Letter to the Editor Tirofiban induced anemia without thrombocytopenia Hüseyin Ede a, ⁎, Mustafa Fatih Erkoç b , Halit Alüzüm c , Zeynep Tuğba Özdemir d , Ali Rıza Erbay a a Bozok University, the Faculty of Medicine, Department of Cardiology, Yozgat, Turkey b Bozok University, the Faculty of Medicine, Department of Radiology, Yozgat, Turkey c Private Sevgi Hospital, Cardiology Clinic, Kayseri, Turkey d Bozok University, the Faculty of Medicine, Department of Internal Medicine, Yozgat, Turkey article info Article history: Received 28 October 2014 Accepted 4 November 2014 Available online 8 November 2014 Keywords: Tirofiban Anemia Hemolytic anemia Dear Editor; Tirofiban is a non-peptide glycoprotein (GP) IIb/IIIa receptor antag- onist which prevents the attachment of fibrinogen and von Willebrand factor to the GP IIb/IIIa receptor on the thrombocyte surface [1]. Tirofiban-induced thrombocytopenia (TCP) (b 100,000/mm 3 ) was re- ported to be 1.1% to 1.3% [2]. Another important clinical adverse event related to tirofiban is bleeding [3]. Rates of major and minor bleedings were reported to be 0.4% and 2.0% accordingly [4]. Tirofiban-induced anemia (without any bleeding or hemorrhage) combined with TCP has been reported and the underlying mechanism of anemia was explained by immune-mediation [5]. Here, we presented a case of tirofiban- induced anemia without TCP following tirofiban usage in an acute setting. A 69-year-old man applied for elective coronary angiography (CAG) after detecting ischemia at inferolateral wall of left ventricle on his myo- cardial perfusion scintigraphy. He had a medical history of hyperlipid- emia without diabetes or hypertension. He had been an ex-smoker for last the ten years. He had experienced elective CAG six years ago for the first time in his life. At that time, one coronary bare metal stent was implanted into proximal segment of first obtuse marginalis (OM1) branch of the left circumflex coronary (LCX) artery without any compli- cation or hematological deterioration at follow-up. And three years later, the CAG repeated and the stent was observed patent without any additional new obstructive coronary artery lesions. At admission, the patient had been taking acetylsalicylic acid of 100 mg/day, met- oprolol of 50 mg/day, and atorvastatin of 20 mg/day for the last six years. He had normal hematological parameters with platelet count of 277,000/ml, hematocrit of 36.4%, and hemoglobin of 12.0 g/dl. He was taken to the angiography laboratory after receiv- ing 100 mg of acetylsalicylic acid. The CAG revealed non-obstructive le- sion (20%) in the left anterior descending coronary artery, proximally located lesion with 90% narrowing in the LCX and 90% stenosis in the ru- dimentary right coronary artery. One bare metal stent was implanted into the LCX following a loading dose of 300 mg clopidogrel and a bolus administration of 8000 IU of unfractionated heparin. Three hours later, the patient developed severe chest pain without obvious electrocardiographic deviation. The patient was transferred into cath- eterization laboratory promptly and the CAG was performed second time at the same day. Second CAG showed thrombus material filling stent lumen in proximal LCX creating 99% obstruction in the luminal di- ameter. Just after observing thrombus material in the LCX, tirofiban was started at a bolus administration of 25 μg/kg over 3 min and then 0.15 μg/kg/min continuous infusion intravenously. In the follow-up, we observed progressively decreasing hemoglobin without any TCP. Hemoglobin level had fallen from 12.0 g/dl to 8.6 g/dl at the end of the 24th hour while platelet count was relatively stable (277,000/ mm 3 vs. 271,000/mm 3 )(Table 1). On observing a trend of decrement in hemoglobin level without any apparent reason, tirofiban was ceased immediately at the 24th hour and an attempt to find possible cause of he- moglobin decrease was started. During 24-hour tirofiban infusion, the pa- tient didn't reveal any clinical signs or symptoms related to hemorrhage except fever of 38.9 °C started approximately 4 h after tirofiban infusion and controlled with paracetamol. Neurological examination was normal and digital rectal examination was without blood. Microscopic examination of the blood film showed hemolytic anemia (schistocytes, acanthocytes, and spherocytes) with single large thrombocytes implying antiaggregant use (Fig. 1a). A computed tomography with intravenous contrast agent revealed negative result for retroperitoneal hematoma or any other source of internal bleeding (Fig. 1b). Both direct and indirect Coombs tests were negative. 24 h after stopping tirofiban infusion, anemia started to recover without any other intervention. One week later he had hematocrit of 32.4% and obvious recovery on the blood film examination. Here, a case of acutely developed anemia without TCP following tirofiban infusion used for a coronary artery intervention in an acute International Journal of Cardiology 179 (2015) 500–501 ⁎ Corresponding author at: Bozok University, Faculty of Medicine, Cardiology Department, Adnan Menderes Bulvarı No:44, 66200 Yozgat, Turkey. E-mail address: huseyinede@gmail.com (H. Ede). http://dx.doi.org/10.1016/j.ijcard.2014.11.041 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved. Contents lists available at ScienceDirect International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard