A CASE OF RENAL CYST INFECTION DEVELOPING FULMINANT DRUG-INDUCED IMMUNE THROMBOCYTOPENIC PURPURA DURING MULTIPLE ANTIBIOTIC THERAPY

Drug-induced thrombocytopenic purpura (DITP) is often characterized by a platelet count falling below 20,000/μL within five to ten days after the administration of a drug. Here, we report a case of DITP in which the patient experienced a rapid decrease in platelet (PLT) count to below the detectable limit within 24 hours.

A 65-year-old male with end-stage kidney disease due to polycystic kidney disease received a kidney transplant from a living donor. The patient presented with fever and left-sided abdominal pain and was diagnosed with an infected renal cyst based on magnetic resonance imaging findings. On Day 1, levofloxacin (LVFX) 500 mg/day was initiated, and on Day 2, clindamycin (CLDM) 1.2 g/day and meropenem (MEPM) 1 g/day were administered intravenously. However, his C-reactive protein level rose, so teicoplanin (TEIC) 2 g/day was added on day 4. On that same day, his PLT count was 257,000/μL. However, 24 hours later, his PLT count was reported to be less than 2,000/μL, with only a very small number visible by visual inspection. On day 4, a retroperitoneal hematoma with a maximum diameter of over 20 cm formed. It originated from bleeding in a left renal cyst and emergency selective renal artery embolization was enforced. Laboratory findings excluded disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, drug-induced and post-transplant thrombotic microangiopathy. Based on the rapid decrease in PLT count after drug initiation, DITP was suspected and all newly initiated drugs were discontinued. The patient received intravenous prednisolone (PSL) at 80 mg (1 mg/kg) and immunoglobulin at 30 g/day. The PLT count slowly increased, reaching 210,000/μL by day 11. However, on day 23, while PSL was being tapered to 10 mg/day, the PLT count dropped again to 125,000/μL. On day 26, the PLT count decreased to 93,000/μL, so PSL was increased to 30 mg/day, starting that day. The PLT count subsequently rose rapidly and recovered to 253,000/μL by day 37. After carefully tapering the PSL dosage, no further decline in the PLT count was observed.

Six drugs were considered potential causes of DITP: asciminib, LVFX, CLDM, MEPM, darbepoetin (DA), and TEIC. Although platelet-reactive antibodies were not detected by serological testing, the characteristic clinical course, with a recurrent decrease in PLT during tapering, suggested that the causative drug might still have been present in the blood on Day 23. Considering the half-lives of each drug, asciminib, LVFX, CLDM, and MEPM's blood concentrations were estimated to be negligible on Day 23, while DA was expected to retain a few percent of its C-max. According to therapeutic drug monitoring (TDM), the estimated TEIC blood concentration on day 23 was 1.1 μg/mL. To our knowledge, there have been four reports of DITP caused by TEIC, but none caused by DA.

We present a case of polycystic kidney disease that required selective arterial embolization due to renal cyst hemorrhage associated with fulminant DITP. Through TDM, analysis using drug half-life data, and a literature review, we estimated that TEIC was the causative agent among the six suspected drugs.

This abstract was also submitted for the 352nd Annual Meeting of the Kyushu Branch of the Japanese Society of Internal Medicine.