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Editor—The heterogeneity of the molecular lesions which underlie the failure of erythropoietic cells to synthesise normal haemoglobin in β thalassaemia1 is a complicating factor in its molecular diagnosis. However, although more than 100 different mutations have been identified, mostly single base substitutions or small deletions and insertions in the β globin gene, in many populations the bulk of β thalassaemia is caused by a population specific spectrum of only a small number of mutations.1The strategy for the detection of mutations in patients, therefore, normally involves screening in the first instance for a small number of mutations that are the most common for the population concerned.
Two of the most commonly used screening procedures are dot blot or reverse dot blot hybridisation2 and the amplification refractory mutation system (ARMS).3 While these procedures are satisfactory in the hands of the more experienced specialised laboratories, the exacting conditions required for the performance of allele specific hybridisation or PCR amplification steps have made them less reproducible in less advanced laboratories.4 5 In south east Asia, where in some regions the frequency of β thalassaemia can be as high as 10%,6 7 many laboratories in medium sized provincial hospitals and universities are suitably …