Vitamin urinary excretion

As shown in Table 9.5, there are a number of indices of vitamin Be status available plasma concentrations of the vitamin, urinary excretion of 4-pyridoxic acid, activation of erythrocyte aminotransferases by pyridoxal phosphate added in vitro, and the ability to metabolize test doses of tryptophan and methionine. None is wholly satisfactory and where more than one index has been used in population studies, there is poor agreement between the different methods (Bender, 1989b Bates et al., 1999a). 

Vitamin C status is generally assessed by estimating the saturation of body reserves or measuring plasma and leukocyte concentrations of the vitamin. Urinary excretion of hydroxyproline-containing peptides is reduced in people with inadequate vitamin C status, but a number of other factors that affect bone and connective tissue turnover confound interpretation of the results (Bates, 1977). The ratio of deoxypyridinolineipyridinoline compounds derived from collagen cross-links provides a more useful index, but is potentially affected by copper status (Tsuchiya and Bates, 1997). 

Riboflavin and riboflavin phosphate that are not bound to plasma proteins are filtered at the glomerulus. Renal tubular resorption of riboflavin is saturated at normal plasma concentrations. There is also active tubular secretion of the vitamin urinary excretion of riboflavin after high doses can be two- to threefold greater than the glomerular filtration rate. 

In humans, studies of urinary excretion of pantothenic acid after oral intakes of either free pantothenic acid or of the pantothenic acid present in food have indicated a relative availability of c. 50% from the food-borne vitamin. Urinary excretion of pantothenate was c. 0.8 mg daywhen a pantothenate-deficient diet... 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Cystic fibrosis is the most common lethal autosomal-recessive disease, in which oxidative stress takes place at the airway surface [274]. This disease is characterized by chronic infection and inflammation. Enhanced free radical formation in cystic fibrosis has been shown as early as 1989 [275] and was confirmed in many following studies (see references in Ref. [274]). Contemporary studies also confirm the importance of oxidative stress in the development of cystic fibrosis. Ciabattoni et al. [276] demonstrated the enhanced in vivo lipid peroxidation and platelet activation in this disease. These authors found that urinary excretion of the products of nonenzymatic lipid peroxidation PGF2 and TXB2 was significantly higher in cystic fibrotic patients than in control subjects. It is of importance that vitamin E supplementation resulted in the reduction of the levels of these products of peroxidation. Exhaled ethane, a noninvasive marker of oxidative stress, has also been shown to increase in cystic fibrosis patients [277]. 

Biochemical findings are variable. The blood cobala-min and folate levels often are normal. Patients often have homocysteinemia with hypomethioninemia, the latter finding discriminating this group from homocystinuria secondary to cystathionine- P-synthase deficiency. Urinary excretion of methylmalonic acid may be high, reflecting the fact that vitamin B12 serves as a cofactor for the methyl-malonyl-CoA (coenzyme A) mutase reaction. 

Chromium compounds interact synergistically or antagonistically with many chemicals. For example, potassium dichromate administered by subcutaneous injection potentiated the effects of mercuric chloride, citrinin, and hexachloro-1,3-butadiene on rat kidneys (USPHS 1993). Chromium effects were lessened by ascorbic acid and Vitamin E, and N-acetyl cysteine was effective in increasing urinary excretion of chromium in rats (USPHS 1993)... 

Cl. Gassmann, B., Knapp, A., and Gartner, L. L., Vitamin Be deficiency and urinary excretion of xanthurenic acid and other tryptophan metabolites in disease. Klin. Wochschr. 37, 189-195 (1959). 

Based on limited epidemiologic evidence, fluoride supplements, with or without calcium, estrogen and vitamin D, are used by clinicians for the treatment of osteoporosis. However, knowledge of the effects of fluoride on calcium and phosphorus metabolism in normal animals is limited although Spencer et al. (32) reported that ingestion of fluoride by three osteoporotic men did not affect calcium absorption but caused a decrease in urinary excretion. Moreover, there is a need to determine the long-term effects of fluoride treatment on bone strength and on soft tissues ( ). 

Excretion of thiamine appears to vary from individual to individual,23 and some other data are available regarding the other better-known B vitamins.24 The differences in the excretion of nicotinic acid-like compounds strongly suggest the existence of individual pattems.25,26 The urinary excretion of vitamin B12, folic acid, and the citrovorum factor by different individuals, even on controlled diets, was found to vary through rather wide ranges (2- to 9-fold) though the study was not concerned with individual differences and individual patterns were not established. 27... 

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. 

Factors which cause a decrease in bioavailability include 111 high urinary excretion (2) destruction by certain mlesiinal bacteria (2) increased urinary excretion caused by vitamin C (4) presence of sulfonamides which block intestinal synthesis and (5) a decrease in absorption mechanisms. Increase in bioavailability can be provided by stimulating intestinal bacterial synthesis in certain species. No toxicity due to folic acid has been reported in humans. 

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

Some mechanisms contributing to bone mineral homeostasis. Calcium and phosphorus concentrations in the serum are controlled principally by two hormones, l,25(OH)2D3(D) and parathyroid hormone (PTH), through their action on absorption from the gut and from bone and on excretion in the urine. Both hormones increase input of calcium and phosphorus from bone into the serum vitamin D also increases absorption from the gut. Vitamin D decreases urinary excretion of both calcium and phosphorus, while PTH reduces calcium but increases phosphorus excretion. Calcitonin (CT) is a less critical hormone for calcium homeostasis, but in pharmacologic concentrations CT can reduce serum calcium and phosphorus by inhibiting bone resorption and stimulating their renal excretion. Feedback effects are not shown. 

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... 

Methylmalonyl-CoA mutase is a cobalamin-linked enzyme of mitochondria that catalyzes the isomerization of methylmalonyl-CoA to succinyl-CoA. A reduction of this enzyme due to vitamin B12 deficiency will result in a metabolic block with the urinary excretion of methylmalonic acid, and the measurement of this metabolite has been used to confirm a deficiency of vitamin B12. The test has also been useful in investigating rare abnormalities of this enzyme that result in the excretion of methylmalonic acid in the presence of adequate vitamin B12. Given an oral loading dose of valine or isoleucine will increase the urinary excretion of methylmalonic acid in patients with a vitamin B12 deficiency (G4). However, Chanarin and his colleagues (CIO) found that one-quarter of their patients with pernicious anemia excreted a normal concentration of methylmalonic acid even after a loading dose of valine. Normal subjects excrete up to 15 mg of methylmalonic acid in their urine over a 24-hour period (Cll). 

S-Methylmalonyl-CoA mutase (EC 5.4.99.2) is a deoxyadenoxyladen-osylcobalamin-dependent enzyme of mitochondria required to catalyze the conversion of methylmalonyl-CoA to succinyl-CoA. A decrease in the activity of methylmalonyl-CoA mutase leads to the urinary excretion of large amounts of methylmalonic acid (C22). The biochemical lesion may be at the mutase level due to an abnormality of apoenzyme protein or an inability to elaborate the required coenzyme form of vitamin B12> i.e., adenosyl-cobalamin. In rare cases the abnormality may be due to an inability to convert the d form of methylmalonyl-CoA mutase to the l form as a result of a defective racemase (EC 5.1.99.1) (Kll). In patients, the nature of the abnormality can be determined by tissue culture studies (D13) and by clinical trial, since patients with a defect in adenosylcobalamin production will show clinical improvement when treated with very large doses of vitamin B12 (Mil). 

Schilling, R. F., Intrinsic factor studies. II. The effect of gastric juice on the urinary excretion of radioactivity after the oral administration of radioactive vitamin B12. /. Lab. CUn. Med. 42, 860-866 (1953). 

Schilling s test assesses the oral absorption of vitamin B12 and is used to diagnose pernicious anaemia. The patient is injected intramuscularly with non-labelled vitamin B12, to saturate body stores. An oral dose of vitamin B12 labelled with cobalt-58 is administered, followed by a second dose labelled with cobalt-57 bound to intrinsic factor. Prior saturation of body stores ensures any absorbed radiolabelled vitamin B12 is rapidly excreted in the urine. Urinary excretion of orally administered vitamin B12 is low in patients with pernicious anaemia due to poor absorption. Absorption is increased when it is administered with intrinsic factor. The ratio of cobalt-57 to cobalt-58 is thus raised in patients with pernicious anaemia. Intrinsic factor antibody testing is now generally used to diagnose pernicious anaemia, though the Schilling s test may occasionally be used. 

Absorption of vitamin B12 can be investigated in several ways after oral delivery of radioactive vitamin B12 (e.g. containing Co) and subsequent measurement of radioactivity in faecal excretion, whole body counting or liver uptake, plasma radioactivity or the popular Schilling test. For the Schilling test, urinary excretion of radioactive vitamin B12 is measured 24 h following oral delivery, and impaired absorption may indicate intrinsic factor deficiency bacterial colonization of the small intestine (stagnant gut syndrome) or ileal disease. 

The principal physiological role of vitamin D is in the maintenance of the plasma concentration of calcium. Calcitriol acts to increase intestinal absorption of calcium, to reduce its excretion by increasing reabsorption in the distal renal tubule, and to mobilize the mineral from bone - of the 25 mol of calcium in the adult body, 99% is in bone. The daily intake of calcium is around 25 mmol, and intestinal secretions add an additional 7 mmol to the intestinal contents 10 to 14 mmol of this is normally absorbed, with 18 to 22 mmol excreted in feces. Bone turnover accounts for exchange of 10 mmol of calcium between bone and plasma daily. The kidneys filter some 240 mmol of calcium daily, almost all of which is reabsorbed urinary excretion of calcium is about 3 to 7 mmol per day. 

The NADPH-dependent reduction of vitamin K quinone to the hydroquinone is not inhibited by warfarin. In the presence of adequate amounts of vitamin K, the carboxylation of glutamate residues can proceed normally, despite the presence of warfarin, with the stoichiometric formation of vitamin K epoxide that cannot be reutilized. Small amounts of vitamin K epoxide, and hydroxides formed by its reduction by other enzymes, are normally found in plasma. In warfarin-treated animals and patients, there is a significant increase in the plasma concentration of both. There is also an increase in the urinary excretion of the products of side-chain oxidation of the epoxide and hydroxides. 

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