Sticky Platelet Syndrome: A Manageable Risk Factor for Posttransplant Thromboembolic Events

Abstract

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...

Sticky Platelet Syndrome: History and Future Perspectives

“…The concomitant occurrence of SPS with other well-defined thrombophilias (elevated factor VIII, antiphospholipid syndrome, prothrombin G20201A, and hyperhomocysteinemia) were subsequently reported. 29,[33][34][35][36][37] In fact, as shown by Ruiz-Argüelles et al, most patients with SPS phenotype might display other thrombophilic conditions, both inherited and acquired. Thus, the coexistence of SPS with other conditions may be required in some cases for the development of vaso-occlusive episodes and clinical manifestation, in accordance with the concept of multifactorial thrombophilia.…”

Sticky platelet syndrome in patients with unexplained venous thrombosis

“…Apart from venous thrombosis, SPS has been associated with various other clinical entities, including acute coronary syndrome with normal coronary angiography findings [6], transient ischemic attack [2], recurrent miscarriage syndrome [7], peripheral arterial microembolism [8], ischemic optic neuropathy [9,10] and post-transplant thromboembolic events [11,12]. The prevalence of SPS in patients with thrombosis varies with the location of involved vessels and study population.…”

Sticky platelet syndrome as a possible cause for free flap failure—A case report

“…In type I, increased platelet aggregation can be induced by ADP and epinephrine, in type II (which is the most common type) by epinephrine alone and in type III only by ADP. 4 Although the overall clinical picture of 4,5,10,11 It is suspected that patients with SPS have a predisposition for vascular thromboses, but do not necessarily experience the possible consequences of aggregational disorders. Furthermore, it is hypothesized that adrenalin release in vivo may induce platelet aggregation.…”