Eptifibatide-induced acute profound thrombocytopenia: a case report.

BACKGROUND: The interactions among cells or among cells and components of the extracellular matrix, is a crucial pathophysiological process involving some molecules collectively known as adhesion molecules (CAMs). Glycoprotein IIb / IIIa receptors are only restricted to blood platelets and they bind fibrinogen and adhesion proteins such as fibronectin, vitronectin, von Willebrand factor to form cross bridges between adjacent platelets. IIb/IIIa receptor antagonists are an object of intense research activity for target therapy worldwide during the last decades. Three GPIIb/IIIa inhibitors, abciximab, tirofiban, and eptifibatide, have been approved for clinical use. Profound thrombocytopenia is an uncommon but clinically important complication of glycoprotein IIb/IIIa inhibitors. CASE PRESENTATION: This case report discusses a forty-four-year-old male patient with acute coronary syndrome who underwent percutaneous coronary intervention and developed profound thrombocytopenia within 4 hours of first administration of eptifibatide. CONCLUSION: This report adds another case of eptifibatide-induced thrombocytopenia to the medical literature and endorses the importance of platelet count monitoring after initiating therapy with this agent.

Acute presentation of vasospastic angina induced by oral capecitabine: a case report.

INTRODUCTION: Oral capecitabine is an oral prodrug of 5-fluorouracil that has been integrated into the management of multiple cancer types because of the convenience of administration and its efficacy compared with 5-fluorouracil. Capecitabine mimics the pharmacokinetics of intravenous 5-fluorouracil. While cardiac events associated with the use of 5-fluorouracil are a well-known side effect, capecitabine-induced cardiotoxicity has only been rarely reported. CASE PRESENTATION: We present a case of a 46-year-old woman of Greek ethnicity who presented to our institution with an operated gastric sarcoma who experienced capecitabine-induced vasospastic angina. Primarily a clinical diagnosis of a possible acute coronary syndrome was proposed and the patient was admitted to the hospital for further investigation which was proved between normal limits. After a witnessed episode of angina, her prior history of capecitabine intake and an undertaken further imaging investigation we associated anginal symptoms and signs with vasospastic angina induced by capecitabine 36 hours prior to hospital admission. CONCLUSION: Cardiologists should be aware of the potential cardiac hazards of capecitabine, especially in patients with cardiovascular risk factors. Due to the increasing usage of capecitabine during the last years, patients should be warned for the possibility of chest pain, particularly during the first few days of capecitabine treatment. Specifically, patients developing acute coronary syndrome should not be retreated with capecitabine. On the other hand, due to its promising antitumoral efficacy, its use should not be discouraged.