Hyperzincuria and selective aminoaciduria in thalassemia

Citation
Y. Yildirmak et al., Hyperzincuria and selective aminoaciduria in thalassemia, J TR EL EXP, 13(2), 2000, pp. 199-204
Citations number
13
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF TRACE ELEMENTS IN EXPERIMENTAL MEDICINE
ISSN journal
0896548X → ACNP
Volume
13
Issue
2
Year of publication
2000
Pages
199 - 204
Database
ISI
SICI code
0896-548X(2000)13:2<199:HASAIT>2.0.ZU;2-E
Abstract
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.