Hypomagnesemia and risk of post-transplant lymphoproliferative disorder in liver transplant recipients.

Liver recipients have substantial risk of post-transplant lymphoproliferative disorder (PTLD) [1]. Most PTLDs result from uncontrolled replication of Epstein-Barr virus (EBV) due to immunosuppressive therapy [1]. A role of magnesium in modulating immune response and in lymphomagenesis is increasingly being recognized [2]. Decreased intracellular magnesium causes impaired T-cell and B-cell function, decreased expression of natural killer-activating receptor (NKG2D) in natural killer and T-cells leading to a blunted anti-EBV response, and increased risk of EBV-positive lymphomas [2, 3]. Hypomagnesemia was associated with EBV viral load and Burkitt lymphoma in Ugandan women, and associations of EBV with other lymphomas are also documented [4].