The purpose of the present study was to quantify the effect of iron deficiency anaemia on the levels of HbA2, HbF, and HbA1C. Complete blood counts (CBC) were performed on 730 university students. Serum ferritin, HbA2, HbF, and HbA1C levels were determined for all microcytic/hypochromic subjects. It was found that 81 (11.1%) of the students were microcytic/hypochromic, of which 47 (58.1%) were found to be iron deficient. Twenty-six (32.1%) were b-thalassemia carriers, 4 (4.9%) were b-thalassemia carriers with iron deficiency and 4 (4.9%) remained undiagnosed. All the anaemic students were treated with oral iron and followed for 20 weeks. The mean HbA2 level rose significantly (from 1.89% ± 0.45 to 2.19% ± 0.53, P < 0.001) after iron treatment. HbF levels were not significantly different after iron treatment (0.94% ± 0.18 before and 0.95% ± 0.17 after treatment, P > 0.05). HbA1C fell significantly after iron treatment, from a mean of 6.15% ± 0.62 to 5.25% ± 0.45 (P < 0.001). In conclusion, iron deficiency must be corrected before making any diagnostic or therapeutic decisions based on HbA2 and HbA1C levels.

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 beta-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) x 1012 L(-1)] and serum ferritin (30.33 +/- 17.99 microg L(-1)) as compared to placebo group values, which were 1.80 +/- 1.10 g dL-1, (0.39 +/- 0.36) x 1012 L(-1), and 20.11 +/- 7.34 microg 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.

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