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Scurvy clinical signs

Most of the other clinical signs of scurvy can be accounted for by effects of deficiency on collagen synthesis as a result of impaired proUne and lysine hydroxylase activity (Section 13.3.3). [Pg.372]

In general, the effects on collagen synthesis are more marked and more important than those of decreased formation of carnitine (as a result of impaired activity of trimethyllysine and y-butyrobetaine hydroxylases Section 14.1.1), impaired xenobiotic metabolism, or hypercholesterolemia (Section 13.3.8). However, depletion of muscle carititine may account for the lassitude and fatigue that precede clinical signs of scurvy. [Pg.372]

The plasma concentration of vitamin C falls relatively rapidly during depletion studies, to undetectably low levels within 4 weeks of initiating a vitamin C-free diet, although clinical signs of scurvy may not develop for a further 3 to... [Pg.374]

The concentration of ascorbate in leukocytes is well correlated with the concentrations in other tissues and falls more slowly than plasma concentration in depletion studies. The reference range of leukocyte ascorbate is 1.1 to 2.8 pmol per 10 cells a significant loss of leukocyte ascorbate coincides with the development of clear clinical signs of scurvy. Predictably, at high levels of ascorbate intake, although the plasma concentration continues to increase with intake, the leukocyte content does not, because the cells, like othertissues, are saturated. [Pg.375]

The minimum requirement for vitamin C was established in the Sheffield study (Medical Research Council, 1948), which showed that an intake of marginally less than 10 mg per day was adequate to prevent the development of scurvy or to cure the clinical signs. Results from the Iowa study (Baker et al., 1969,... [Pg.376]

A priori, the best means of determining vitamin C requirement would seem to be determination of the total body pool and its fractional rate of loss or catabolism. An appropriate intake would then be that to replace losses and maintain the body pool. Clinical signs of scurvy are seen when the total body pool of ascorbate is below 1.7 mmol (300 mg). The pool increases with intake, reaching a maximum of about 8.5 mmol (1,500 mg) in adults -114 /rmol (20 mg) per kg of body weight. The fractional turnover rate of ascorbate is 3% to 4% daily, suggesting a need for 45 to 60 mg per day for replacement. The basis for the 1989 U.S. Recommended Daily Allowance (RDA) of 60 mg (National Research Council, 1989) was the observed mean fractional turnover rate of 3.2% of a body pool of 20 mg per kg of body weight per day, with allowances for incomplete absorption of dietary ascorbate and individual variation. [Pg.378]

One could more readily explain the clinical signs of scurvy on the basis of the function of vitamin C in collagen formation, than one could explain the development of wet beriberi for thiamine, or of cheilosis for riboflavin function. For instance, why shouldn t riboflavin cause beriberi, and thiamine cause cheilosis—rather than the reverse We cannot explain this. The situation exemplifies that we often cannot explain the clinical findings on the basis of what is known about the biochemical function of the vitamin. There is still much more to be learned about vitamin nutrition, and this is exemplified by vitamin C. [Pg.370]

The amount of vitamin C sufficient to alleviate and cure the clinical signs of scurvy is only lOmg/day, which is probably near the minimum requirement in man. This amount, however, is not adequate to maintain near saturation of tissue in the adult human male, who has a body pool of 1.5 to 2 g and shows chnical symptoms of deficiency when this total pool falls below about 300 mg. Acknowledgment of functions of vitamin C beyond the antiscorbutic, particularly the antioxidant function, has led to the development of the concept of the optimal nutrition state, and the intake... [Pg.1106]

Mobilization and Metabolism. The total ascorbic acid body pool in healthy adults has been estimated to be approximately 1.5 g, which increases to 2.3—2.8 g with intakes of 200 mg/d (151—158). Depletion of the body pool to 600 mg initiates physiological changes, and signs of clinical scurvy are reported when the body pool falls below 300 mg (149). Approximately 3—4% of the body pool turns over daily, representing 40—60 mg/d of metabolized, or consumed, vitamin C. Smokers have a higher metaboHc turnover rate of vitamin C (approximately 100 mg/d) and a lower body pool than nonsmokers, unless compensated through increased daily intakes of vitamin C (159). The metaboHsm of ascorbic acid varies among different species. [Pg.22]


See other pages where Scurvy clinical signs is mentioned: [Pg.21]    [Pg.375]    [Pg.372]    [Pg.375]    [Pg.375]    [Pg.21]    [Pg.375]    [Pg.378]    [Pg.328]    [Pg.375]    [Pg.375]    [Pg.255]    [Pg.174]    [Pg.175]    [Pg.137]    [Pg.150]    [Pg.423]    [Pg.52]    [Pg.53]    [Pg.178]    [Pg.179]    [Pg.98]   
See also in sourсe #XX -- [ Pg.328 ]




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