Early success has been achieved in hand transplantation with the use of currently available immunosuppressive drugs.

We read with great interest the article by Mühlfeld et al.(1) in which the authors report three patients with clinical symptoms of sticky platelet syndrome (SPS) following kidney transplantation, resulting in graft loss in one case and life-threatening thromboembolic and respiratory complications in the other two cases, respectively. SPS is a disorder of platelet hyperresponsiveness first described at our institution (2). Among 259 renal allograft recipients transplanted at our center from July 2001 through August 2007, three (1.2%) had SPS type I. All three of these renal allograft recipients were begun on an individualized anticoagulation regimen in the pretransplant period, including titration of acetylsalicylic acid (ASA) dose to normalize the platelet response to both adenosine diphosphate (ADP) and epinephrine; continued on the same therapy posttransplantation, with perioperative modification if necessary; maintained on tacrolimus-based immunosuppression; have sustained no hemorrhagic or thrombotic complications and have excellent renal function with 100% patient and graft survival.The first patient is a 49-year-old African-American female with a history of recurrent access thromboses who was found to have SPS, hyperhomocysteinemia and antiphospholipid antibodies. She was managed with vitamin B12, folic acid and ASA 81 mg twice daily, and received enoxaparin, 40 mg subcutaneously (SQ) daily, for the first 3 months after transplantation. The second patient is a 46-year-old African-American female with a history of systemic lupus erythematosus and central as well as lower extremity recurrent deep venous thromboses. She was managed with folic acid and vitamin B12 for hyperhomocysteinemia, warfarin for protein S deficiency and increased inflammatory markers and ASA 81 mg daily. At the time of transplantation, her warfarin was discontinued; she was bridged with enoxaparin, 50 mg SQ daily for 6 weeks followed by tinzaparin, 6500 units SQ daily until 3 months posttransplant; and then converted back to warfarin. The third patient is a 55-year-old African-American female with a history of recurrent access thromboses who was diagnosed with SPS and hyperhomocysteinemia. She was managed with vitamin B12, folic acid and ASA 325 mg daily, and required no perioperative adjustment in her regimen.Several differences between the two series of patients are noteworthy, and may have contributed in varying degrees to the divergent outcomes obtained. In the German cases: (i) none of the patients, except perhaps for Case 3 with a history of right retinal vein thrombosis in addition to (presumably catheter-induced) right internal jugular vein thrombosis, had a history that would prompt the performance of a pretransplant hypercoagulability workup; (ii) all three patients were SPS type II rather than type I (although this would seem to predispose to a lesser, rather than greater, risk of perioperative thrombosis) and (iii) two of the three patients were maintained on cyclosporine-based, rather than tacrolimus-based, immunosuppressio...

The increases in phosphodiesters seen in this study indicate that phospholipid synthesis and turnover were stimulated by 6 weeks of oral citicoline. These results in humans support previous in vitro and animal studies and suggest that the administration of oral citicoline may be of use in reversing age-related changes in the brain.

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