Abstract
Drug-induced thrombotic microangiopathy (DITMA) is a potentially life-threatening condition causing hemolytic anemia with microvascular damage. DITMA is generally associated with calcineurin inhibitor use when observed in solid organ transplant recipients. Herein, we describe a rare case of ciprofloxacin-induced TMA in a lung transplant recipient who recovered immediately after discontinuation of the drug.
A 67-year-old female bilateral lung transplant recipient presented 21 months post-transplant with a one-week history of weakness and increasing fatigue. Maintenance immunosuppression consisted of tacrolimus, prednisone, and mycophenolate mofetil. The patient was receiving antibiotic therapy with ciprofloxacin prior to admission for recent Nocardia infection. Physical exam revealed multiple ecchymoses on the bilateral upper extremities, attributed to frail skin in the setting of chronic prednisone use. Complete blood count on admission revealed anemia (hemoglobin, 7.6 g/dL), leukopenia (3 × 109/L), and thrombocytopenia (26 × 109/L). Urea and creatinine were elevated (36 mmol/L and 136 μmol/L, respectively). Coagulation panel was normal with no evidence of disseminated intravascular coagulation. Peripheral blood smear showed marked red cell fragmentation consistent with TMA. Further investigation revealed elevated serum lactate dehydrogenase (560 U/L) and total bilirubin (39 μmol/L), with low haptoglobin levels (<8 mg/dL). Given the association between calcineurin inhibitors and DITMA in solid organ transplant recipients, tacrolimus was discontinued. Despite these efforts, no improvements were noted in the patient's hematological profile.
On review of literature, we identified a rare association of ciprofloxacin with DITMA, and thus this medication was discontinued immediately. Within 48 hours, platelet count and haptoglobin levels improved. Rarely, clinicians may need to consider other possible offending agents when TMA persists after discontinuing calcineurin inhibitor use in transplant recipients.