Download Advances in Clinical Chemistry, Vol. 23 by A.L & Schwartz, Morton Latner PDF

By A.L & Schwartz, Morton Latner

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Sideroblastic anemia has been reported in pyridoxine-deficient animals and in patients receiving pyridoxine antagonists. Treatment of the condition with oral pyridoxine may lead to hematological improvement. However, response to the pyridoxine is usually suboptimal, if it occurs, and very large doses are required. Hines and Grasso (H6) suggest that a block in the conversion of pyridoxine to pyridoxal phosphate might be the underlying cause of sideroblastic anemia. Hines and Cowan (H7) showed that conversion was defective in alcoholinduced sideroblastic anemia and thought pyridoxine kinase activity was inhibited.

C ystathioninuria Cystathionine is a key intermediate in the transsulfuration pathway of methionine metabolism, where it fills its only known biological function in the transfer of the sulfur atom from methionine to cysteine. 1) requires pyridoxal phosphate as a cofactor. Clinically, patients with cystathioninuria show no consistent signs or symptoms, although several have been retarded. On the other hand, sibs of affected cases who have been shown to have the biochemical disease have been clinically normal.

The mechanism of the malabsorption here is probably a combination of decreased transit time through the absorptive area of the gut, slightly reduced absorptive area, and temporarily reduced intake. The chronic inflammatory condition, Crohn’s disease, is also associated with low plasma pyridoxal phosphate levels (M),as well as low plasma folate levels. Whether this deficiency is a result of malabsorption or due to an increased requirement induced by the inflammatory process requires further investigation.

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