Th1/Th2 LYMPHOCYTE SUBSETS IN PURE RED CELL APLASIA

I read with interest the article by Fujisao & Tsuda (1998) entitled ‘Th1/Th2 balance alteration in the clinical course of a patient with pure red cell aplasia’. The authors conclude, based on the analysis of Th1/Th2 ratios pre- and post-thymectomy and during a subsequent relapse and remission of pure red cell aplasia (PRCA), that polarization of T-helper lymphocyte subsets to Th2 type, induced by clonally expanded T cells in thymoma, are involved in the pathogenesis of PRCA. I would like to point out that the data provided in the article fail to support the authors' conclusions and that their inferences are misleading.

Firstly, their report suggests that the T-helper cell subset changes were induced by clonally expanded T cells in thymoma. Although the initial normalization from the previously low Th1/Th2 ratio immediately following thymectomy may suggest a link between thymoma and an altered Th subset ratio, the observation that a similar fall and normalization of the ratio occurred subsequently without any clinical evidence of a relapse (and later remission) of thymoma argues against such an aetiological connection.

Secondly, it should be mentioned that although the ratio of Th1/Th2 subsets declined (4.9) during relapse of PRCA, it was, however, still within the normal range (8.04 ± 3.16 as quoted by the authors) and the subsequent remission was accompanied by a concomitant rise in the ratio towards upper end of the normal range. In other words, the observed change in Th1/Th2 ratio was a fluctuation within the normal range and therefore there was, in my opinion, insufficient evidence to be able to conclude that polarization of Th subsets of Th2 is involved in the pathogenesis of PRCA.

In summary, the data provided in the article do not support the authors' conclusions that Th2 lymphocyte subset polarization is (1) induced by thymoma and (2) involved in the pathogenesis of PRCA. It is likely that the subset changes observed in this case were epiphenomena rather than indicative of a pathogenetic mechanism.