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Carotenoderma (also carotenodermia or carotenosis) is the name given to the yellow to yellow-orange discoloration of the skin that is caused by increased serum carotenoids (carotenemia) and their subsequent deposition in the outermost layer of skin[1]. Carotenoids are lipid-soluble compounds that include alpha- and beta-carotene, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin. The primary serum carotenoids are beta-carotene, lycopene, and lutein. Serum levels of carotenoids vary between region, ethnicity, and sex in the healthy population. All are absorbed by passive diffusion from the gastrointestinal tract and are then partially metabolized in the intestinal mucosa and liver to vitamin A. From there they are transported in the plasma into the peripheral tissues. Carotenoids are eliminated via sweat, sebum, urine, and gastrointestinal secretions. Carotenoids contribute to normal-appearing human skin color and are a significant component of physiologic ultraviolet photoprotection.
Carotenemia is a benign condition most commonly occurring in vegetarians and young children. Carotenemia is more easily appreciated in light-complexioned people, and it may present chiefly as yellowing of the palms and the soles in more darkly pigmented persons.[2] Carotenemia does not cause selective yellowing of the conjuctiva of the eyes (yellowing over the sclera), and thus is usually easy to distinguish from the yellowing of the skin caused by bile pigments, in states of jaundice.
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 conjunctivae 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, which can be visualized on ultrasound.
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. In certain disease states, the metabolism and conversion of carotenoids to retinol is slowed, which can lead to decreased clearance and increased plasma levels. Carotenoderma can be divided into two major types, primary and secondary. Primary carotenoderma is that developing 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[3] include:
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 through 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.[4] 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.[5] 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.[6]
Infants and small children are especially prone to carotenodermia 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.
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