
of topical metronidazole, oral erythromycin, or both.1 Response is generally noted within 23
months. Other options include topical clindamycin or erythromycin, topical sulfur-based
preparations, and topical azelaic acid.30 Reports of successful use of topical calcineurin inhibitors
exist, particularly in adults; however, caution is advised given the occasional reports of
granulomatous eruptions after the use of these agents.3135 Ointment preparations should
generally be avoided in the treatment of perioral dermatitis. Photodynamic therapy with topical 5-
aminolevulinic acid has shown promise for treating perioral dermatitis in one report.36
PREVENTION
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The only widely accepted factor that may predispose to the development of perioral dermatitis is
the use of topical corticosteroids. Avoiding facial skin exposure to these products may prevent the
eruption in some case