CASE #1: Xanthelasma palpebrarum
Xanthelasma (or xanthelasma palpebrarum) is a yellow plaque that occurs on the eyelids. The word is derived from the Greek terms xanthos (yellow) combined with the elasma (beaten metal plate). The yellow color is a visual manifestation of esterified cholesterol in the middle and superficial layers of the dermis (and more rarely in the subcutaneous fat) that has been swallowed by macrophages. The upper eyelid is more affected than the lower eyelid, and the inner canthus of the eye is more affected than the lateral canthus.
The term xanthoma refers to fatty deposits that are histologically the same as xanthelasma but occur off the eyelid. However, a variant system of nosology suggests that xanthelasma may instead be referred to as a xanthoma when becoming larger and nodular, manifesting in tumorous dimension. Xanthelasma is not uncommon and is much more prevalent than xanthoma.
Xanthelasma is usually yellow in color but can appear white, particularly if the epidermis is removed. On palpation, the lesion can be soft or hard. Frequently, xanthelasmas are symmetrical, involving upper and lower and right and left eyelids. Xanthelasmas have a tendency to progress, coalesce and become permanent. It is thought that xanthelasma occurs on the eyelid because that structure is mechanically stressed and the surrounding is usually in rapid positional flux.
Once formed, xanthelasma typically remains static or increases in size; the lesions rarely disappear spontaneously. More common in women,1 xanthelasma can manifest at any age. The lesions seem to occur in all groups, and may be more frequent in people of Asian origin and those from the Mediterranean region.1 The mechanism that starts macrophage accumulation, cholesterol uptake, and foam-cell formation in a normolipemic patient following an inflammatory skin disorder remains undefined. It is thought that increased plasma lipid peroxidation (coming from oxidized LDL) could initiate accumulation of cholesterol in macrophages and the transformation to foam cells.
Xanthelasmata are cosmetically unacceptable to most patients. Some note that the lesions obscure vision, but the pupil, sclera, or eyelid are not affected directly.
Some types and cases of xanthoma suggest coincident lipid metabolism disorders (e.g. hyperlipidemia or high blood fats). Half of xanthelasmata are associated with elevated plasma lipid levels.1 Thus, xanthoma can be linked to heart disease, circulatory disease (i.e., atheromatous disease, high lipids), and, occasionally, pancreatitis (acute pancreatitis during hyperlipoproteinemic crisis, aggravation of insulin resistance and decompensation of type 2 diabetes mellitus).
Xanthelasma most likely manifest in patients with type II and type IV hyperlipidemia.1 A study of almost 13,000 people found that individuals with xanthelasma are 12% more likely to suffer from heart disease and more likely to have a heart attack or die within 10 years.2 Treating these conditions can aid in the resolution of the xanthomas.
Xanthelasma presents a wide differential diagnosis that includes: (1) xanthogranulomatous inflammation of the orbit with a prominent population of immunoglobulin (Ig)G4-positive plasma cells, which might be a novel variant of IgG4 sclerosing disease of the orbit; (2) diffuse plane xanthomas are characterized by the presence of yellowish plaques on the eyelids, neck, upper trunk, buttocks, and flexural folds; histology shows foamy histiocytes in the dermis; approximately half of diffuse plane xanthomas are associated with lymphoproliferative disorders; (3) atypical lymphoid hyperplasia; (4) necrobiotic xanthogranuloma; (5) sebaceous hyperplasia; (6) sebaceous carcinoma; and (7) Erdheim-Chester disease.
Treatment of xanthomas is surgical rather than medical. A variety of options exist for the removal of xanthelasma palpebrarum, including surgical excision, argon and carbon dioxide laser ablation, chemical peeling, electrodesiccation and curettage, and cryotherapy.3
Surgery can involve simple excision, as scarring tends to blend in with the surrounding eyelid wrinkles. Techniques can entail blepharoplasty with extension of the excision and incision parameters. Smaller bulging xanthelasmata may be “uncapped” and excised with a flap that can be replaced and sutured.
Another method uses a surgical microscope to undermine between the xanthelasma and the orbicularis oculi with a #11 scalpel blade, raise the flap, carefully remove the xanthelasma bit by bit with microscissors from the reverse side and then suture the flap with 7-0 nylon.4
There are surgical risks, however. Full-thickness and lower-lid lesions are more complex to remove than thinner upper-lid xanthelasma. Side effects include risk of eyelid retraction and ectropion. An individual who has repeated excision and blepharoplasty should be warned of lagophthalmos secondary to the medial position and absence of medial dermatochalasis. Scar tissue will complicate subsequent surgeries. Xanthelasma can infiltrate into surgical scars, again complicating repeat surgeries.
Laser ablation is often used to treat xanthelasma. Carbon dioxide5 and argon lasers3 are the most common lasers used. Laser treatment obviates the need for sutures, does not involve bleeding, minimizing issues with hemostasis, and does not involve direct contact with the xanthelasma, allowing for improved visualization and is a rapid procedure. Scarring and pigment alteration are the chief side effects of laser treatment of xanthelasma.
The 1064-nm Q-switched Nd:YAG laser has also been used to treat xanthelasma.6 This valuable treatment option eliminates lesions rapidly and results in good healing. The absence of any associated skin destruction allows treatment to be repeated when necessary.
Peeling agents are useful for treating xanthelasma when the epidermis of the eye is very thin and the dermis is close to the outside air. Such chlorinated acetic acids as monochloroacetic acid, dichloroacetic acid and trichloroacetic acid (TCA) precipitate and coagulate proteins and dissolve lipids. These agents have been found to be effective in the removal of xanthelasma.7 Haygood et al deployed ≤0.01 mL of 100% dichloroacetic acid, noting excellent effect and minimal scarring.8 In my experience, 20%-30% TCA is the most widely used type and concentration of acid used in the treatment of this condition.
Electrodesiccation and curettage and cryotherapy can destroy superficial xanthelasmas but may require repeated treatments. Electrodessication and curettage is inexpensive, effective and does not cause bleeding. While this procedure occasionally leaves some fatty histiocytes behind, it flattens lesions and renders them much more cosmetically acceptable. Cryotherapy may cause scarring and hypopigmentation and is disfavored.
This patient’s yellow plaque and papule were removed with electrodesiccation and curettage. Three days later, the regions had healed, and the patient was happy with the cosmetic results.