A Case of Tacrolimus-Induced Thrombotic Thrombocytopenic Purpura in a Heart-Liver En Bloc Transplant Patient

Case Report

Ann Hematol Oncol. 2017; 4(12): 1185.

A Case of Tacrolimus-Induced Thrombotic Thrombocytopenic Purpura in a Heart-Liver En Bloc Transplant Patient

Lee R*, Mukherji J, Maxfield B and Chow J

Department of Anesthesiology, Loyola University Medical Center, USA

*Corresponding author: Lee R, Department of Anesthesiology, Loyola University Medical Center, USA

Received: October 24, 2017; Accepted: November 30, 2017; Published: December 19, 2017

Abstract

Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy (TMA) most often described as a classic pentad of microangiopathic hemolytic anemia, thrombocytopenia, neurologic involvement, renal abnormalities and fever.

Keywords: Thrombotic thrombocytopenic purpura; Heart-Liver En Bloc transplant; NASH cirrhosis

Introduction

It can present primarily, due to a deficiency of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), or secondary to pregnancy, solid organ or bone marrow transplant, malignancy, autoimmune or medications [1]. Cases of TMA secondary to antirejection medications such calcineurin inhibitors after solid organ transplantation has been reported [2] and here we describe a case of TTP secondary to tacrolimus.

Case Presentation

A 56 year old female with history of NASH (nonalcoholic steatohepatitis) cirrhosis, ischemic cardiomyopathy and heart failure with reduced ejection fraction who had left ventricular assist device placed with a plan for bridge to transplant BTT), presented for an orthotopic heart and liver transplant. Her intraoperative and immediate postoperative period was largely uneventful and she was started on tacrolimus for antirejection on POD#4. On POD#9, the patient was found to have an altered mental status, fever and leukocytosis. Pancultures and imaging revealed no signs of active infection. She was continued on tacrolimus and on POD#11, she was noted to have decreased UOP refractory to diuretics. Her creatinine was noted to be elevated as well as worsening thrombocytopenia. Peripheral blood smear revealed schistocytes (Figure 1). Lactate dehydrogenase (LDH) was noted to be elevated at 535 IU/L (normal 98-192) and haptoglobin decreased at <15 mg/dL (normal 36-195), consistent with hemolysis. There was a clinical suspicion of TTP on POD#16, her platelet count dropped even further to 25 k/UL (normal 150-400), for which she underwent plasmapheresis. On POD#17, she underwent a renal biopsy which revealed cortical necrosis as well as microthrombi, consistent with a diagnosis of TMA, likely TTP. On POD#18, tacrolimus was discontinued and she was started on cyclosporine. She underwent a renal ultrasound which revealed no flow to the left kidney. ADAMST13 activity was found to be mildly below normal limits at 62% (normal 67%). A diagnosis of tacrolimus induced TTP was made given her lab findings, pathology, and improving clinical picture once tacrolimus was discontinued.

Citation:Lee R, Mukherji J, Maxfield B and Chow J. A Case of Tacrolimus-Induced Thrombotic Thrombocytopenic Purpura in a Heart-Liver En Bloc Transplant Patient. Ann Hematol Oncol. 2017; 4(12): 1185. ISSN:2375-7965