Journal of Dermatology & Dermatologic Surgery

: 2022  |  Volume : 26  |  Issue : 3  |  Page : 5--7

Madarosis in a normolipidemic woman: Is giant xanthelasma palpebrarum the culprit?

Saloni Desai, Hari Pathave, Abigail Syiemlieh, Chitra Nayak 
 Department of Dermatology, BYL Nair Ch. Hospital and TNMC, Mumbai, Maharashtra, India

Correspondence Address:
Dr. Hari Pathave
Department of Dermatology, BYL Nair Ch. Hospital and TNMC, Mumbai, Maharashtra


Xanthelasma palpebrarum (XP) is the most common cutaneous xanthoma. It is triggered by hyperlipidemia, thyroid dysfunction, and diabetes mellitus. Madarosis, loss of eyebrows, occurs in various diseases ranging from local dermatological disorders to complex systemic diseases. Herein, we present a case of giant XP in a middle-aged female in whom bilateral partial madarosis developed. In polarized contact dermoscopy, the number of hairs on xanthoma plaque was reduced compared to normal.

How to cite this article:
Desai S, Pathave H, Syiemlieh A, Nayak C. Madarosis in a normolipidemic woman: Is giant xanthelasma palpebrarum the culprit?.J Dermatol Dermatol Surg 2022;26:5-7

How to cite this URL:
Desai S, Pathave H, Syiemlieh A, Nayak C. Madarosis in a normolipidemic woman: Is giant xanthelasma palpebrarum the culprit?. J Dermatol Dermatol Surg [serial online] 2022 [cited 2023 Mar 21 ];26:5-7
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Full Text


Cutaneous xanthomas are plaque-like infiltrations and present in a variety of morphologies with a characteristic yellow or orange hue. They develop due to intracellular and dermal deposition of lipid. Xanthelasma palpebrarum (XP) is the most common cutaneous xanthoma, characterized by yellowish plaques occurring most commonly near the inner canthus of the eyelid. Madarosis is the decrease or complete loss of eyebrows, known as supraciliary madarosis, or eyelashes, known as ciliary madarosis. We present a case where giant XP was the probable reason for madarosis in a middle-aged female.

 Case Report

A 30-year-old female presented to us with asymptomatic, yellowish, raised areas around both eyes for 2 years with partial loss of both eyebrows that started immediately following the lesions. The hair loss progressed gradually over the next 2 years from lateral to medial side but remained confined to bilateral eyebrow areas. The patient denied any hair removal, trauma, or application of local irritants. There was no history of red, raised or scaly or light-colored, hypoesthetic lesions or decrease in sensations elsewhere on the body, or any history suggestive of atopic diathesis. There was no history of diabetes mellit'yroid disease, hypertension, or cardiovascular disease.

Cutaneous examination revealed bilaterally symmetrical, yellowish plaques with irregular, geographic borders on upper and lower lids, extending to malar and bilateral zygomatic areas and upward to eyebrows, with no surface changes [Figure 1]a. There was evident loss of bilateral eyebrows, more on the lateral side than medial [Figure 1]b and [Figure 1]c. Polarized contact dermoscopy showed a significant decrease in number of hairs on xanthelasma areas [Figure 2]a and [Figure 2]b. Sensations on the lesion as well as elsewhere were intact, and the supraorbital, supratrochlear, and infraorbital nerves were nonpalpable. Serum lipid profiles including serum triglyceride, total cholesterol, and high-density lipoprotein (HDL) levels were normal, with normal blood sugar and thyroid profile.{Figure 1}{Figure 2}

Biopsy from the yellow plaque on the eyebrow showed interstitial and perivascular infiltrate of lipid-laden, foamy histiocytes and lymphocytes in the mid and deep dermis [Figure 3]a and [Figure 3]b. The infiltrate was granulomatous with foamy histiocytes, few epithelioid cells, and lymphocytes without Touton giant cells [Figure 3]c. There was no proliferation of histiocytes and no background of inflammatory stroma. There was no palisading xanthogranulomas with foci of necrobiosis in the dermis or panniculus. The upper dermis showed widely spaced collagen fibers without foamy cells, and the sparing of nerves as well as arrector pili. Ziehl-Neelsen and Fite-Faraco stains did not reveal bacilli. We could not perform special stains (Oil Red O or Sudan Black B) due to unavailability of the facility in our institute.{Figure 3}

Weekly application of trichloroacetic acid was planned to be carried out in sections due to the extensive lesions; however, the patient has since been lost to follow-up.


XP is seen more commonly in females (prevalence of 1.1% in females as compared to 0.3% in males)[1] with peak incidence in the age group of 30–50 years.[2] In about 50% of patients, it is associated with hyperlipidemias such as type II hyperlipidemia and type IV hyperlipidemia, also known as familial hypertriglyceridemia. Secondary hyperlipidemias, which can result from hypothyroidism; diabetes mellitus; primary biliary cirrhosis; drug intake such as glucocorticoids, estrogens, and anabolic steroids; and diets rich in saturated fats, cholesterol, and alcohol have also been associated with XP. It also occurs in normolipidemic persons with low HDL levels and in patients with allergic contact dermatitis, erythroderma, or other inflammatory skin disorders.

The lesions of XP present as soft, yellowish papules and plaques over the medial canthus of the upper lid, and do not show spontaneous regression. Xanthelasmas, in general, are a major cause for cosmetic concern, and treatment options include surgical excision, radiofrequency excision, ablative laser therapy, trichloroacetic acid, or cryotherapy.

Madarosis is derived from the Greek word “madaros,” meaning “bald.” Supraciliary madarosis is the most common ocular lesion (76%) in leprosy patients.[3] Other systemic causes include syphilis, myxedema, scleroderma, and systemic lupus erythematosus. Local causes include trauma, burns, radiation therapy, squamous cell carcinoma, basal cell carcinoma,[4] alopecia areata, and trichotillomania.[5] Medications that can cause madarosis include anticoagulants and anticholinergics.

Our patient presented with loss of eyebrows following the appearance of xanthelasma without any other associated skin lesions or systemic comorbidities and histopathology consistent with XP. Hence, the most probable cause of the madarosis in our patient, by exclusion, is xanthelasma.

Although lipids are a small part of hair composition, cholesterol plays important roles in hair biology.[6] Peroxisome proliferator-activated receptor-gamma deficiency is associated with cicatricial alopecia.[7],[8] Accumulation of sterol precursors in the hair follicle epithelium of mice, causes distortion of whiskers and hair shafts; ectatic, keratin-plugged distal follicles; and abnormally arrested catagen/telogen forms.[9] We propose that a similar such effect caused by local lipid deposition may have led to loss of hair follicles in our case.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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