Iron Zinc Vitamin A and selenium

Some diet-treated patients with PKU have exhibited altered iron, zinc, vitamin A, and selenium status. With the exception of selenium, aberrations have been demonstrated even when patients consumed close to or greater than the RDI levels of the vitamin/mineral in question. The mechanisms of these changes are unclear and may be multifactorial. The actual impact of these changes on the health of the individual patients is unknown.

Low serum ferritin but appropriate hemoglobin and mean erythrocyte volumes have been noted, even in patients consuming close to three times the recommended dietary allowance (RDA) for iron. Iron absorption or bioavailability may be inhibited by the presence of calcium and phosphorous salts, diets high in PUFAs, and dietary fiber. The presence of alterations in the PUFA composition of gut cell membranes could affect iron absorption. In vitamin A-deficient rats, anemia occurred, which was not remedied by the administration of oral iron. This suggests that vitamin A deficiency in PKU patients could result in anemia unresponsive to iron therapy. The iron status of diet-treated patients should be serially monitored.

Low serum zinc has occurred in infants and children receiving greater than or equal to 70% of the RDA for zinc. Low serum zinc occurred more often in patients receiving casein hydrolysates than in patients receiving L-amino acids alone. Serum zinc may not be an accurate marker for assessment of zinc deficiency. Zinc absorption in general is inhibited by a PUFA-rich diet, fiber, phosphorous, and large amounts of iron. Competitive inhibition between calcium and zinc also occurs.

Low plasma retinol levels have been observed in infants and young children despite consumption of up to three times the RDA for vitamin A. Retinol is transported on retinol-binding protein (RBP); zinc is needed for the synthesis of RBP. Prealbumin is a carrier for RBP. RBP and zinc levels have been normal in nearly all patients with low retinol levels. Low prealbumin levels or abnormal release of RBP from prealbumin may be responsible for the low serum retinol levels. In fact, a number of children have low prealbumin levels despite receiving adequate protein and energy intakes.

Until recently, selenium was not routinely added to PKU formulas. In the past it was supplied to patients via contamination of foods grown in selenium-containing soil. Low serum, whole blood, urine, and hair levels of selenium have been observed in some patients with PKU on strict diet therapy. Low activity of the selenium-containing enzyme glutathione peroxidase also occurs. Clinical symptoms of selenium deficiency in the patients studied have not been reported.

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