Plasma levels of vitamin

Some hydroxy metabolites of coplanar PCBs, such as 4-OH and 3,3 4,5 -tet-rachlorobiphenyl, act as antagonists of thyroxin (Chapter 6, Section 6.2.4). They have high affinity for the thyroxin-binding site on transthyretin (TTR) in plasma. Toxic effects include vitamin A deficiency. Biomarker assays for this toxic mechanism include percentage of thyroxin-binding sites to which rodenticide is bound, plasma levels of thyroxin, and plasma levels of vitamin A. 

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). 

Borel, P, M. Moussa et al. (2007). Human plasma levels of vitamin E and carotenoids are associated with genetic polymorphisms in genes involved in lipid metabolism. J. Nutr. 137(12) 2653-2659. 

Mangialasche F, Kivipelto M, Mecocci P, Rizzuto D, Palmer K, Winblad B, Fratiglioni L. (2010) High plasma levels of vitamin E forms and reduced Alzheimer s disease risk in advanced age. J Alzheimers Dis 20 1029-1037. 

Italian Collaborative Groupon Preterm Delivery (ICGPD). (1993). Supplementation and plasma levels of vitamin A premature newborns at risk for chronic lung disease. Dev. Pharmacol. Ther. 20,144—151. 

Blood tests were performed and had the following results hematocrit 33% (normal is 38%-45%) reticulocyte count 2.0% (normal is 0.5%-1.5%) mean corpuscular volume 90 (normal). A decreased erythrocyte sedimentation rate and a prothombrin time (PT) of 15 s (normal 11-13 s) were noted. A complete blood cell count values for total protein and albumin, ALT, and AST, fasting glucose, Hb-Alc, as well as amylase and lipase were within normal range. Plasma levels of vitamins A and K were below normal, and there was near absence of vitamin E. Dysmorphic red blood cells (RBC) with multiple thorny projections (acanthocytes) were present on a blood smear. All other laboratory tests and findings were within normal limits. 

For a review, see Sachse etal. (1982). Combining acarbose with sulphonylurea or metformin or insulin may lead to hypoglycaemia, although acarbose itself will not produce hypoglycaemia (doses have to be corrected). The effect of acarbose may be reduced by antacids, cholestyramine, pancreatic enzymes and adsorbants. Plasma levels of vitamin B6 increased, and vitamin A concentrations decreased with acarbose (Couet et al., 1989). 

Loerch JD, Underwood BA, Lewis KC. Response of plasma levels of vitamin A to a dose of vitamin A as an indicator of hepatic vitamin A reserves in rats. J Nutr 1979 109 778-86. 

Vitamin E deficiency occurs due to genetic defects in the formation of hepatic a-tocopherol transfer protein. This transport protein plays a central role in the liver and one of its functions is to facilitate incorporation of a-tocopherol into nascent very low density lipoproteins (VLDLs). Since there are no specific transport proteins for vitamin E in plasma, the delivery of vitamin E to the tissues is primarily mediated by VLDL-LDL transport mechanisms (Chapter 20). Thus, deficiency of hepatic a-tocopherol transport protein causes low plasma levels of vitamin E with impairment of delivery to the tissues. Patients with the transport protein deficiency exhibit peripheral neuropathy and ataxia. Early and vigorous vitamin E supplementation in patients with neurological symptoms and with low plas-mal levels of vitamin E has yielded therapeutic benefits. 

A CBC, including a peripheral smear and reticulocyte count, should be performed in any elderly patient with symptoms that may be attributed to anemia, along with a physical exam to look for signs of renal or hepatic failure as well as to evaluate for gastrointestinal or genitourinary blood loss. If the reticulocyte count is adequate, blood loss or RBC destruction should be suspected, whereas a low level will indicate decreased RBC production. With a low reticulocyte count, RBC indices should be evaluated and if the MCV is > 100 fL, further evaluation should be performed to discern vitamin B12 deficiency and folate deficiency as possible causes. A vitamin B12 deficiency may be present even when plasma levels of vitamin B12 are within normal range, but elevated levels of MMA will detect the deficiency. A refractory macrocytic anemia in the elderly should raise suspicion of a myelodysplastic or leukemic syndrome. 

I should say that there is very little evidence that vitamin C ever acts as a pro-oxidant in people. There are a few indications that the body is aware of the danger, however. In particular, we control our blood plasma levels of vitamin C carefully. Even if we take mega-doses of vitamin C, plasma levels hardly rise. There are two main controls on vitamin C levels in blood plasma — absorption and excretion. The absorption of vitamin C from the intestine falls off drastically the larger the dose. Mega-doses... 

During the Industrial Revolution, there was widespread incidence of rickets in both children and adults, because inadequate exposure to sunlight prevented the biosynthesis of active vitamin D in the skin. Both rickets and osteomalacia are metabolic bone diseases that are characterized by poor bone mineralization. Without adequate plasma levels of vitamin D and calcium, deposition of the calcium salts in the bone markedly decreases. Vitamin D supplementation (to improve intestinal absorption of calcium and mineralization of the bone) as well as oral calcium supplementation are required to treat these diseases once established. The incidence of rickets in the United States dropped dramatically through vitamin D-supplemented food programs. The increased use of milk substitutes (e.g., soy) and reduced exposure to sunlight has recently led to a rise in rickets. Rickets is still considered to be a worldwide health problem. 

Not understood. One study showed that norethandrolone did not alter the metabolism of dicoumarol, and did not alter the plasma levels of vitamin-K dependent clotting factors. However, a more recent study of oxandrolone and warfarin shows a pharmacokinetic basis for this interaction. ... 

A syndrome associated with low plasma levels of vitamin E was reported by Hassan et al (1966) in premature infants receiving formula mixtures with relatively high content of polyunsaturated fatty acids. S3nnptoms included edema, skin lesions, an elevated platelet count and morphologic changes in erythrocytes. These were relieved or prevented by supplementation with vitamin E. 

Newill, A., Habibzadeth, N., Bishop, N., and Schorah, C. J., 1984, Plasma levels of vitamin C components in normal and diabetic subjects, Ann. Clin. Biochem. 21 488-490. 

Zinc deficiency accompanied by a depression in plasma retinol has been noted in several studies. Some investigators have reported an increased liver vitamin A in several species of zinc-deficient animals (Stevenson and Earle, 1956 Saraswat and Arora, 1972 J. C. Smith et aL, 1973, 1976 Brown et aL, 1976 Jacobs et al., 1978 Carney et aL, 1976). There are also reports in humans in an association between lowered zinc, retinol, and RBP (Jacobs et a/., 1978 Solomons and Russell, 1980). J. C. Smith et al, (1973) suggested that hepatic mobilization of vitamin A was impaired by zinc deficiency and their follow-up studies demonstrated a depression in liver and plasma RBP in the zinc-deficient rat compared to pair-fed controls (Brown et al., 1976 Smith et al., 1974). The depression was hypothesized to be the result of a depressed synthesis rather than an increased turnover of RBP. That preformed RBP is present in zinc-deficient rats was demonstrated by Carney et al. (1976) using labeled vitamin A. Zinc-deficient rats, whether or not they were also vitamin A-deficient, were able to mobilize over a short time span a small oral dose of vitamin A as well as could their pair-fed controls. Those animals deficient only in zinc excreted metabolites of the labeled vitamin in a similar quantitative manner as the pair-fed controls for 6 days postdosing. These data suggest that the release of retinol from retinyl ester stores, as well as a depressed RBP synthetic rate, contributed to low plasma levels of vitamin A in zinc deficiency. 

Fig. 4. The effect of fluctuations in the seasonal availability of foods with vitamin A activity on plasma levels of vitamin A and carotenoids in one area of Southern Mali. (From Le Francois et al., 1980.)...

Effect of Dietary Source of Retinol Equivalents (RE), Preformed versus Precursor, on Plasma Levels of Vitamin A and Carotenoids in Senegal" and the United States ... 

Total RBP measurements, however, are indicative of plasma levels of vitamin A under most survey conditions and would be equivalent to direct vitamin A determination for assessment purposes, providing the population excludes those suffering from relatively short-term or chronic severe calorie and/or protein deficit and those suffering from diseases (e.g., of the liver) that will affect RBP levels (see Chapter 7). Currently there has been no report of a large-scale survey in which both parameters have been measured to determine their comparability as assessment tools for vitamin A nutriture. Reddy et al. (1979) found children with mild forms of PEM had values for both RBP and retinol similar to normal children. 

A number of studies have examined RBP levels (and usually TTR and vitamin A levels as well) in patients with various kinds of acute and chronic diseases of the liver (Smith and Goodman, 1971 Kindler, 1972 Prellwitz et al., 1974 Skredeeta/., 1975 Brissot er a/., 1978 Vahlquist a/., 1978a Russell et a/., 1978 McClain et al., 1979). In patients with clinically significant hepatic parenchymal disease, the plasma levels of vitamin A, RBP, and TTR have usually been found to be substantially depressed. The low levels of RBP and TTR presumably reflect a reduced rate of production of the proteins by the diseased liver. 

In 63 patients with liver disease, the levels of vitamin A, RBP, and TTR were all markedly decreased and were highly significantly correlated with each other over a wide range of concentrations (Smith and Goodman, 1971). Nineteen patients with acute hepatitis were studied with serial samples as the disease improved, the plasma levels of vitamin A, RBP, and TTR all increased. In these patients, the RBP concentrations correlated negatively with the values of standard tests of liver function (plasma bilirubin, glutamic-oxaloacetic transaminase, and alkaline phosphatase). It has been reported that the level of RBP is of value clinically in assessing the course of acute infectious hepatitis and, to a limited extent, in the differentiation of various forms of jaundice (Kindler, 1972). It seems clear that measurements of plasma RBP levels in patients with liver disease could, if available, be used as an index of hepatic parenchymal functional status and hence could serve as a useful clinical liver function test. 

Relationships between plasma vitamin A and zinc were explored in 45 children with clinical vitamin A deficiency and 20 children with PEM (Shingwekar et al., 1979). Mean levels of plasma vitamin A, RBP, and zinc were low in these malnourished children compared to controls. Supplementation with zinc resulted in a small but significant increase in plasma vitamin A and RBP levels in children with PEM but not in the vitamin A-deficient group. There was no correlation between plasma levels of vitamin A and zinc. It was suggested that in children with PEM, apart from deficiencies of protein and vitamin A, zinc deficiency may also contribute in part to low plasma vitamin A levels. Other clinical studies on the interaction between zinc and vitamin A are discussed in the above-mentioned reviews. Zinc deficiency is an uncommon but potential contributor to abnormal vitamin A transport in a number of gastrointestinal and hepatic diseases, as well as in PEM. 

Figure 7.2 suggests very strongly that a high plasma level of vitamin E is protective against coronary heart disease. Table 7.5 shows the results of the Cambridge Heart Anti-Oxidant Study. 

Newborn infants (especially the premature) have low plasma levels of vitamin E (the vitamin E concentration in full-term newborn infants is about one-third that of adults and that of premature infants is even lower), because transfer of vitamin through the placenta to the fetus is limited. As a result, hemolytic anemia (caused by shortened life span of red cells) may occur in the early weeks of life. In this condition, the membranes of the red blood cells are weakened by the action on them of the products of peroxidation of polyunsaturated fats and the cells rupture easily, producing a condition characterized by edema, skin lesions, and blood abnormalities. Supplements of vitamin E bring about increeises in blood levels of the vitamin, decreases in red blood cell hemolysis, and a return to normal hemoglobin levels. 

The highest plasma level of vitamin A was found in the 4 hour after its administration in every case and plasma level was not influenced by the different fatty acid composition and absorption mechanisms of the oils and fats. 

Shingwekar AG, Mohanram M, Reddy V (1979) Effect of zinc supplementation on plasma levels of vitamin A and retinol-binding protein in malnourished children. Clin ChimActa 93 97-100... 

The effects of dietary vitamin E have been examined in several studies, many of which have reported a clear association between the reduction in the relative risk of CVD and high intake or supplement of vitamin E, although some have shown no such association. The Vitamin Substudy of the WHO/MONICA Project showed that in Em-opean populations whose classical risk factors for CVD were very similar, the 7-fold differences in CVD mortality could be explained at least to approximately 60% by differences in the plasma levels of vitamin E and up to 90% by the combination of vitamins E, A, and C. The Edinburgh Case Control Study and Basel Prospective Study consistently revealed an increased risk of ischemic heart disease and stroke for low plasma levels of vitamin E. 

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