Thrombotic microangiopathy and cytomegalovirus in liver transplant recipients: a case‐based review

• Published in: Transplant infectious disease 2003-06, Vol.5 (2), p.98-103
• Main Authors: Ramasubbu, K., Mullick, T., Koo, A., Hussein, M., Henderson, J.M., Mullen, K.D., Avery, R.K.
• Format: Article
• Language: English
• Subjects: Adult; Anemias. Hemoglobinopathies; Antibiotics. Antiinfectious agents. Antiparasitic agents; Antiviral agents; Biological and medical sciences; Cytomegalovirus; Cytomegalovirus - isolation & purification; cytomegalovirus infection; Cytomegalovirus Infections - complications; Cytomegalovirus Infections - virology; Diseases of red blood cells; Female; Gastritis - diagnosis; Gastritis - virology; Hematologic and hematopoietic diseases; Hemolytic-Uremic Syndrome - etiology; Humans; Immunosuppressive Agents - administration & dosage; liver transplant; Liver Transplantation - adverse effects; Medical sciences; Pharmacology. Drug treatments; Purpura, Thrombotic Thrombocytopenic - etiology; tacrolimus; Tacrolimus - administration & dosage; thrombotic microangiopathy
• ISSN: 1398-2273; 1399-3062
• DOI: 10.1034/j.1399-3062.2003.00019.x

: Background. Thrombotic microangiopathy (TMA) is a rare but potentially lethal complication encountered in solid organ and bone marrow transplant recipients, requiring rapid recognition, diagnosis, and initiation of therapy. Several potential causes have been identified in this setting, including viral infections and medications. Methods. We report a case of TMA in a liver transplant recipient with active cytomegalovirus (CMV) gastritis. A 41‐year‐old female presented 3 months after liver transplantation with a 5‐week history of nausea, vomiting, anorexia, and diarrhea. CMV serology was donor seropositive and recipient seronegative (D+/R−). The immunosuppressive regimen consisted of tacrolimus, mycophenolate mofetil, and prednisone. Evaluation revealed CMV viremia with a high viral load and intravenous ganciclovir was started. A decline in hemoglobin and platelets with an increase in lactate dehydrogenase (LDH) warranted hematologic evaluation, which revealed findings consistent with microangiopathic hemolytic anemia. Ganciclovir and tacrolimus were discontinued. Intravenous immunoglobulin was administered and daily plasmapheresis was initiated. As the patient's blood counts and LDH started to improve, ganciclovir was cautiously reinstituted. The patient's gastrointestinal symptoms gradually resolved and her blood counts continued to improve with prolonged plasmapheresis (a total of 23 plasmapheresis sessions). Tacrolimus and possibly CMV infection were suspected to be the cause for her TMA, and cyclosporine was substituted. Conclusions. TMA is an important entity in the differential diagnosis of acute hemolytic anemia in liver transplant recipients. Many cases seem to be medication‐induced. However, in treatment‐resistant or relapsing cases, a possibility of concomitant CMV infection should be considered.