An 11-year-old comes into the office with an asymptomatic slowly progressive eruption that began 3 years prior. The problem is finally resolved with topical and/or systemic treatment.
» How would you treat her?
» What's the diagnosis?
An unhappy mother tells you that she is not leaving the office until you make her daughter's face normal again. The healthy 11-year-old girl has had an asymptomatic, slowly progressive eruption that started around her mouth three years ago.
Diagnosis: Periorificial dermatitis
Periorificial dermatitis (PD) is a common acneiform eruption of unknown origin most commonly found around the mouth, but lesions often spread around the nose and eyes.1-8 Although PD may develop without antecedent use of topical steroids, it is often triggered by the chronic use of topical steroids for a pre-existing dermatosis, such as a contact dermatitis, and may persist for months to years.
This primarily facial eruption affects young women most commonly as well as children, and has an incidence of 0.5% to 1% in industrialized countries independent of geographic factors.1 Medications in use at the time of diagnosis included topical steroids (66%) and topical antifungals (20%).8
PD's clinical and histologic features overlap with acne rosacea, suggesting common triggering factors.
Clusters of follicular-bases red papules, papulo-vesicles, and papulopustules develop on a red base. They may become confluent around the mouth, but typically spare the vermillion border and the immediately surrounding skin. Similar lesions may develop around the nose and on the eye lids.
In a recent case series of about 80 affected children, erythema, scaling, or both were noted in 86% of patients, papules were noted in 66%, and pustules in 11%. Isolated perioral involvement was seen in 39% of patients, perinasal alone in 13%, periocular alone in 1%, perioral and perinasal in 14%, perinasal and periocular in 6%, perioral and periocular in 6%, and perioral and perinasal and periocular in 10%.8 Although PD is usually asymptomatic, mild pruritus is reported in 19% of patients, and 4% complained of burning or tenderness.8
The etiology of periorificial dermatitis is unknown; however, the chronic use of topical steroids for minor facial dermatoses has been implicated as a causative factor in many patients. Recently, neurogenic inflammation has also been proposed as a pathogenic mechanism. For some, skin care ointments and creams, especially those with a petrolatum or paraffin base, and the vehicle isopropyl myristate may trigger the eruption.1 Gastrointestinal disturbances, such as malabsorption, may be a predisposing factor. Although Fusiform spirilla bacteria, Candida species, and other fungi have been cultured from lesions, their role in PD is unclear.
The histopathologic findings in periorificial dermatitis are variable. Characteristic pathology described in 26 patients showed spongiotic changes in the external root sheaths of the follicles without similarity to rosacea.9 However, many histologic findings overlap with acne rosacea. They include follicular hyperkeratosis, edema and vasodilation of the papillary dermis, and perivascular and parafollicular infiltrates of lymphocytes, histiocytes, and polymorphonuclear leukocytes with occasional epithelioid granulomas and giant cells.5,10
The differential diagnosis for periorificial dermatitis includes acne vulgaris, contact dermatitis, rosacea, seborrheic dermatitis and folliculitis.11 Rosacea can be distinguished by its association with frequent flushing, erythema and telangiectasia, ocular involvement (eg, blepharitis, conjunctival hyperemia, keratitis, and iritis), and associated rhinophyma.12 In seborrheic dermatitis there is usually accentuation along the nasolabial folds. Contact dermatitis, which is most frequently caused by food, saliva and tartar control toothpaste, involves the vermillion border and immediately surrounding perioral skin. Comedones, which are characteristic of acne vulgaris, are absent in periorificial dermatitis. Bacterial or fungal folliculitis are not restricted to a periorificial distribution.
Topical antibiotics including metrinidazole, erythromycin, mupirocin, and sulfacetamide have been reported to successfully treat PD.8 However, when these agents fail or the skin is too irritated to tolerate topical therapy, oral antibiotics including erythromycin (30 mg/kg/day divided in three doses) in preadolescents and tetracycline derivatives in adolescents (at doses used for acne vulgaris) are usually effective. Providers should emphasize that patients may require two to three months of therapy to clear, and they should not anticipate much improvement for at least two to four weeks.7
MS. FATUSIN is a fourth-year medical student at Johns Hopkins University School of Medicine, Baltimore.
DR. PUTTGEN is an assistant professor of pediatric dermatology at Johns Hopkins University School of Medicine.
DR. COHEN, who serves as section editor for Dermatology: What's your Dx?, is director, Pediatric Dermatology and Cutaneous Laser Center, and professor of pediatrics and dermatology, Johns Hopkins University School of Medicine, Baltimore. He is a contributing editor of Contemporary Pediatrics.
The authors and section editor have nothing to disclose in regard to affiliations with, or financial interests in, any organization that may have an interest in any part of this article.
Vignettes are based on real cases which have been modified to allow the authors and editor to focus on key teaching points. Images may also be edited or substituted for teaching purposes.
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