Carotenosis

Carotenosis is a benign and reversible medical condition where an excess of dietary carotenoids results in orange discoloration of the outermost skin layer. The discoloration is most easily observed in light-skinned people and may be mistaken for jaundice. 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.^{[citation needed]} Carotenoids contribute to normal-appearing human skin color, and are a significant component of physiologic ultraviolet photoprotection.

Carotenemia most commonly occurs in vegetarians and young children with light skin. Carotenemia is more easily appreciated in light-complexioned people, and it may present chiefly as an orange discolouration of the palms and the soles in more darkly pigmented persons. Carotenemia does not cause selective orange discoloration of the conjunctival membranes over the sclerae (whites of the eyes), and thus is usually easy to distinguish from the yellowing of the skin and conjunctiva caused by bile pigments in states of jaundice.

Carotenoderma is deliberately caused by beta-carotenoid treatment of certain photo-sensitive dermatitis diseases such as erythropoietic protoporphyria, where beta carotene is prescribed in quantities which discolor the skin. These high doses of beta carotene have been found to be harmless in studies, though cosmetically displeasing to some. In a recent meta analysis of these treatments, however, the effectiveness of the treatment has been called into question.

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. The average adult intake in the U.S. is around 2.3 mg/day. One medium-sized carrot has about 4.0 mg.^{[citation needed]}

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.^{[citation needed]}

Foods associated with high levels of carotenoids include:

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.^{[citation needed]}

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.^{[citation needed]}