Wednesday, January 5, 2011

Carotenodermia

Carotenemia is present in the blood of yellow pigment carotenic by excessive intake of carrots or other vegetables that contain the carotenoid pigment in the blood increases. It can lead to changes in skin color (or carotenodermia xantodremia) and dep [UnErase secondary to deep skin layers.Carotenemia is a benign condition that occurs mainly in vegetarians and young children. It is easier to see in people with pale skin and can be presented directly to the palms and soles orange to darker people. Not cause discoloration of whites of eyes orange selective and thus is easily distinguished from jaundice caused by bile pigments.
Excessive intake of vitamin A precursors in food, especially carrots can lead to yellow discoloration of the skin and whites but not oral cavity. This condition occurs mostly in children with liver disease, hypothyroidism or diabetes mellitus. Food carotenes requires dietary fat absorption. Conversion of beta-carotene to vitamin A is accelerated by thyroxine and hyperthyroidism. Excessive intake of carotenoids is not toxic and does not cause hypervitaminosis A because the conversion of carotene to vitamin A is slow.
Carotenodremia is deliberately caused by treatment with beta-carotene in some photosensitive dermatitis as erythropoietic protoporfiria, prescribing the amounts of beta carotene to color the skin. These high doses of beta-carotene does not cause pathology in studies, although the cosmetic appearance may bother.
Carotenodermia is pathological and requires no treatment. The primary form when using large quantities of carotene is interrupted will return to normal skin color. This may require several months, however children with this condition should not take vitamins. The secondary form of treatment depends on the cause.
Pathogenesis and causes:Carotenoids are fat-soluble components including alpha and beta carotene, beta-cryptoxanthin, lycopene, lutein and zeaxanthin. The main carotenoid in the blood is beta carotene, lycopene and lutein. Serum levels of carotenoids vary INRE regions, ethnicity and sex in healthy population. All are absorbed by passive diffusion from the gastrointestinal tract and then metabolized partly in the intestinal mucosa and liver to vitamin A. Here are transported in plasma and peripheral tissues. Are eliminated through sweat, sebum, urine and gastrointestinal secretions. Contribute to a normal human skin and are a significant component of ultraviolet fotoprotectiei skin.They are deposited in the stratum corneum intercellular lipids and the color change especially in regions that are sweating a lot and a thick skin. These include hands, feet, knees and nasolabial folds although the color change can be generalized. Primary factor that differentiates jaundice carotenodermia feature is to avoid the conjunctiva. Girl carotenodermia jaundice does not respond to artificial light. Licopenemia is typically associated with changing the color of the soft palate and storage of liver parenchyma can be visualized at ultrasound.Causes and risk factors:There are three main mechanisms involved in carotenemie: excess dietary carotenoids, increased serum lipid and carotenoid metabolism decrease. The most common cause is excessive intake of carotenoids reported or supplements nutrotionale. This amendment requires 4-7 weeks to clinically recognized. Many ingested substances are rich in carotenes.Increased serum lipids can also cause carotenemia due to increased circulating lipoproteins containing carotenes bound. Finally, some diseases, and converting carotenes to retinol metabolsimul is slowed, leading to a decrease in their elimination and increase in plasma.Carotenemia can be divided into two main types: primary and secondary.Carotenemia primary is one that develops from the oral ingestion acroteni while the secondary is caused by some diseases that result in increased serum carotene their normal oral intake. Primary and secondary Carotenodermia can coexist in the same patient.Carotenodermia secondary:Diseases associated with this condition is hypothyroidism, diabetes mellitus, anorexia nervosa, nephrotic syndrome and liver disease. In carotenemiei hipotiridism and diabetes is affecting conversion mechanism in increasing retinol and lipids. Diabetes mellitus is also associated with fostd carotenodermia aliemntare various diets that are rich in plant-specific. The nephrotic syndrome is associated with increased lipid carotenemia similar to the above diseases. Renal dysfunction is generally associated with skin color change as a result of a fall in excretion of carotenoids. Cause liver dysfunction regardless of origin as a result of damage carotenemie carotenes to retinol conversion. This is especially important because jaundice and carotenemia can coexist. Anorexia nervosa carotenemie determine the diets that are rich in corotenoizi and associated hypothyroidism. Tends to be more restrictive type of joint disease and is associated with various dermatological manifestations such as brittle hair, lanugo hair and body type xerosis.Although Alzheimer's disease was not associated with serum carotene caroterodermia in some studies in these patients was low way it can be associated with dementia.
Canthaxanthin and astaxanthin are carotenoids that are found naturally and are used in self-tanning pills in the U.S. and Europe but not approved yet by the Association of Food and Drug Administration because of adverse effects. These include retinopathy, rash, anemia and hepatitis. Children are especially prone to carotenodermie because they eat cooked vegetables. Processing and mixing make carotene more available to be absorbed.

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