Facial hyperpigmentation caused by pigmented demodicosis

Dear Editors,

We present a case of facial hyperpigmentation caused by demodicosis in an adolescent. Demodicosis is a skin condition due to the overgrowth of Demodex mites, primarily Demodex folliculorum and Demodex brevis. These ectoparasites are obligate inhabitants of human skin, particularly in the sebaceous glands and hair follicles, but can become relevant under certain conditions, such as immunosuppression, pityriasis folliculorum, or chronic skin disorders like rosacea. ¹ Recently, it has also been described as a cause of facial hyperpigmentation, leading to the term “pigmented demodicosis”. We report a case of facial hyperpigmentation caused by Demodex mites and successful treatment.

A 16‐year‐old male patient presented with progressing asymptomatic hyperpigmentation on his face. His medical history was devoid of any significant findings. Previous treatments included topical retinoid (0,1% adapalene) and hydroquinone 5% without any noticeable improvement. Two months before the consultation at our clinic, the patient initiated treatment with oral isotretinoin at 10 mg per day.

Dermatological examination revealed dusky brown‐grey macules on his cheeks, forehead, and temples, developing into larger patches over the past 2 years (Figure 1a). A previous biopsy described lymphocytic infiltration and melanophages in favor of postinflammatory hyperpigmentation or lichenoid dermatitis. Therefore, we repeated the biopsy to differentiate between our differential diagnoses, including lichen planus pigmentosus, erythema dyschromicum perstans, and rosacea. Histopathological examination presented Demodex mites in dilated hair follicles, melanophages and perivascular lymphocytic infiltration (Figure 1b).

FIGURE 1.

(a) A 16‐year‐old patient with dusky brown‐grey macules on his cheeks, forehead, and temples. (b) Histologic evaluation with hematoxylin‐eosin staining reveals a dilated hair follicle with Demodex folliculorum (arrowhead).

Taking histopathology findings, such as a combination of mites, interface reaction of the hair follicle epithelium into account with the clinical presentation we diagnosed pigmented demodicosis. In addition to systemic retinoid treatment, we initiated ivermectin 1% cream once daily. During the follow‐up visit, a significant improvement in overall hyperpigmentation and skin texture was observed after just 3 months of treatment (Figure 2).

FIGURE 2.

Follow‐up visit after three months.

Demodex mites are commensal ectoparasites. Only Demodex brevis and Demodex folliculorum have been identified on human skin. ² The overproliferation of Demodex mites can trigger inflammatory responses and play a role in skin conditions such as rosacea. Treatment generally includes topical anti‐demodectic agents, such as ivermectin, aimed at reducing mite populations and alleviating symptoms. Demodex‐induced facial hyperpigmentation is still an underdiagnosed cause of facial hyperpigmentation. Feuerstein et al. published a case series and proposed the term “pigmented demodicosis”. ³ To diagnose demodicosis, the literature has also described additional dermoscopic findings, such as white gelatinous protrusions from the hair follicle (representing mite abdomen) and lesional perifollicular reticulated pigmentation. ³

Facial hyperpigmentation is among the top five major concerns in patients with skin of color, significantly impacting quality of life. ⁴ , ⁵ Common differential considerations in facial hyperpigmentation are lichen planus pigmentosus, melasma, post‐inflammatory hyperpigmentation, and erythema dyschromicum perstans.

With this case, we want to highlight that demodicosis should be considered a differential diagnosis in cases of chronic or treatment‐resistant facial hyperpigmentation. Early recognition and appropriate therapy can lead to significant clinical improvement.

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