Her platelets continued to improve, and the patient was discharged having a platelet count of 114?k/mm3. receptors have been one of the major focuses on in the management of high risk acute coronary syndrome and in conjunction with angioplasty, especially for bailout during thrombotic complications [2]. Tirofiban, a small, non-peptide and a highly specific Glycoprotein IIb/IIIa (GPI), is definitely a competitive inhibitor of the platelet fibrinogen receptor and when given intravenously, tirofiban inhibits ex lover vivo platelet aggregation inside a dose and concentration-dependent manner. It is a risk element for severe thrombocytopenia [1,3]. The pathogenesis for this phenomenon is not completely obvious but is believed to be due to drug-dependent antibodies that abide by platelets only in the presence of the offending drug [1,3C6]. There is growing body of evidence to suggest that tirofiban alters the set up of glycoprotein receptors within the platelets, hence creating a new antigen which is definitely then acknowledged and removed Propyzamide from the blood circulation due to immune-mediated reaction. This, in essence, is the Propyzamide disposal of thrombocytes which is the cause of the sudden and severe thrombocytopenia [7]. Severe thrombocytopenia can set in immediately after exposure to Tirofiban [6]. We hereby statement a case of 69-year-old female with tirofiban-induced thrombocytopenia in which the platelet count fallen to within 12C24 h of administration with no other alternative explanation. 2.?Case demonstration A 69-year-old woman with past medical history significant for diabetes mellitus, coronary artery disease, and hypertension presented to the emergency department with issues of chest pain that was substernal in nature, not associated with any radiation, diaphoresis, nausea, or vomiting. At the time of admission, patient physical exam was unremarkable. Her platelet levels were 224?k/mm3 at baseline and troponins ( 0.01). She was initially started on aspirin 81?mg. She experienced an invasive angiogram (Number 1) due to high pre-test probability the next day and was given tirofiban infusion during the heart catheterization, she experienced two drug eluting stents placed in mid and distal portion of remaining anterior descending artery that were found to have 85% stenosis and 80% stenosis, respectively. Open in a separate window Number 1. Invasive angiogram identifying mid and distal LAD lesions. The next day after percutaneous coronary treatment, patient had developed ecchymosis and slight epistaxis, on further evaluation it was identified that her platelets experienced decreased from 224 to 2?k/mm3. Her antiplatelets were held due to acute severe thrombocytopenia. Hematology services was consulted, patient was started on steroids and given 2 models platelet transfusion. The peripheral smear ruled out thrombotic thrombocytopenic purpura (TTP) due to the absence of schistocytes. In the subsequent days, as the individuals platelets count recovered, aspirin and plavix were restarted. Her platelets continued to improve, and the patient was discharged having a platelet count of 114?k/mm3. After a week, repeat laboratory work revealed an improved platelet count to 442?k/mm3. The etiology of thrombocytopenia was concluded to be tirofiban induced as platelet count was not affected by antiplatelets when they were restarted and additional alternate explanations for thrombocytopenia were ruled out. 3.?Conversation Thrombocytopenia is a prominent complication of GPIs with an incidence of severe thrombocytopenia (platelet count 50?k/mm3) to be 0.2C0.5% [1,3,5,8]. Five different presentations of GPI-induced thrombocytopenia have been reported: (i) Acute Severe Thrombocytopenia (platelets 10?k/mm3) within 12 h of 1st TRIB3 dose administration, (ii) Acute Thrombocytopenia within 12 h of second dose administration, (iii) Delayed Thrombocytopenia (5C7?days after exposure), (iv) Anaphylaxis after first or second exposure, and (v) Pseudo thrombocytopenia [1,3]. Drug-induced thrombocytopenia is definitely a analysis of exclusion and additional alternative diagnoses should be cautiously evaluated. Heparin-induced thrombocytopenia?is similar to tirofiban-induced thrombocytopenia, both happening within 1C4 h or 7C14?days, but this can be ruled out if the patient has had no previous exposure [1]. Aspirin and clopidogrel have not reported to result in instances of isolated acute severe thrombocytopenia [3]. Studies have shown clopidogrel to Propyzamide Propyzamide occasionally become associated with TTP, which typically encompasses microangiopathic hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever, and renal dysfunction [3]. Pseudo thrombocytopenia, which is definitely clumping of platelets, can be excluded on a peripheral smear [4]. Dual anti-platelet medicines are another potential cause of thrombocytopenia, however, its onset happens after days or weeks unlike our individuals case [5]. To validate the hypothesis that tirofiban Propyzamide is definitely, in fact, the offending agent, a case reported in 2007 used ELISA and circulation cytometry to confirm the drug-dependent antibodies were indeed formed only in the presence of tirofiban [9]. Studies explain how important it is to understand the life-threatening effects associated with intracoronary use.