Teicoplanin-suspected drug-induced immune thrombocytopenia causes fulminant platelet drop in polycystic kidney disease patient

Patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) are prone to complications like renal cyst infections, which often necessitate aggressive, broad-spectrum antimicrobial therapy. While effective, such regimens increase the risk of adverse drug reactions. Drug-induced immune thrombocytopenia (DITP) is a rare but severe adverse event characterized by an abrupt, profound drop in platelet count, often leading to life-threatening hemorrhage. Identifying the causative agent in polymedicated patients can be challenging, underscoring the need for heightened clinical suspicion and monitoring, especially when multiple drugs are initiated concurrently.

A 65-year-old man with polycystic kidney disease and a history of kidney transplantation presented with fever and left flank pain, diagnosed as renal cyst infection. He was initiated on combination antimicrobial therapy: levofloxacin, clindamycin, meropenem, and teicoplanin. Platelet counts were monitored daily as part of routine care. The primary endpoint was the occurrence and severity of thrombocytopenia and the clinical course following its onset, including management and suspected drug identification.

On day 5 of antimicrobial therapy, the patient's platelet count was 257,000/µL. However, it precipitously declined overnight to an undetectable level, <2,000/µL. This fulminant thrombocytopenia was followed by a massive retroperitoneal hematoma, presumed to be from the infected renal cyst, necessitating emergency selective arterial embolization. All recently initiated medications were discontinued, and the patient was treated with high-dose intravenous dexamethasone and intravenous immunoglobulin, which led to a transient recovery of the platelet count. > However, thrombocytopenia recurred during prednisolone tapering, highlighting the persistent immune challenge. Although drug-dependent platelet-reactive antibodies were not detected in the patient's serum, teicoplanin was considered the most plausible causative agent based on pharmacokinetic considerations and prior case reports of teicoplanin-induced DITP.