Possible ameliorative effect of taurine in the treatment of iron‐deficiency anaemia in female university students of Gaza, Palestine

• Published in: European journal of haematology 2002-10, Vol.69 (4), p.236-242
• Main Authors: Sirdah, Mahmoud M., El‐Agouza, Ibrahim M. A., Abu Shahla, Abdel Nasser K.
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; anaemia; Anemia, Iron-Deficiency - blood; Anemia, Iron-Deficiency - drug therapy; Biological and medical sciences; Blood. Blood coagulation. Reticuloendothelial system; Double-Blind Method; Erythrocyte Count; Female; ferrous sulfate; Hemoglobin A2 - metabolism; Humans; Iron - blood; Iron Compounds - pharmacology; Iron Compounds - therapeutic use; iron deficiency; Medical sciences; Middle East; Pharmacology. Drug treatments; Students; taurine; Taurine - blood; Taurine - pharmacology; Taurine - therapeutic use; treatment
• ISSN: 0902-4441; 1600-0609
• DOI: 10.1034/j.1600-0609.2002.02722.x

: The aim of the study was to evaluate the haematological effects of adding the antioxidant taurine to iron sulfate in the treatment of iron‐deficiency anaemia (IDA). A sample of 730 students from Al‐Azhar University, Gaza, in Palestine underwent screening with complete blood counts and serum samples. In subjects with microcytosis/hypochromasia, Alpha2 delta2 (HbA2) and serum concentrations of iron, total iron binding capacity (TIBC), ferritin and taurine were determined. Samples from 17 normocytic, normochromic, and non‐anaemic subjects were used as baseline controls. At base‐line, 81 of the 730 subjects (11.1%) had microcytosis/hypochromasia, 26 (3.6%) were diagnosed as β‐thalassemia carriers, none of which was iron deficient. Four subjects had microcytosis of unknown cause. Fifty‐one subjects (all females) had iron‐deficiency anaemia and were included in the therapeutic study, which lasted for 20 wk. They were matched for Hb into pairs and were treated with oral iron (325 mg of slow‐release iron sulfate). In addition, they were, in a double‐blind procedure, randomised to additional oral taurine (1000 mg d−1 at a cost comparable to that of adding ascorbic acid) or placebo. Mean S‐taurine was significantly lower in the IDA subjects than in the controls. After 20 wk of iron supplementation, both the taurine and placebo group significantly improved their Hb concentrations and normalised the markers of iron deficiency. Apart from the expected, albeit in this study mild side‐effects of oral iron, no significant side‐effects were noted. In the taurine group, there was a statistically significant additive positive change from the baseline values on Hb (2.67 ± 1.24 g dL−1), red blood cell (RBC) count [(0.57 ± 0.25) × 1012 L−1] and serum ferritin (30.33 ± 17.99 μg L−1) as compared to placebo group values, which were 1.80 ± 1.10 g dL−1, (0.39 ± 0.36) × 1012 L−1, and 20.11 ± 7.34 μg L−1, respectively. Oral taurine appears to increase the effectiveness of oral iron in the treatment of IDA, and has no significant side‐effects. This merits further cost–benefit and clinical analyses.