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Vitamin serum levels

One of the major problems In the treatment of patients with vitamin D compounds (l.e., patients with hypoparathyroidism) has been the unpredictable development of hypercalcemia and the syndrome of vitamin D Intoxication. Although this problem may become less serious when some of the faster-acting metabolites and analogues of metabolites of vitamin D become available for clinical use. It Is likely that monitoring of serum levels of... [Pg.53]

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. [Pg.240]

There is very little evidence relating to the role of ROMs in cholestatic liver disease. Serum selenium and glutathione peroxidase activity are decreased in humans with intrahepatic cholestasis of pregnancy (Kauppila et al., 1987). Low levels of vitamin E have been reported in patients with primary biliary cirrhosis, and in children with Alagille s syndrome or biliary atresia (Knight et al., 1986 Jeffrey etal., 1987 Lemonnier etal., 1987 Babin etal., 1988 Kaplan et al., 1988 Sokol etal., 1989). Serum levels of Mn-SOD are increased in patients with all stages of primary biliary cirrhosis compared with patients with other forms of chronic liver disease, although whether this causes or results from the disease process is unclear (Ono etal., 1991). [Pg.156]

In the bile-duct-ligated rat, hepatic mitochondrial lipid peroxides are increased and correlate with serum levels of alkaline phosphatase, bilirubin and alanine aminotransferase (Sokol et al., 1991). Dietary vitamin E deficiency resulted in relatively higher lipid peroxide and bilirubin... [Pg.156]

Maldigestion results in decreased serum levels of the fat-soluble vitamins A, D, E, and K. [Pg.248]

CF patients with low bone mineral density and low serum vitamin D levels may improve bone health through supplemental vitamin D analogs beyond those found in standard CF vitamins. The optimal dose and analog have not been determined. For ergocalciferol, a minimum of 400 IU and 800 IU... [Pg.253]

Increased serum phosphorus levels Low to normal serum calcium levels Increased Ca-P product Increased PTH levels Decreased vitamin D levels... [Pg.388]

Cameron C, Lodes MW and Gershan WM. 2007. Facial nerve palsy associated with serum vitamin A level in an infant with cystic fibrosis. J Cyst Fibros 6 241-243. [Pg.212]

When utilization tests were run on a group of 18 male and 7 female human subjects, wide variations in blood level responses were found, particularly among the males.36 [Both in animals (rats) and humans the two sexes respond somewhat differently.] When 134,000 ig. of vitamin A in four different forms, viz., vitamin A alcohol, vitamin A acetate, vitamin A natural ester No. 1, and vitamin A natural ester No. 2, was fed to the group of 18 males on four different occasions, the serum levels found after 6 hours ranged from 178 to 1423 ig. per 100 ml., 122 to 1170 ig. per 100 ml., 110 to 1183 ig. per 100 ml., and 114 to 1230 ig. per 100 ml., respectively. These nearly 10-fold variations in serum levels do not, of course, indicate 10-fold variation in need, but they do show that the vitamin when given in relatively large doses does behave very differently in different individuals. [Pg.190]

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone. Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.
Calcium/Vitamin Bq Low serum calcium and low plasma vitamin 85 levels were... [Pg.287]

Vitamin Bf2 levels A decrease of previously normal serum vitamin B-12 levels has been observed in patients receiving metformin. [Pg.324]

Serum calcium and phosphorus levels (vitamin D levels also helpful, although less frequently)... [Pg.888]

Thyroid function, serum glucose (especially in drug-treated diabetics), vitamin Bjj levels... [Pg.894]

A daily multivitamin supplement may prevent reduction in serum levels of vitamins D, E, K, and folic acid... [Pg.1124]

Once a diagnosis of megaloblastic anemia is made, it must be determined whether vitamin B12 or folic acid deficiency is the cause. (Other causes of megaloblastic anemia are very rare.) This can usually be accomplished by measuring serum levels of the vitamins. The Schilling test, which measures absorption and urinary excretion of radioactively labeled vitamin B12, can be used to further define the mechanism of vitamin Bi2 malabsorption when this is found to be the cause of the megaloblastic anemia. [Pg.738]

The most common toxic effects of metformin are gastrointestinal (anorexia, nausea, vomiting, abdominal discomfort, and diarrhea), which occur in up to 20% of patients. They are dose-related, tend to occur at the onset of therapy, and are often transient. However, metformin may have to be discontinued in 3-5% of patients because of persistent diarrhea. Absorption of vitamin B12 appears to be reduced during long-term metformin therapy, and annual screening of serum vitamin B12 levels and red blood cell parameters has been encouraged by the manufacturer to determine the need for vitamin B12 injections. In the absence of hypoxia or renal or hepatic insufficiency, lactic acidosis is less common with metformin therapy than with phenformin therapy. [Pg.943]

In mild forms of malabsorption, vitamin D (25,000-50,000 units three times per week) should suffice to raise serum levels of 25(OH)D into the normal range. Many patients with severe disease do not respond to vitamin D. Clinical experience with the other metabolites is limited, but both calcitriol and calcifediol have been used successfully in doses similar to those recommended for treatment of renal osteodystrophy. Theoretically, calcifediol should be the drug of choice under these conditions, because no impairment of the renal metabolism of 25(OH)D to l,25(OH)2D and 24,25(OH)2D exists in these patients. Both calcitriol and 24,25(OH)2D may be of importance in reversing the bone disease. However, calcifediol is no longer available. [Pg.970]

The major form of vitamin D in both cows and human milk is 25(OH)D3. This compound is reported to be responsible for most of the vitamin D in the blood serum of exclusively breast-fed infants. Whole cows milk contains only about 0.03 pg vitamin D per 100 g and 1 litre of milk per day will supply only 10-20% of the RDA. Therefore, milk is often fortified (at the level of c. 1-10 fig 1 ) with vitamin D. Fortified milk, dairy products or margarine are important dietary sources of vitamin D. The concentration of vitamin D in unfortified dairy products is usually quite low. Vitamin D levels in milk vary with exposure to sunlight. [Pg.191]

Probstfield JL, Lin TL, Peters J, Hunninghake DB. Carotenoids and vitamin A the effect of hypocholesterole-mic agents on serum levels. Metabolism 1985 34(1) 88—91. [Pg.557]

Serum vitamin B12 levels decrease with age, and serum methylmalonic acid concentrations increase with age. These findings reflect a decline in vitamin B12 status in elderly people. [Pg.344]

Folate deficiency results in a megaloblastic anemia that is microscopically indistinguishable from the anemia caused by vitamin B12 deficiency (see above). However, folate deficiency does not cause the characteristic neurologic syndrome seen in vitamin B12 deficiency. In patients with megaloblastic anemia, folate status is assessed with assays for serum folate or for red blood cell folate. Red blood cell folate levels are often of greater diagnostic value than serum levels, since serum folate levels tend to be quite labile and do not necessarily reflect tissue levels. [Pg.750]

Type IE vitamin D-dependent rickets is caused by a target tissue defect in response to l,25(OH)2D. Studies have shown a number of point mutations in the gene for the l,25(OH)2D receptor, which disrupt the functions of this receptor and lead to this syndrome. The serum levels of l,25(OH)2D are very high in type II but not in type I. Treatment with large doses of calcitriol has been claimed to be effective in restoring normocalcemia. Such patients are totally refractory to vitamin D. One recent report indicates a reversal of resistance to calcitriol when 24,25(OH)2D was given. These diseases are rare. [Pg.1031]

Dog (NS) 13-14 d 1x/d (GO) Hepatic 0.2 (impaired liver functions as indicated by decreased serum vitamin A levels increased prothrombin time and BSP retention increased urinary excretion of administered choline) Sigal et al. 1954... [Pg.57]


See other pages where Vitamin serum levels is mentioned: [Pg.269]    [Pg.392]    [Pg.259]    [Pg.312]    [Pg.300]    [Pg.190]    [Pg.215]    [Pg.264]    [Pg.100]    [Pg.34]    [Pg.782]    [Pg.137]    [Pg.307]    [Pg.985]    [Pg.970]    [Pg.136]    [Pg.263]    [Pg.158]    [Pg.1028]    [Pg.108]    [Pg.97]    [Pg.147]    [Pg.239]   
See also in sourсe #XX -- [ Pg.363 ]




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