Vitamin plasma level

Dihydroxyvitamin (283) is the endogenous ligand for the vitamin receptor (VDR). It modulates genomic function in a tissue and developmentaHy specific manner and affects ceU proliferation, differentiation, and mineral homeostasis (74). Vitamin mobilizes calcium from the bone to maintain plasma Ca " levels. Vitamin and VDR are present in the CNS where they may play a role in regulating Ca " homeostasis. Vitamin D has potent immunomodulatory activity in vivo. 

The most recent RDA has included a vitamin C recommendation of 100 mg/day for cigarette smokers. An increasing number of investigators have concluded that the current RDA for vitamin C may not be adequate for elderly individuals. Plasma vitamin C level is generally accepted as an indicator of vitamin C status. 

With investigations of phytochemicals and functional foods, the outcome measure is generally going to be a biomarker of disease, such as serum cholesterol level as a marker of heart disease risk, or indicators of bone turnover as markers of osteoporosis risk. Alternatively, markers of exposure may also indicate the benefit from a functional food by demonstrating bioavailability, such as increased serum levels of vitamins or carotenoids. Some components will be measurable in both ways. For instance, effects of a folic acid-fortified food could be measured via decrease in plasma homocysteine levels, or increase in red blood cell folate. 

Epidemiological studies in Europe reveal an inverse relationship between plasma vitamin E levels and the incidence of ischaemic heart disease (Gey and Puska 1989), and the risk of angina pectoris appears to increase with low plasma levels of vitamins E, A and C (Rie-mersma et al., 1991). These interesting observations require further population-based controlled intervention trials with specific supplements of antioxidant vitamins (Gey etal., 1991). 

Sinclair, A.J. Taylor, P.B., Lunec, J., Girling, A.J. and Barnett, A.H. (1994). Low plasma ascorbate levels in patients with type 2 diabetes mellitus consuming adequate dietary vitamin C. Diabet. Med. 11, 893-898. 

The final mechanism of action of PTH involves the activation of vitamin D3 through the stimulation of la-hydroxylase in the kidney. In the gastrointestinal tract, vitamin D3 is essential for the absorption of calcium. Enhanced absorption of calcium from dietary sources serves to further increase the concentration of calcium in the blood. Many foods, in particular, dairy products, which are rich in calcium, are fortified with vitamin D. The release of PTH from the parathyroid glands is regulated by plasma calcium levels through negative feedback. A decrease in the level of calcium in the blood stimulates the secretion of PTH and an increase in the calcium level in the blood inhibits it. 

The polypeptide parathormone is released from the parathyroid glands when plasma Ca + level falls. It stimulates osteoclasts to increase bone resorption in the kidneys, it promotes calcium reabsorption, while phosphate excretion is enhanced. As blood phosphate concentration diminishes, the tendency of calcium to precipitate as bone mineral decreases. By stimulating the formation of vit D hormone, parathormone has an indirect effect on the enteral uptake of Ca + and phosphate. In parathormone deficiency, vitamin D can be used as a substitute that unlike parathormone, is effective orally. 

Hypocalcemia - To correct plasma calcium levels (eg, neonatal tetany and tetany due to parathyroid deficiency, vitamin D deficiency, alkalosis) prevention of hypocalcemia during exchange transfusions conditions associated with intestinal malabsorption. 

Calcium/Vitamin Bq Low serum calcium and low plasma vitamin 85 levels were... 

Recently we published data that even in countries with excellent food sources and availability, insufficient vitamin A supply will occur (Schulz et ah, 2007). The aim of this trial was to analyze vitamin A and p-carotene status and investigate the contribution of nutrition to vitamin A and p-carotene supply in mother-infant pairs of multiparous births or births within short birth rates. Twenty-nine volimteers aged between 21 and 36 years were evaluated for 48 hours after delivery. In order to establish overall supply, retinol and p-carotene were determined in maternal plasma, cord blood, and colostrum via HPLC analysis. A food frequency protocol was obtained from all participants. Regardless of the high-to-moderate socioeconomic background, 27.6% of participants showed plasma retinol levels below 1.4 pmol/liter, which can be taken as borderline deficiency. In addition, 46.4% showed retinol intake <66% of RDA and 50.0% did not consume liver at all, although liver contributes as a main source for preformed retinol. Despite a high total carotenoid intake of 6.9 3.9mg/day, 20.7% of mothers showed plasma levels <0.5 pmol/liter p-carotene. 

Hypercalcemia is a common clinical condition that can accompany a variety of other medical conditions, such as sarcoidosis, vitamin D toxicity, hyperparathyroidism, and malignancy. When calcium levels are exceptionally high, adjunctive measures for the control of plasma calcium levels are necessary, as this is a medical emergency. Various modalities in combination are used to treat this condition intravenous hydration with normal saline and the use of loop diuretics (e.g., furosemide) to induce calcium diuresis are the most important supportive measures. 

Vitamin A absorption from the small intestine requires dietary fat and pancreatic lipase to break down retinyl esters and bile salts to promote the uptake of retinol and carotene. Drugs, such as mineral oil, neomycin and cholestyramine, that can modify lipid absorption from the gastrointestinal tract can impair vitamin A absorption. The use of oral contraceptives can signihcantly increase plasma vitamin A levels. 

Plasma calcium level is precisely regulated by three hormones e.g. parathormone, calcitonin and calciferol (which is a active form of vitamin D). They control its absorption, exchange with bone and excretion. 

Calcium is present in three forms e.g., as free calcium ion, bound to plasma protein albumin and in diffusable complexes. The endocrine system, through parathyroid hormone and calcitonin, helps in keeping the concentration of ionized plasma calcium in normal level. Decrease in plasma levels of ionized calcium leads to increased parathyroid hormone secretion. Parathyroid hormone tends to increase plasma calcium level by increasing bone resorption, increasing intestinal absorption and increasing reabsorption of calcium in kidney. Vitamin D acts by stimulating... 

Vitamins B6, B12, and folate An elevated plasma homocysteine level is associated with increased cardiovascular risk (see p. 263). Homocysteine, which is thought to be toxic to the vascular endothelium, is converted into harmless amino acids by the action of enzymes that require the B vitamins—folate, B6 (pyridoxine), and B12 (cobalamin). Ingesting foods rich in these vitamins can lower homocysteine levels and possibly decrease the risk of car diovascular disease. Folate and B6 are found in leafy green veg etables, whole grains, some fruits, and fortified breakfast cereals. B12 comes from animal food, for example, meat, fish, and eggs. 

In human subjects, however, 8 weeks of vitamin E supplementation (800 IU/day) to the diet produced a lowered plasma PGI2 level, as measured by 6-keto-PGF1(X, compared with that in non-supplemented controls [129]. Addition of vitamin E to human platelets in concentrations which resemble normal plasma levels produced a moderately potent but consistent reduction in cyclo-oxygenase activity, with a dose-dependent response up to 1 mM. a-Tocopherol quinone was equally effective in this test [ 130]. 

Fyfe (F10) has investigated plasma vitamin A levels. He observed that the fasting levels in infants with idiopathic hypercalcemia were higher than in the normal and that after a large oral dose of vitamin A,... 

Fyfe (F10), too, in showing that the fasting plasma vitamin A levels and the levels 4 hours after a standard dose of vitamin A are significantly higher in idiopathic hypercalcemia than in the normal, has adduced this... 

In the Heart Outcomes Prevention Evaluation 2 (HOPE-2) study, 5522 patients aged 55 or older with vascular disease or diabetes were randomized to treatment with either placebo or a combination 2, 5 mg of folic acid, 50 mg vitamin B6, and I mg vitamin B 2, for an average of five years. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, and stroke. Mean plasma homocysteine levels decreased by 2.4 jimol/L in the treatment group and increased by 0.8 jimol/L in the placebo group. The primary outcome occurred in 18.8% of patients assigned to active therapy and in 19.8% of those assigned to placebo (relative risk = 0.95 95% Cl = 0.84-1.07 P = 0.41) (68). 

Chronic malabsorption does not fully explain the different extents of fat-soluble vitamin deficiencies associated with ABL. More specifically, why are plasma vitamin E levels more severely affected than those of vitamins A or K The answer for this can be traced to apoB lipoprotein biosynthesis and catabolism (Fig. 27-2). Just as observed for lipids, hydrophobic, fat-soluble vitamins require apoB lipoproteins as vehicles for plasma transport. The reliance of each fat-soluble vitamin on apoB lipoproteins varies, and this variable dependency is directly related to the severity of symptoms observed in ABL. 

IU/day by the oral route with routine blood work to monitor plasma levels. Toxicity due to excess vitamin A is not common but is potentially fatal. Acute toxicity presents as vertigo, diplopia, seizures, and exfoliative dermatitis. Chronic toxicity manifests very differently (i.e., dry skin, alopecia, amenorrhea, symptoms of liver fibrosis, etc.). It is imperative to monitor plasma vitamin A levels regularly, especially in the setting of the large doses required to treat ABL. 

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