Acne-like rash around the nose and mouth
 - Clinical Advisor

Acne-like rash around the nose and mouth


Slideshow

  • 2014 November Dermatology Clinic

A 71-year-old woman presents with a worsening rash of red bumps on her face that burned and was itchy for 5 months. A topical ointment of hydrocortisone 1% provided some symptom improvement, but the rash seemed to flare when the patient stopped using the ointment, so she used it regularly.

She had not used any new personal-care products and had applied the same moisturizer, day cream, and night cream for years. On physical exam, coalescing erythematous papulovesicles with overlying scale were seen concentrated on the paranasal skin and in the nasolabial folds. Comedones were not present.



This The Clinical Advisor CME activity consists of 3 articles.To obtain credit, read itchy, tense blisters and a desquamating rash on an infant. Then take the post-test here.


Perioral dermatitis is an inflammatory condition characterized by coalescing erythematous papules, vesicles, and pustules around the nose and mouth. As in our case, patients often report use of topical corticosteroids to the face preceding or concurrent with the onset of...

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Perioral dermatitis is an inflammatory condition characterized by coalescing erythematous papules, vesicles, and pustules around the nose and mouth. As in our case, patients often report use of topical corticosteroids to the face preceding or concurrent with the onset of the eruption, but it is unclear if the corticosteroids are causative or curative.


The term perioral dermatitis was coined by Mihan and Ayers in 1964 to describe a cohort of mainly young adult women with a mildly pruritic or burning cyclical eruption of discrete, pinpoint, erythematous papules, vesicles, and pustules around the mouth with variable scaling.1

In searching for a cause, these authors were unable to find Demodex mites on skin scrapings (usually associated with rosacea), and patch testing for an allergic contact dermatitis reaction to cosmetic ingredients was negative. They commented that the condition was refractory to treatment and said caution was needed in prescribing topical medications, which they found to produce local irritation followed by an exacerbation.1

Perioral dermatitis preferentially affects young adult women, usually aged 20 to 45 years.2 Men account for only 10% of cases.2 While uncommon, the condition can also occur in older (as in our case) and pediatric patients.


Patients with perioral dermatitis classically present with multiple, small, coalescing, pink-to-erythematous papules and pinpoint vesiculopustules on an erythematous base with variable scaling

Lesions tend to be more concentrated in the nasolabial folds, around the opening of the nostrils, and on the upper and lower cutaneous lip and chin, with a characteristic 3- to 5-mm zone of sparing at the vermilion border.2,3 Patients may complain of burning, stinging, or itching but are often asymptomatic.3Severity ranges from a few lesions in the typical locations to numerous lesions that can involve nearly the entire face.3

The pathogenesis of perioral dermatitis is unknown. The role of topical corticosteroids in the etiology of perioral dermatitis is unclear, but patients frequently report using them before the appearance of or as therapy for the eruption.

It has been postulated that the immunosuppressive action of topical corticosteroids can modify the skin’s flora toward proliferation of pathogenic microbes, some of which have been cultured from perioral dermatitis lesions.3 In addition, topical corticosteroids cause thinning of the epidermis and reduction in the synthesis of collagen, elastin, and lipids.3

Collectively, these changes lead to increased permeability of the skin, which may predispose patients to increased facial sensitivity to topical agents.3 However, some practitioners employ topical corticosteroids in the treatment of perioral dermatitis for their anti-inflammatory effect. 


Fritsch et al have suggested that perioral dermatitis is caused by the regular use of multiple cosmetics and skin creams.4 They proposed that these emollients alter the barrier function of the stratum corneum with resultant overgrowth of normal skin flora and found that the condition resolved in their study patients within a month of cessation of all topical products.

Similarly, a study by Malik and Quirk demonstrated that use of a foundation, moisturizer, and night cream led to a 13-fold increase in the risk for development of perioral dermatitis.5 Many other factors have been reported as possible causes of this condition, including oral corticosteroids, fluorinated toothpaste, infectious agents, and hormonal therapy.2

The differential diagnosis for perioral dermatitis includes acne, rosacea, seborrheic dermatitis, and other facial eruptions that are more rare. Acne differs from perioral dermatitis in that patients present with open and closed comedones in addition to erythematous papules and pustules; it is more common in adolescents; and lesions are usually localized to the forehead, cheeks, chin, and jawline.

Rosacea tends to affect older adults, and examination reveals facial telangiectasias with papulopustules on the nose and cheeks. Patients often report flushing, which is absent in perioral dermatitis. Seborrheic dermatitis may involve the nasolabial folds but can usually be found on the scalp, eyebrows, beard area, and ears as well. The morphology of seborrheic dermatitis is that of erythematous patches with greasy yellow scale, which helps differentiate it from the discrete papulopustules of perioral dermatitis. 


Skin biopsy is usually not needed, as this is a clinical diagnosis. However, if the presentation is not classic or response to treatment is poor, a small punch biopsy of a given papule should be considered. Histopathology reveals eczematous changes of the follicular epidermis with acanthosis, spongiosis, and parakeratosis, and some have postulated that these superficial changes indicate that there is an externally applied irritant that plays a role in the pathogenesis of the condition.6

There may also be sparse perivascular and perifollicular lymphohistiocytic inflammation. Later lesions may demonstrate granulomatous infiltrates. These histopathologic features resemble those of rosacea, with the exception of the superficial changes.2,6

Many therapies have been used successfully in perioral dermatitis, but the use of these agents is off-label. Minimizing use of topical preparations (e.g., cosmetics, moisturizing creams) can be beneficial, but patients are often reluctant to comply with this option.2

If patients are using topical corticosteroids at presentation, discontinuation is recommended. Despite the possibility that topical agents may play a role in causing the eruption, topical therapies have been effective in clearing the lesions, although preparations that are not ointments are preferred.

Interestingly, some advocate treating patients who had not previously used topical corticosteroids with a low-potency, nonfluorinated topical corticosteroid, but use of these agents should be slowly decreased over time to prevent rebound.2 Topical antibiotics, such as metronidazole, erythromycin, and clindamycin, can be beneficial, but clearance of the eruption often takes a few months, and some patients may experience irritation.3 The anti-inflammatory effects of topical calcineurin inhibitors can also provide relief.3

However, the first-line therapy for perioral dermatitis in patients older than age 8 years and who are not pregnant or breastfeeding is oral tetracycline for a 1- to 2-month treatment course.3 Oral doxycycline and minocycline are also effective but not as well studied as tetracycline.3

Systemic therapy eliminates the need to apply another topical treatment that could potentiate irritation.2 The prognosis is excellent, as the condition tends not to scar. Recurrences are not uncommon.


Our patient discontinued the topical steroids she had been using and initiated treatment with a topical metronidazole cream, which she used twice daily for 1 month. Her rash has cleared with no recurrence after 2 years.

Puja Bharucha is a fourth-year medical student at Virginia Commonwealth University School of Medicine in Richmond, Virginia.

Erin L. Reese, MD, is an assistant professor of dermatology at Virginia Commonwealth University.



This The Clinical Advisor CME activity consists of 3 articles.To obtain credit, read itchy, tense blisters and a desquamating rash on an infant. Then take the post-test here.


References


  1. Mihan R, Ayres Jr S. Perioral dermatitis. Arch Dermatol. 1964;89(6):803-805.

  2. Lipozenčić J, Hadžavdić SL. Perioral dermatitis. Clin Dermatol. 2014;
32(1):125-130.
  3. 
Tempark T, Shwayder TA. Perioral dermatitis: a review of the 
condition with special attention to treatment options. Am J Clin Dermatol. 2014;15(2):101-113.

  4. Fritsch P, Pichler E, Linser I. Perioral dermatitis [article in German]. Hautarzt. 1989;40(8):475-479.

  5. Dirschka T, Tronnier H, Fölster-Holst R. Epithelial barrier function and atopic diathesis in rosacea and perioral dermatitis. Br J Dermatol. 2004;150(6):1136-1141. 

  6. Marks R, Black MM. Perioral dermatitis. a histopathologic study of 26 cases. Br J Dermatol. 1971;84(3):242-247.

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