We read with great interest the paper by Premawardhena et al (2008), in which the authors investigated the clinical findings in a group of β-thalassaemia heterozygotes. They found that there was no significant difference in the frequency of palpable spleens between normal controls and those with β-thalassaemia trait (2·25% vs. 2·3% respectively, P = 0·949) and concluded that, if an individual with β-thalassaemia trait has a palpable spleen, other causes should be sought (Premawardhena et al, 2008).
Almost simultaneously, Karimi et al (2007) published their findings concerning the prevalence of splenomegaly in β-thalassaemia minor in 74 cases (and 185 controls), using ultrasonography to calculate splenic volume. They found that splenic volume was significantly increased in thalassaemia trait compared to controls (163·48 ± 133·97 mm3 vs. 126·29 ± 53·98 mm3 respectively, P = 0·0016). This difference corresponded to an average increase in splenic volume by 29·4%. However, as a general rule, the size of the spleen should be enlarged by more than 40% in order to be palpable on physical examination (Blackburn, 1953).
Previous studies on splenomegaly in beta thalassaemia minor yielded conflicting results (Weatherall & Clegg, 2001). In our opinion, the combination of these two recent studies (Karimi et al, 2007; Premawardhena et al, 2008) points towards the conclusion that, indeed, the spleen is enlarged in β-thalassaemia minor but usually not to such a degree to be palpable. This was also evident in an older study (Tassiopoulos et al, 1995), in which all beta-thalassaemia heterozygotes had increased splenic volume compared to controls (132·94 ± 41·76 mm3 vs. 80·29 ± 25·88 mm3 respectively) but only 17·8% of them had a palpable spleen. It seems that radio-imaging techniques, such as ultrasonography or computed tomography scan, may detect a slightly enlarged spleen in beta thalassaemia trait without, however, being palpable in most cases.