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Тежкият дефицит на витамин Д нарушава костния метаболизъм и функционирането на мускулите, като води до развитието на рахит, остеомалация и миопатии. Недостигът на витамин Д е особено чест при постменопаузални жени и се асоциира с повишен риск не само за остеопороза, но и за сърдечносъдови заболявания, неоплазми, диабет и неврологични нарушения. Рискови фактори за дефицит на витамин Д Основните рискови фактори за появата на дефицит на витамин Д включват: недостатъчна експозиция на слънчева светлина, неадекватен прием с храната (основни източници са тлъстите риби, яйцата и млякото), затлъстяване, малабсорбция, прием на медикаменти (антиконвулсанти, антиретровирусни). Жените са по-предразположени към хиповитаминоза Д, съпоставени с мъжете. Витамин Д и сърдечносъдов риск Системен анализ на данните от проспективни проучвания доказва два до пет пъти по-висока смъртност сред хората с ниски серумни нива на 25-ОН-витамин Д. Допълнителният прием на витамина при тях намалява значимо сърдечносъдовия риск, докато калциевите добавки нямат съществен ефект върху сърдечносъдовата заболеваемост.Счита се, че витамин Д е ангажиран в патогенезата на артериалната хипертония, нарушенията в липидния и глюкозния метаболизъм, исхемичната болест на сърцето, миокардния инфаркт, инсулта. Витамин Д и костна плътност Остеопоротичните фрактури са често усложнение при жените в менопауза. Серумните нива на 25-ОН-витамин Д под 19 ng/ml са асоциирани с най-висок риск за фрактури, съпоставени с нива над 28 ng/ml Витамин Д и диабет Наличието на рецептори за витамин Д върху клетките на панкреаса показва, че витаминът е ангажиран в регулацията на инсулиновата секреция. При възрастни без диабет, серумните нива на 25-ОН-витамин Д демонстрират обратна зависимост със стойностите на инсулина и на кръвната глюкоза на гладно, и са асоциирани правопропорционално с индекса на инсулинова чувствителност, и стойностите на холестерола в липопротеините с висока плътност (HDL-С). Витамин Д и злокачествени заболявания Витамин Д стимулира клетъчната диференциация и потиска пролиферацията, поради което се счита, че има антиапоптозна активност.. Витамин Д и инфекции Възприемчивостта към инфекции корелира с витамин Д статуса Витамин Д и когнитивни функции Резултатите от наблюдателни проучвания и няколко малки рандомизирани изпитвания предполагат позитивен ефект от слънчевата експозиция и приема на добавки с витамин Д върху когнитивните функции, паметта, деменцията и болестта на Parkinson. С грижа за своите пациенти Първа МДЛ разработи пакет от изследвания : остеометрия, калций , фосфор и Витамин Д тотал на цена от 29.50 лв
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Vitamin D deficiency Vitamin D deficiency exists when the concentration of 25-hydroxy-vitamin D (25-OH-D) in the blood serum occurs at 12 ng/ml (nanograms/milliliter), or less. The normal concentration of 25-hydroxy-vitamin D in the blood serum is 25-50 ng/ml. When vitamin D deficiency continues for many months in growing children, the disease commonly referred to as rickets will occur. A prolonged deficiency of the vitamin in adults results in osteomalacia. Both diseases involve defects in bones. Vitamin D is a fat-soluble vitamin, meaning it is able to be dissolved in fat. While some vitamin D is supplied by the diet, most of it is made in the body. To make vitamin D, cholesterol, a sterol that is widely distributed in animal tissues and occurs in the yolk of eggs, as well as in various oils and fats, is necessary. Once cholesterol is available in the body, a slight alteration in the cholesterol molecule occurs, with one change taking place in the skin. This alteration requires the energy of sunlight (or ultraviolet light). Vitamin D deficiency, as well as rickets and osteomalacia, tends to occur inpersons who do not get enough sunlight and who fail to eat foods that are rich in vitamin D. Once consumed, or made in the body, vitamin D is further altered to produce ahormone called 1,25-dihydroxy-vitamin D (1,25-diOH-D). The conversion of vitamin D to 1,25-diOH-D does not occur in the skin, but in the liver and kidney. First, vitamin D is converted to 25-OH-D in the liver; it then enters the bloodstream, where it is taken-up by the kidneys. At this point, it is converted to 1,25-diOH-D. Therefore, the manufacture of 1,25-diOH-D requires the participation of various organs of the body--the liver, kidney, and skin. The purpose of 1,25-diOH-D in the body is to keep the concentration of calcium at a constant level in the bloodstream. The maintenance of calcium at a constant level is absolutely required for human life to exist, since dissolved calcium is required for nerves and muscles to work. One of the ways in which 1,25-diOH-D accomplishes this mission is by stimulating the absorption of dietary calcium by the intestines. The sequence of events that can lead to vitamin D deficiency, then to bone disease, is as follows: a lack of vitamin D in the body creates an inability tomanufacture 1,25-diOH-D, which results in decreased absorption of dietary calcium and increased loss of calcium in the feces. When this happens, the bones are affected. Vitamin D deficiency results in a lack of bone mineralization(calcification) in growing persons, or in an increased demineralization (decalcification) of bone in adults. Vitamin D deficiency can be caused by conditions that result in little exposure to sunlight. These conditions include: living in northern countries; having dark skin; being elderly or an infant, and having little chance to go outside; and covering one's face and body, such as for religious reasons. Many Arab women cover the entire body with black cloth, and wear a veil and black gloves when they go outside. These women may acquire vitamin D deficiency, eventhough they live in a sunny climate. Most foods contain little or no vitamin D. As a result, sunshine is often a deciding factor in whether vitamin D deficiency occurs. Although fortified milk and fortified infant formula contain high levels of vitamin D, human breastmilk is rather low in the vitamin. The term fortified means that vitamins are added to the food by the manufacturer. No harm is likely to result from vitamin D deficiency that occurs for only afew days a year. If the deficiency occurs for a period of many months or years, however, rickets or osteomalacia may develop. The symptoms of rickets include bowed legs and bowed arms. The bowed appearance is due to the softening of bones, and their bending if the bones are weight-bearing. Bone growth occurs through the creation of new cartilage, a soft substance at the ends of bones. When the mineral calcium phosphate is deposited onto the cartilage, a hardstructure is created. In vitamin D deficiency, though, calcium is not available to create hardened bone, and the result is soft bone. Other symptoms of rickets include particular bony bumps on the ribs called rachitic rosary (beadlike prominences at the junction of the ribs with their cartilages) and knock-knees. Seizures may also occasionally occur in a child with rickets, becauseof reduced levels of dissolved calcium in the bloodstream. Although osteomalacia is rare in the United States, symptoms of this diseaseinclude reduced bone strength, an increase in bone fractures, and sometimes bone pain, muscle weakness, and a waddling walk. Rickets and osteomalacia are almost always treated with oral supplements of vitamin D, with the recommendation to acquire daily exposure to direct sunlight. An alternative to sunlight is the use of an ultraviolet (UV) lamp. When using UV lamps, the eyes must be covered to protect them against damage. Many types of sunglasses allow UV light to pass through, so only those that are opaque to UV light should be used. Attempts to acquire sunlight through glass windows fail to help the body make vitamin D. This is because UV light does notpass through window glass. The prognoses for correcting vitamin D deficiency, rickets, and osteomalaciaare excellent. Vitamin D treatment results in the return of bone mineralization to a normal rate, the correction of low plasma calcium levels, the prevention of seizures, and a recovery from bone pain. On the other hand, deformities such as bowed legs and the rachitic rosary persist throughout adult life. Food fortification has almost completely eliminated rickets in the United States. Vitamin D deficiency can be prevented by acquiring the RDA through drinking fortified milk and eating fortified cereals. For those who cannot drink milk, supplements of pills might be considered. In some older people, a 400 IUsupplement may not be enough to result in the normal absorption of calcium;therefore, daily doses of 10,000 IU per day may be needed. For infants who are fed only breast milk (and rarely exposed to sunshine), a daily supplement of 200-300 IU is recommended.