In thalassemia, the reasons of growth retardation are tissue hypoxia due to
insufficient blood transfusions, iron accumulation, somatomedin C deficien
cy, and chronic zinc deficiency. In our previous studies on thalassemia, we
documented zinc deficiency in the presence of hyperzincuria. The cause of
increased urinary zinc excretion in thalassemia is not clear. Zinc is known
to bind avidly to certain amino acids, especially cystine and histidine. W
e investigated the urinary excretion of 13 amino acids and their possible r
ole in hyperzincuria in thalassemic patients with serum amino acid assays.
Mean urinary zinc excretion was found to be 1,263 +/- 20.72 mu g/24 hours,
a value significantly higher than the normal urinary zinc excretion. In 24-
hour urine samples, the levels of amino acids that have high affinity to zi
nc, as cystine, histidine, tyrosine, and lysine, were found to be higher th
an controls, and the increase in levels of serine and valine amino acids wa
s significant when compared with controls (P < 0.01). In addition, serum le
vels of histidine, lysine, tyrosine, serine, valine, isoleucine tryptophane
, and ornitine were increased (P < 0.01). It is concluded that selective am
ino aciduria may be one of the factors causing hyperzincuria in thalassemia
and the mechanisms may be clarified by further studies in future. J. Trace
Elem. Exp. Med. 13:199-203, 2000. (C) 2000 Wiley-Liss, Inc.