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The technique of liver splitting offers an effective way of increasing the donor pool and decreasing pediatric waiting list mortality. A donor liver is divided in such a way that the left lateral liver graft can be transplanted into a small child and the right extended liver graft into an adult. This innovative technique did not harm the adult recipient pool. Because of its technical complexity and the initial poor results after split liver transplantation (SLT) this procedure has slowly gained acceptance in the Transplantation Community after its first introduction in 1988 (4). Small children with end stage liver disease suffered the most from the extreme shortage of cadaveric donor organs due to the difficulty of finding size-matched donors. The successful surgical development of SLT and a better donor and recipient selection have led to a reduction of the pediatric pretransplant mortality to nearly zero and to results comparable with those after whole organ transplantation (WLT). By splitting a donor organ into two 'full' hemi-grafts and providing a small adult ( < 60 kg) or a big child ( > 30 kg) with the full left graft and a medium-sized adult (60-80 kg) with the full right graft, a small-for-size situation for adolescents or adults can be avoided and the total number of available grafts can be increased. It is the goal to provide each recipient with its customized graft in the near future. However, splitting for two adults requires high technical skills and profound knowledge of the anatomic variations and should be performed in centers with large transplantation experience.

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Hypogammaglobulinemia has been reported after solid organ transplantation in adults, however immunoglobulin replacement [intravenous immunoglobulins (IVIG)] is only necessary in a minority of affected patients. We here present three pediatric patients with severe post-transplant hypogammaglobulinemia following liver transplantation (LTx) receiving a cyclosporine-based standard immunosuppression. Patient 1 was transplanted at the age of 10 months for biliary atresia. Eight weeks post-Ltx the serum IgG was 1.7 g/L. Patient 2 was transplanted at the age of 12 yr for acute liver failure. Four weeks post-Ltx the IgG dropped to 2.6 g/L. Patient 3 was transplanted at the age of 4 months for biliary atresia. Ten weeks post-Ltx severe hypogammaglobulinemia (IgG < 1.48 g/L) was diagnosed during a severe infectious complication. Patients 1 and 3 received a steroid bolus therapy for acute graft rejection. All patients had normal IgG concentrations prior to Ltx and lymphocyte subsets were post-operatively in the normal range. There was no extensive loss of protein by ascites. IGIV were replaced in the three patients monthly without further complications. In two of the patients (1 and 3) IVIG therapy was discontinued 8 and 10 months after Ltx when the immunosuppression has been reduced and serum IgG concentrations were found in the normal range without further immunoglobulin replacement. Severe hypogammaglobulinemia is a rare phenomenon following pediatric LTx and seems to be mainly caused by immunosuppressive drugs, however, the exact underlying mechanisms are unclear. A screening for hypogammaglobulinemia is useful after pediatric LTx, especially in patients with an intensified immunosuppression. Moreover, further immunologic research in affected patients is necessary.

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