Xanthelasma palpebrarum is a prevalent, benign dermatologic condition characterized by the formation of yellow-white, lipid-laden plaques on the upper and lower eyelids, most commonly near the inner canthus.[1, 2] While xanthelasma can be associated with dyslipidemias, the majority of patients do not exhibit abnormal lipid profiles.
Clinically, xanthelasma can present as soft, semisolid, or calcareous plaques, often symmetrical, and may involve all four eyelids. The condition is progressive, with lesions tending to coalesce and become permanent over time. The term "xanthelasma" is derived from the Greek words "xanthos" (yellow) and "elasma" (beaten metal plate), indicative of its distinctive coloration and texture. Regular monitoring and patient education regarding potential lipid abnormalities are recommended.
![]() View Image | Xanthelesma of four eyelids in patient with hyperlipidemia. |
Diagnosis is primarily clinical, based on the characteristic appearance of the lesions.[1, 2] Although treatment is not medically necessary, excision or other removal methods may be considered for cosmetic reasons. It is essential to evaluate and manage any underlying dyslipidemias, as they may pose cardiovascular risks.
Xanthelasma are a specific type of xanthoma that appear on the eyelids. They are deposits of yellowish, cholesterol-rich material that can develop in various parts of the body due to different disease conditions. Xanthomas represent cutaneous signs of lipidosis, where lipids accumulate in foam cells within the skin; they often are linked to hyperlipidemias, which can be either primary or secondary. Some cases are associated with changes in lipoprotein composition or structure, such as reduced levels of high-density lipoprotein (HDL). These lesions commonly are found in patients with type II hyperlipidemia and the type IV phenotype.
Individuals with XP exhibit higher levels of atherogenic LDL and a significantly increased risk for atherosclerosis compared to controls, highlighting the need for careful monitoring and targeted interventions to prevent cardiovascular diseases in these patients.[1]
United States
Xanthelasma are not uncommon.
International
In India, the incidence of xanthelasma may range from 0.3%-1.5%.[3]
These lesions have no premalignant potential; however, see Differentials.
A study by Christoffersen et al finds that xanthelasmata can be a predictor of risk for myocardial infarction, ischemic heart disease, severe atherosclerosis, and death in the general population, independent of well-known cardiovascular risk factors (eg, plasma cholesterol, triglyceride concentrations). On the other hand, arcus senilis of the cornea has been found not to be an important independent predictor of risk.[4]
In case studies of patients with xanthomatosis, a predominance of xanthelasma in women has been seen; women, 32%, and men, 17.4%.
The age of onset ranges from 15-73 years, with a peak in the fourth and fifth decades.
Recurrence is common. Patients need to be aware that studies completed after surgical excision showed recurrence in up to 40% of patients. This percentage is higher with secondary excisions. Of these failures, 26% occurred within the first year and were more likely to occur in patients with hyperlipidemia syndromes and in those with all four eyelids affected.
Xanthelasma are the most common type of xanthoma.[2] They often present in the absence of xanthomas elsewhere on the body, although, histologically, they are the same.
Once plaques are established, they will remain static or increase in size.
Patients generally present with concerns of their appearance, rather than symptoms of discomfort or inflammation.
Xanthelasma or xanthoma palpebrarum usually are located on the medial side of the upper eyelids.
Lesions are yellowish and soft, and they form plaques.
Generally, these lesions do not affect the function of the eyelids, but ptosis has been known to occur.
Many individuals with xanthelasma have a lipid disorder. Many xanthelasma occur in normolipemic persons who may have low HDL cholesterol levels or other lipoprotein abnormalities.
Eruptive xanthomas can be seen in primary and secondary causes of hyperlipidemia.
Examples of primary genetic causes include familial dyslipoproteinemia, familial hypertriglyceridemia, and familial lipoprotein lipase deficiency.
Secondary causes of hyperlipidemia include those related to various diets, drugs, disorders of metabolism, and some diseases. Diets rich in saturated fats and cholesterol, alcohol excess, and weight gain can cause severe but reversible hypercholesterolemia. Drugs that may cause altered lipid profiles include glucocorticoids, estrogens, anabolic steroids, some antihypertensive medications, retinoids, cyclosporine, cimetidine, certain antiepileptic drugs, and tamoxifen. Hypothyroidism is the most common secondary cause of hyperlipidemia after dietary causes are considered.
Uncontrolled diabetes is a common cause of secondary hyperlipidemia.
More than 50% of patients with xanthelasma have lipid disorders; therefore, it is recommended that plasma lipid levels initially be obtained on all patients presenting with significant xanthelesma.[1] These should include LDL cholesterol and HDL cholesterol levels, triglyceride level, and apolipoprotein B100 level. Xanthelasma usually are an obvious clinical diagnosis, but, in rare cases, other lesions can simulate the appearance and may be associated with disorders of a more serious nature. If there is any doubt, surgical excision and pathologic analysis should be performed.
Xanthelasma are composed of xanthoma cells. These are foamy histiocytes laden with intracellular fat deposits primarily within the upper reticular dermis. The main lipid that is stored in hyperlipidemic and normolipidemic xanthelasmas is cholesterol. Most of this cholesterol is esterified.
Dietary restriction and pharmacologic reduction of serum lipids, although important in the overall care of a patient with abnormal lipids, yield only limited response in the treatment of xanthelasma.
Numerous options are available for the removal of xanthelasma palpebrarum, including surgical excision, argon and carbon dioxide laser ablation, chemical cauterization, electrodesiccation, and cryotherapy.
For small linear lesions, excision is recommended, as scarring should blend in with the surrounding eyelid tissue. Smaller bulging lesions can be "uncapped" and removed; then, the flap can be replaced and sutured.
Doi recommends using a surgical microscope, undermining between the tumor and the orbicularis oculi with an 11 blade, raising the flap and carefully removing the tumor piece by piece with microscissors from the reverse side, and then suturing the flap with 7-0 nylon.[6]
In full-thickness excisions, the lower lid is more prone to prominent scarring, as the tissue tends to be thicker. Simple excision of larger lesions risks eyelid retraction, ectropion, or the need for more complicated reconstructive procedures. When xanthelasma removal has been incorporated into routine blepharoplasty, extending the incisional limits increases the risk for ectropion or webbing.
![]() View Image | Case presentation of excision of recurrent xanthelasma. Recurrent xanthelasma bilateral upper lids; previous excision combined with blepharoplasty; pa.... |
![]() View Image | Close-up view of recurrent xanthelasma right upper lid. Note the scar from previous excision by a plastic surgeon. Careful examination reveals subtle .... |
![]() View Image | Xanthelasma. External view, 1 week after surgery. Sliding and rotational flaps from residual lateral dermatochalasis used for medial excisional gap. |
![]() View Image | Xanthelasma. Top image, 4 weeks after surgery; lower image, before surgery. |
Carbon dioxide, yttrium aluminum garnet, pulsed dye, argon, and 1450 nm diode laser have been laser modalities used in treatment of xanthelesma.[7] The carbon dioxide laser was the most commonly reported modality. Enhanced hemostasis, better visualization, lack of suturing, and speed have been cited as reasons to use these techniques. Scarring and pigmentary changes can occur. In a retrospective study involving the use of a 1064-nm, Q-switched Nd:YAG laser, 46 patients had significant clearing of lesions after 4 laser sessions.[8]
Tuan et al studied the efficacy and safety of fractional carbon dioxide (CO2) laser versus fractional Er:YAG laser in treating xanthelasma palpebrarum (XP).[9] Patients with bilaterally symmetrical lesions were recruited from two centers, with one lesion randomly assigned to receive CO2 laser treatment and the other assigned to Er:YAG laser treatment (39 patients; 82 lesions available for final assessment).
There was a significantly higher percentage of "Excellent Improvement" for the CO2 laser group at the third visit (60.98% compared to 39.02%) and at the fourth visit (90.24% compared to 63.41%), with p < 0.05. In the follow-up period of 12 to 25 months. Recurrence rates were similar for both treatments, with 22% for CO2 laser and 24% for Er:YAG laser. The researchers concluded that fractional CO2 laser therapy is more effective, as it requires fewer treatments to achieve significant clinical improvement in patients with XP.
The use of chlorinated acetic acids has been found to be effective in the removal of xanthelasma. These agents precipitate and coagulate proteins and dissolve lipids. Monochloroacetic acid, dichloroacetic acid, and trichloroacetic acid (TCA) have been used with good results. Haygood used less than 0.01 mL of 100% dichloroacetic acid with excellent results and minimal scarring.[10] TCA treatment has been advocated prior to surgical excision to cause initial shrinkage of the lesions.[11] Intralesional heparin sodium[12] and pingyangmycin[13] have been described for xanthelasma but are not yet conventional treatments.
Electrodesiccation and cryotherapy can destroy xanthelasmas when they are superficial but may require repeated treatments. Cryotherapy may cause scarring and hypopigmentation.
Ectropion and cutaneous nasal webbing may occur after excision of xanthelasma lesions.
Hypopigmentation may occur after trichloroacetic acid application.
If xanthelasma extend deep into the orbicularis muscle, the lesions may not respond to surface ablation techniques.
Patients should receive follow-up care for medical and surgical treatment.