Develops more commonly in older individuals, especially women, on the eyelids and periorbital area as flat, slightly elevated, soft papules or plaques of round, oval, or elongated shape, ranging in diameter from 2-3 to 10 mm or more. They are straw-yellow in color, have a smooth or wrinkled surface, and cause no subjective sensation. Approximately 50% of patients with xanthelasma have normal plasma lipid levels, while the remainder usually have elevated cholesterol levels (this is particularly characteristic of younger patients).

Main Causes:

• Type II hyperlipoproteinemia (familial)
• Type III hyperlipoproteinemia (familial)
• Mixed hyperlipidemia (Type IV)
• Apolipoprotein E phenotypes
• Primary biliary cholangitis

It is characterized by the appearance of yellow-orange flat stripes in the folds of the palms and fingers with clear borders, as well as flat papules of the same color, 4-6 mm in diameter, localized only in the palm area. The condition appears after the age of 30. It can be inherited as an autosomal recessive trait (more common) or as an autosomal dominant trait (less common). It is associated with early atherosclerosis of the peripheral vessels, ischemic heart disease, liver disease, diabetes, often with obliterative atherosclerosis of the arteries of the lower limbs.

Main Causes:

• Homozygous familial hyperlipidemia
• Type III hyperlipoproteinemia (familial)
• Diabetic Xanthomatosis
• Prolonged cholestasis
• Monoclonal gammopathy

It is characterized by flat, oval, or linear yellow plaques that are more elevated above the skin surface than xanthelasma. These plaques may start as localized lesions but gradually, due to slow progression, spread to the skin of the face, neck, upper trunk, upper limbs and folds.

It may develop either for no apparent reason in cases of normolipidemia or in patients with multiple myeloma (sometimes long before its clinical manifestation), paraproteinemia, as well as acquired deficiency of C1 esterase inhibitor.

Main Causes:

• Primary hyperlipidemia type III
• Secondary hyperlipidemia
• Monoclonal gammopathy associated with myeloma, lymphoma, leukemia, rheumatoid arthritis
• IgA gammopathy with hypolipidemia

It begins with the appearance of small, soft, yellow, red, or flesh-colored papules on the extensor surfaces of the knees, elbows, shoulders, and buttocks. Over time, these become large (up to 1-5 cm) nodules with a denser consistency due to fibrous tissue infiltration. They may be yellow, orange, or purplish red in color and often coalesce into massive conglomerates. Some elements may be surrounded by a reddish-blue rim.

There is an elevated plasma cholesterol level with an unchanged ratio of free and esterified fractions (there are cases of normocholesterolemia), rarely triglycerides. Patients often have a very high frequency of vascular atherosclerosis. Cases of transformation of xanthomas into keloid scars have been described. Mucous membranes may be involved. Early involvement of blood vessels, joints, and bones is noted. The liver and spleen are often involved.

Main Causes:

• Hyperlipoproteinemia type II (familial)
• Hyperlipoproteinemia type III (familial)
• Secondary hyperlipidemia, associated with, hypothyroidism, primary biliary cholangitis, nephrotic syndrome
• Monoclonal gammopathy
• Xanthomatosis ceribrotendinosus

Classically, tendinous xanthomas are dense, smooth, deep-seated, slowly growing tumor-like formations within the tendons of the wrist extensor, knee, and Achilles tendons. The latter may cause pain and tenderness to palpation due to an inflammatory reaction. The skin overlying the xanthoma remains unchanged and is not adherent to the xanthoma. Trauma is considered a predisposing factor for their formation.

Main Causes:

• Primary systemic hyperlipidemia
• Hyperlipoproteinemia type II (familial)
• Apolipoprotein E phenotypes
• Secondary hyperlipidemia with prolonged cholestasis
• Xanthomatosis ceribrotendinosus

It occurs exclusively in association with elevated plasma triglyceride levels, often in cases of secondary hypertriglyceridemia caused by uncontrolled diabetes. The eruptions occur suddenly, typically in clusters, and, unlike other forms of xanthomatosis, may be accompanied by pruritus.

Papules are small (1-4 mm in diameter), soft, flat or (more commonly) hemispherical, yellowish or yellow-orange in color, and surrounded by an erythematous halo. They are most commonly localized over areas subjected to pressure and on the extensor surfaces of the limbs (joint areas, buttocks), sometimes widespread, including mucous membranes. Perifollicular and follicular xanthomas with cystic changes have been described.

Main Causes:

• Hyperlipoproteinemia type I (familial lipoprotein lipase deficiency)
• Hyperlipoproteinemia type III (familial)
• Hyperlipoproteinemia type IV (familial hypertriglyceridemia)
• Hypertriglyceridemia type V
• Secondary hyperlipidemia associated with diabetes mellitus, alcoholism, estrogens and contraceptives, retinoids, hyperthyroidism, nephrotic syndrome

A rare form of xanthoma characterized by small, painful, dense, slightly elevated red plaques along the course of nerves (often on the feet).

Considered a reactive process. Tumor-like formations with verrucous surfaces are typically localized on the oral mucosa, less commonly on the genitals.

Also known as Montgomery Syndrome. Some authors classify this condition as normolipidemic xanthomatosis, while others associate it with the group of non-Langerhans cell histiocytoses. The eruptions appear as reddish-brown papules 2-10 mm in diameter that rapidly evolve into larger yellow-brown confluent patches resembling eruptive xanthomas. They are typically clustered and localized on the proximal parts of the limbs, flexures, trunk, and face. Dark brown plaques may form on the flexural areas of adults.

Mucous membranes of the mouth, larynx, trachea, conjunctiva, cornea, and sclera are often involved. Respiratory lesions may cause hoarseness and shortness of breath.

The prognosis is generally good. The disease resolves spontaneously with involution and scarring of the xanthomas. However, there are cases of fatal outcome due to airway obstruction by xanthomas and development of xanthomatous tumors in brain tissue.

Papular xanthoma is a normolipemic histiocytosis not associated with Langerhans cells. It is observed between the ages of 13 and 57 years with a male to female ratio. Clinically, it manifests as single or multiple yellow-red or yellow-brown papules on the skin of the face, trunk, and extremities. In adults, the mucous membranes may also be involved.

In children, the disease usually resolves on its own, leaving a scar-like appearance, but in adults the disease may progress. There is no systemic involvement. Serum lipid levels remain within normal limits, although qualitative abnormalities of lipoproteins may be present.

Also known as familial hyperlipoproteinemia or familial chylomicronemia. It is an inherited disorder of lipid metabolism characterized by xanthomatosis and neurological and cardiovascular symptoms.

Characteristic features include multiple tuberous xanthomas around the elbows and knees and eruptive xanthomas on the trunk, eyelids, palms, and soles. The skin is yellowish or golden in color. The disease is associated with hepatosplenomegaly, fever, and involvement of the nervous and cardiovascular systems.

There are six types of familial hyperlipoproteinemia: lipoprotein deficiency due to lipase deficiency (gene 8p22); hyperbeta lipoproteinemia (gene 19qB2); lipoidosis with low-density lipoproteins (gene 19q13. 2); lipoidosis with high levels of very-low-density lipoproteins (gene 11q23); lipoidosis combined with high levels of triglycerides and glucose (gene 11q23); and combined lipoidosis characterized by elevated levels of triglycerides and cholesterol. The inheritance of the pathological gene can be autosomal dominant (types 2, 3, 4, and 6) or autosomal recessive (types 1 and 5).

It's a unique form of normolipidemic xanthomatosis with autosomal dominant inheritance. The syndrome manifests as lipidosis of the skin, bones, and cornea. It is characterized by yellowish papules (xanthomas) localized on the extensor surfaces of the upper and lower limbs, around joints, on the buttocks, and other areas of the trunk. There are also disturbances in the ossification of the epiphyses of small bones and corneal dystrophy. Liver and spleen are not enlarged.

Also known as phytosterolemia or β-sitosterolemia. It's a lipid metabolism disorder characterized by tendon and nodule xanthomas and a predisposition to premature coronary atherosclerosis. Xanthomas of the tendon, earlobes, extensor musculature, and tendons are observed from early childhood. In the elbow area they take on a nodular character.

Blood tests show significantly elevated levels of beta-sitosterol, while cholesterol levels are normal. It's thought that the absorption of β-sitosterol in the intestine is disturbed. Inheritance of the disease gene is autosomal recessive.

It's a normolipidemic xanthomatosis characterized by xanthomas of the tendons, lungs, and central nervous system. This autosomal recessive disorder is characterized by increased synthesis of bile acids, disruption of cholesterol metabolism, and deposition in various organs.

The disease begins with generalized symptoms. Intellectual disability develops in early childhood and progresses each year. Ataxia, spastic paralysis, and cataracts develop between the ages of 12 and 15. Later, xanthomas appear around the Achilles and other tendons. Early atherosclerosis often develops.

Blood cholesterol levels remain unchanged, while cholestanol levels are significantly elevated. The prognosis for recovery and life is poor; patients often die before the age of 20.