Updated: Mar 02, 2021
Author: Andrew A Dahl, MD, FACS; Chief Editor: Edsel B Ing, MD, PhD, MBA, MEd, MPH, MA, FRCSC 



Xanthelasma are yellowish plaques that occur most commonly near the inner canthus of the eyelid, more often on the upper lid than the lower lid. Xanthelasma palpebrarum is the most common cutaneous xanthoma. 

Xanthelesma of four eyelids in patient with hyperl Xanthelesma of four eyelids in patient with hyperlipidemia.

Xanthelasma can be soft, semisolid, or calcareous. Frequently, they are symmetrical, and all four lids are sometimes involved. Xanthelasma tends to progress, coalesce, and become permanent.

The term xanthelasma is derived from the Greek xanthos (yellow) and elasma (beaten metal plate).

See Can You Recognize Benign Skin Lesions From Cancerous Ones?, a Critical Images slideshow, to help identify various skin lesions.


Xanthelasma are a type of xanthoma appearing on the eyelids. Xanthomas are depositions of yellowish cholesterol-rich material that can appear anywhere in the body in various disease states. They are cutaneous manifestations of lipidosis in which lipids accumulate in foam cells within the skin. They are often associated with hyperlipidemias, of both primary and secondary types. Some occur with altered lipoprotein composition or structure, such as lowered high-density lipoprotein (HDL) levels. They frequently occur in patients with type II hyperlipidemia and in the type IV phenotype.



United States

Xanthelasma are not uncommon.


In India, the incidence of xanthelasma may range from 0.3%-1.5%.[1]


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.[2]


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 4 eyelids affected.

Patient Education

For excellent patient education resources, see eMedicineHealth's Cholesterol Center. Also, visit eMedicineHealth's patient education articles High Cholesterol, Cholesterol Charts, Lifestyle Cholesterol Management, and Cholesterol Lowering Medications.




Xanthelasma are the most common type of xanthoma. 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.



Diagnostic Considerations

Familial hypercholesterolemia types IIa and IIb

Familial dysbetalipoproteinemia type III

Familial hypertriglyceridemia type IV

Other lipid disorders, to include the following:

  • Low HDL cholesterol levels as compared to low-density lipoprotein (LDL) levels

  • Diabetes, uncontrolled with associated hypertriglyceridemia

  • Necrobiotic xanthogranuloma

  • Tuberous xanthomata

  • Diffuse planar xanthoma

  • Orbital lipogranulomata

  • Juvenile xanthogranulomata

  • Erdheim-Chester disease

  • Wegener granulomatosis

  • Lipoid proteinosis

  • Primary systemic amyloidosis

  • Necrobiosis lipoidica

  • Sarcoid

  • Atypical lymphoid infiltrate

Pseudoxanthelasma - One case history describes retinal surgery with silicone oil in tissue mimicking xanthelasma.[3]

Differential Diagnoses



Laboratory Studies

Since more than 50% of patients with xanthelasma have lipid disorders, it is recommended that plasma lipid levels initially be obtained on all patients presenting with significant xanthelesma.  These should include LDL cholesterol and HDL cholesterol levels, triglyceride level, and apolipoprotein B100 level. Xanthelasma are usually 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.

Histologic Findings

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.



Medical Care

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.

Surgical Care

Numerous options are available for the removal of xanthelasma palpebrarum, including surgical excision, argon and carbon dioxide laser ablation, chemical cauterization, electrodesiccation, and cryotherapy.

Surgical excision

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.[4]

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.

Case presentation of excision of recurrent xanthel Case presentation of excision of recurrent xanthelasma. Recurrent xanthelasma bilateral upper lids; previous excision combined with blepharoplasty; patient insistent on repeat excision and blepharoplasty; advised of lagophthalmos risk due to medial position and lack of medial dermatochalasis.
Close-up view of recurrent xanthelasma right upper Close-up view of recurrent xanthelasma right upper lid. Note the scar from previous excision by a plastic surgeon. Careful examination reveals subtle infiltration in the lateral aspect of scar.
Xanthelasma. External view, 1 week after surgery. Xanthelasma. External view, 1 week after surgery. Sliding and rotational flaps from residual lateral dermatochalasis used for medial excisional gap.
Xanthelasma. Top image, 4 weeks after surgery; low Xanthelasma. Top image, 4 weeks after surgery; lower image, before surgery.

Laser ablation

Carbon dioxide, yttrium aluminum garnet, pulsed dye, argon, and 1450 nm diode laser have been laser modalities used in treatment of xanthelesma.[5]  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.[6]

Chemical cauterization

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.[7] TCA treatment has been advocated prior to surgical excision to cause initial shrinkage of the lesions.[8]  Intralesional heparin sodium[9] and pingyangmycin[10] have been described for xanthelasma but are not yet conventional treatments.

Electrodesiccation and cryotherapy

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.

Further Outpatient Care

Patients should receive follow-up care for medical and surgical treatment.


Questions & Answers