Abstract | April 6, 2022

A Rare case of Immune Thrombocytopenic Purpura Secondary to Clopidogrel

Presenting Author: Haroutiun Hamzoian, Doctor of Medicine, Internal Medicine Resident PGY1, Department of Medicine, HCA Kingwood, Kingwood, Texas; Lakshmi Tatineni, MD, Internal Medicine, PGY1, HCA Healthcare, Kingwood, TX

Coauthors: Haroutiun Hamzoian, MD, Internal Medicine, PGY1, HCA Healthcare, Kingwood, TX; Lakshmi Tatineni, MD, Internal Medicine, PGY1, HCA Healthcare, Kingwood, TX; Muhammad Monk, MD, Internal Medicine, PGY1, HCA Healthcare, Kingwood, TX; Aswin Srinivasan, DO, Internal Medicine, PGY2, HCA Healthcare, Kingwood, TX; Branden Wilson, DO, Internal Medicine, PGY2, HCA Healthcare, Kingwood, TX; Ahmed Qadri, MD, Internal Medicine, Hospitalist, HCA Healthcare, Kingwood, TX

Learning Objectives

  1. To familiarize with the possible severe thrombocytopenia of clopidogrel, commonly known as a safe and effective medication.
  2. To quickly recognize and treat patients experiencing thrombocytopenia due to clopidogrel induced immune thrombocytopenic purpura.
  3. To stress the importance of checking the platelet levels prior to and after starting clopidogrel.

Introduction: Immune Thrombocytopenic Purpura (ITP) is an autoimmune condition in which pathogenic antibodies bind platelets, accelerating their clearance from circulation leading to profound thrombocytopenia. In this case report, we present a unique case of an acute and severe drop in platelet count after initiation of clopidogrel.

Case Description: A 69-year-old male with PMH of CAD with recent left circumflex drug-eluting stent placement, presented with two weeks history of bruising on his upper extremities and petechiae on his abdomen and bilateral lower extremities. Laboratory studies were unremarkable except for platelet count of 4K/uL. Peripheral smear showed decreased platelets without platelet clumping. Iron panel, TSH and vitamins B1/B12/C were within normal limits. HIV, HIT antibodies, COVID-19 and ANA were negative. Bone marrow biopsy was unremarkable. One notable finding was that the patient underwent left heart catheterization a month prior and was discharged with aspirin and clopidogrel. During his hospitalization, all antiplatelet and anticoagulation were held and the patient was transfused 4 units of platelets. He was started on Prednisone daily and IVIG for three days. Aspirin was restarted when platelets had improved to 50K/uL. Ticagrelor was substituted for clopidogrel as an alternative antiplatelet therapy upon discharge.

Discussion: In this case, we excluded causes from decreased production of platelets (aplastic anemia, hematologic malignancies) and from other causes of increased destruction of platelets (DIC, HUS, TTP, HIT, sepsis, viral infections) or pseudothrombocytopenia. The only concerning change was the recent addition of clopidogrel to our patient’s medication regimen. Two known mechanisms for clopidogrel-inducedthrombocytopenia have been reported in the literature. One is clopidogrel-induced thrombotic thrombocytopenic purpura (TTP) which was ruled out in our patient. TTP is more commonly reported with an incidence of 1:26,000. A second mechanism is Clopidogrel-induced ITP which occurs at a much lower incidence, and which our patient was found to have. Clopidogrel-induced ITP is treated by drug withdrawal, steroids and immunoglobulin. Our patient’s thrombocytopenia was successfully treated with this regimen.

Conclusion: This case illustrates the importance of being aware about life threatening complications of clopidogrel. It also highlights the need to measure platelet levels before and after initiating clopidogrel therapy.

References and Resources:

  1. https://pubmed.ncbi.nlm.nih.gov/9360060/
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2999053/