Aparna Tiwari

The etiopathogenesis of COVID-19 and its differential geographic spread suggest some populations are apparently ‘less affected’ through many host-related factors that involve angiotensin-converting enzyme 2 (ACE2) protein, which is also the entry receptor for SARS-CoV-2. The role of ACE2 has been well studied in COVID-19 but not in the context of malaria and COVID-19. We have previously suggested how malaria might intersect with COVID-19 through ACE2 mutation and here we evaluate the currently available data that could provide a link between the two diseases. Based on the existing global and Indian data on malaria, COVID-19 and the suggested ACE2 mutation, the association could not be examined robustly, neither accepting nor refuting the suggested hypothesis. We strongly recommend targeted evaluation of this hypothesis through carefully designed robust molecular epidemiological studies.

Patients admitted to the hospital can develop thrombocytopenia due to multifactorial causes. It can be pseudo-thrombocytopenia or true thrombocytopenia. Among patients admitted for chest pain, coronary angiography (CAG) is a common diagnostic test to evaluate patients for coronary artery disease (CAD). Normally, patients undergoing angiogram receive antiplatelets and anticoagulants pre-catheterization, and platelet aggregation inhibitor agents are sometimes used during and after CAG like in patients with high thrombus burden. Glycoprotein IIb/IIIa receptor inhibitors are a type of platelet antiaggregant agents that can cause severe thrombocytopenia in few cases. We present a case of a 68-year-old patient who came to the emergency department with inferior wall ST-segment elevation myocardial infarction and underwent angiography and had percutaneous coronary intervention (PCI) done. He was administered tirofiban during the angiogram that caused acute severe thrombocytopenia decreasing platelets count to 4000/microliter within one day. Patients' platelets gradually recovered after platelets transfusion.