A 55-Year-Old Woman With Bumps on Her Face

Amin Esfahani, MD; Mary E. Lohman, BA; Anne Laumann, MBChB, MRCP(UK)


October 11, 2017

Clinical exacerbation of the flushing associated with rosacea has been linked to numerous "triggers." This extensive list includes sun exposure, alcohol consumption, exercise, exposure to extremes of temperature, various emotions, and spicy foods.

Rosacea is a clinical diagnosis. Diagnostic studies, including skin biopsy, are rarely indicated. The differential diagnosis varies, depending on the type of rosacea. For the erythematotelangiectatic type, the differential diagnosis includes chronic sun-damaged skin. Location can be used to distinguish rosacea from sun damage. Rosacea is generally limited to the centrofacial region, whereas chronic sun damage usually includes the lateral cheeks and neck. Seborrheic dermatitis can present with similar eyelid findings; however, perinasal erythema, the presence of greasy, yellow scale and the involvement of eyebrows, ears (retroauricular), and scalp are distinguishing features.

When evaluating patients with centrofacial erythema, it is important to keep in mind the malar erythema seen in patients with systemic lupus erythematosus. Patients with lupus may or may not be aware of photosensitivity; however, their malar lesions are often more floridly red in character, with well-demarcated borders. A clinical history and a detailed review of systems are useful when distinguishing these entities. This is especially important in people with darker skin tones because erythema in darker skin tones can appear violaceous. In general, unless suspicion is high, an autoimmune panel and other laboratory tests are not indicated. Other flushing disorders are included in the differential diagnosis, such as medication-induced flushing menopausal hot flashes and malignancies, like carcinoid syndromepheochromocytoma, and medullary thyroid carcinoma.[1]

The differential diagnosis for papulopustular rosacea includes acne vulgarisperiorificial dermatitis, steroid-induced rosacea, Demodex folliculitis, papulopustular eruptions due to epidermal growth-factor receptor (EGFR) inhibitors, and keratosis pilaris rubra faciei. Unlike acne, papulopustular rosacea lacks comedones. Periorificial dermatitis can be distinguished from rosacea by location (surrounding mouth, eyes) and papulopustules at the same stage of development. Patients with periorificial dermatitis can have a history of topical or inhaled corticosteroid use, and might describe symptoms of sun intolerance or sensitivity to cosmetics and hot water. No relapse typically occurs after successful treatment; in contrast, in patients with rosacea, flaring is seen after the discontinuation of therapy.

The use of potent topical steroids can lead to steroid-induced rosacea. An example is shown in Figure 6. Papulopustular lesions in this entity are monomorphic. However, given that the appearance is similar to rosacea, a detailed history of medications is crucial. The appearance of Demodex folliculitis (demodicosis) and papulopustular rosacea is similar.

Figure 6.

Immunocompromised patients are at increased risk for demodicosis. Diagnosis can be made on the basis of clinical history and a potassium hydroxide (KOH) preparation that demonstrates many mites. Demodex mites are also present in those with normal skin, but at a lower concentration.

Similar lesions have been seen in patients treated with EGFR inhibitors, so a detailed disease-course, medication, and medical history is necessary. Keratosis pilaris rubra faciei can occur as a manifestation of keratosis pilaris, with rough, erythematous, symmetric triangular patches of skin on both cheeks, at times with overlying 1 to 2 mm follicular-based papules. The presence of keratosis pilaris and a lack of pustules can guide diagnosis.


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