Hyperzincuria and selective aminoaciduria in thalassemia
Journal of Trace Elements in Experimental Medicine, cilt.13, sa.2, ss.199-204, 2000 (Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 13 Sayı: 2
- Basım Tarihi: 2000
- Dergi Adı: Journal of Trace Elements in Experimental Medicine
- Derginin Tarandığı İndeksler: Scopus
- Sayfa Sayıları: ss.199-204
- Anahtar Kelimeler: thalassemia, hyperzincuria, aminoaciduria
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
In thalassemia, the reasons of growth retardation are tissue hypoxia due to insufficient blood transfusions, iron accumulation, somatomedin C deficiency, 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. We investigated the urinary excretion of 13 amino acids and their possible role in hyperzincuria in thalassemic patients with serum amino acid assays. Mean urinary zinc excretion was found to be 1263 ± 20.72 μg/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 zinc, as cystine, histidine, tyrosine, and lysine, were found to be higher than controls, and the increase in levels of serine and valine amino acids was significant when compared with controls (P < 0.01). In addition, serum levels of histidine, lysine, tyrosine, serine, valine, isoleucine tryptophane, and ornitine were increased (P < 0.01). It is concluded that selective amino aciduria may be one of the factors causing hyperzincuria in thalassemia and the mechanisms may be clarified by further studies in future. (C) 2000 Wiley-Liss, Inc.