Carotenosis

Carotenosis
Other names: Carotenaemia, xanthaemia, carotenoderma, carotenodermia
Carotenoderma of the palm (left) in comparison with a normal appearing hand
Specialty	Dermatology
Symptoms	Orange skin discoloration
Usual onset	1 to 2 months
Types	Primary, secondary
Causes	Diet high in β-carotene, diabetes, anorexia
Diagnostic method	Usually based on symptoms and examination
Differential diagnosis	Jaundice, lycopenemia
Treatment	None, dietary changes
Prognosis	Non serious
Frequency	Relatively common

Carotenosis is an orange discoloration of the skin. It is more apparent in light-skinned people; while, in those with darker skin it may only be apparent in the palms and soles. Other commonly involved areas include the nose and forehead. Onset is one to two months after increased intake. It does not affect the whites of the eyes, like jaundice.

Those who eat a diet high in β-carotene are most affected including vegetarians, young children, and those from West Africa. Common foods high in β-carotene include mango, pumpkin, carrots, and sweet potato. Those in West Africa are particularly affected due to red palm oil. It may also occur in diabetes, low thyroid, liver problems, and anorexia. Diagnosis can usually based on symptoms and examination; though, blood carotene and liver function tests may be helpful.

Specific treatment is not generally required. In those who have concerns, dietary changes can be recommended. In those with associated health conditions, these should be treated. It is non serious and generally resolves following a few months of dietary changes. Cases due to the tanning pill canthaxanthin; however, may be associated with eye problems. Carotenosis is relatively common. It was first described by Hess and Meyers in 1919. It was even more common around the Second World War due to food rationing.

Signs and symptoms

The presentation of this condition is consistent with yellowish color on the palms of hands and feet.

• 
  Carotenoderma visible on the nose
• 
  Carotenaemia

Causes

There are three main mechanisms involved in hypercarotenemia: excessive dietary intake of carotenoids, increased serum lipids, and decreased metabolism of carotenoids. The most common reported cause of hypercarotenemia (and thus carotenoderma) is increased intake, either through increased dietary foods or nutritional supplements. This change takes approximately 4 to 7 weeks to be recognized clinically. Numerous ingested substances are rich in carotenoids. Increased serum lipids also cause hypercarotenemia because there are increased circulating lipoproteins that contain bound carotenoids. Finally, in certain disease states, the metabolism and conversion of carotenoids to retinol is slowed, which can lead to decreased clearance and increased plasma levels. Elevated serum beta-carotene does not necessarily result in carotenosis, but the latter is likely to show up when intake is more than 20 mg/day. Average adult intake in the U.S. around 2.3 mg/day. One medium-sized carrot has about 4.0 mg.

Carotenoderma can be divided into two major types, primary and secondary. Primary carotenoderma is from increased oral ingestion of carotenoids, whereas secondary carotenoderma is caused from underlying disease states that increase serum carotenoids with normal oral intake of these compounds. Primary and secondary carotenoderma can coexist in the same patient.

Foods associated with high levels of carotenoids include:

Alfalfa Apples Apricots Asparagus Beans Beet greens Broccoli Brussels sprouts Butter Cabbage Cantaloupes Carrots Cheese

Collard greens Cucumbers Eggs Figs Kale Kiwi Lettuce Mangoes Mustard Oranges Palm oil (unrefined) Papayas

Parsley Peaches Pineapples Plums Pumpkins Seaweed Spinach Squash Sweet potatoes Tomatoes Yams Yellow corn Red palm oil

Secondary

Disease states associated with carotenoderma include hypothyroidism, diabetes mellitus, anorexia nervosa, nephrotic syndrome, and liver disease. In hypothyroidism and diabetes mellitus, the underlying mechanism of hypercarotenemia is thought to be both impaired conversion of beta-carotene into retinol and the associated increased serum lipids. Diabetes mellitus has also been associated with carotenoderma through disease-specific diets that are rich in vegetables. In the nephrotic syndrome, the hypercarotenemia is related to the associated increased serum lipids, similar to the above entities.

It is of note that kidney dysfunction in general is associated with hypercarotenemia as a result of decreased excretion of carotenoids. Liver dysfunction, regardless of origin, causes hypercarotenemia as a result of the impaired conversion of carotenoids to retinol. This is of particular interest because jaundice and carotenoderma can coexist in the same patient. Anorexia nervosa causes carotenoderma mainly through diets that are rich in carotenoids and the associated hypothyroidism. It tends to be more common in the restricting subtype of this disease, and is associated with numerous other dermatologic manifestations, such as brittle hair and nails, lanugo-like body hair, and xerosis. Although Alzheimer's disease has been associated with carotenoderma in some reports, most studies on serum carotenoids in these patients show that their levels of carotenoids and retinol are depressed, and may be associated with the development of dementia. A true association between Alzheimer's disease and carotenoderma is unclear at this time. There have been case reports in the literature of increased serum carotenoids and carotenoderma that is unresponsive to dietary measures, with a genetic defect in carotenoid metabolic enzymes proposed. Canthaxanthin and astaxanthin are naturally occurring carotenoids that are used in the British and US food industry to add color to foods such as sausage and fish. Canthaxanthin has been used in over-the-counter “tanning pills” in the United States and Europe, but is not currently Food and Drug Administration (FDA)-approved for this purpose in the United States because of its adverse effects. These include hepatitis, urticaria, aplastic anemia, and a retinopathy characterized by yellow deposits and subsequent visual field defects.

Infants and small children are especially prone to carotenoderma because of the cooked, mashed, and pureed vegetables that they eat. Processing and homogenizing causes carotene to become more available for absorption. A small 2.5 ounce jar of baby food sweet potatoes or carrots contains about 400-500% of an infant's recommended daily value of carotene. In addition to that source of carotene, infants are usually prescribed a liquid vitamin supplement, such as Tri-Vi-Sol, which contains vitamin A.

It may be deliberately brought about by beta-carotenoid treatment in certain photo-sensitive conditions such as erythropoietic protoporphyria. They contribute to normal-appearing skin color, and are a component of physiologic ultraviolet photoprotection.

Mechanism

Carotenoids are deposited in the intercellular lipids of the stratum corneum, and the color change is most prominent in regions of increased sweating and thickness of this layer. This includes the palms, soles, knees, and nasolabial folds, although the discoloration can be generalized. The primary factor differentiating carotenoderma from jaundice is the characteristic sparing of the sclerae in carotenoderma, which would be involved in jaundice if the bilirubin is at a level to cause skin findings. In contrast to jaundice, carotenoderma is reported to be better observed under artificial light. It is of note that lycopenemia is specifically associated with discoloration of the soft palate and deposition in the liver parenchyma.

Diagnosis

Differential

Hyperbilirubinemia is the main differential diagnosis to be considered.

Excessive consumption of lycopene, a plant pigment similar to carotene and present in tomatoes, can cause a deep orange discoloration of the skin. Like carotenodermia, lycopenemia is harmless.

Excessive consumption of elemental silver, silver dust or silver compounds can cause the skin to be colored blue or bluish-grey. This condition is called argyria. A similar skin color can result from prolonged exposure to gold, typically as a little-used medical treatment. The gold-induced greyish skin color is called chrysiasis. Argyria and chrysiasis, however, are irreversible, unlike carotenosis.

Treatment

Carotenemia and carotenoderma is in itself harmless, and does not require treatment. In primary carotenoderma, when the use of high quantities of carotene is discontinued the skin color will return to normal. It may take up to several months, however, for this to happen. Infants with this condition should not be taken off prescribed vitamin supplements unless advised to do so by the child's pediatrician.

As to underlying disorders in secondary carotinemia and carotenoderma, treatment depends wholly on the cause.

See also

• Argyria
• Diabetic dermadromes
• List of cutaneous conditions
• Xanthochromism

External links

Classification	ICD-10: L81.9 ICD-9-CM: 709.00
External resources	eMedicine: derm/789

• "Carotenemia: Overview, Pathophysiology, Etiology". 3 April 2018. Archived from the original on 27 June 2018. Retrieved 8 May 2018. {{cite journal}}: Cite journal requires |journal= (help)