Common coagulation-related observations in COVID-19 patients include increased D-dimer level, decreased platelet count, increased interleukin level, abnormal tumor necrosis factor, increased lactate dehydrogenase, and prolonged prothrombin time (PT) [
11]. The patient of this report also showed increased D-dimer and PT and decreased platelet count [
11,
12]. However, another differential diagnosis for this patient was APS. This disease usually targets phospholipid proteins, and the persistent abnormal presence of these antibodies over a period of at least 3 months is essential for the diagnosis of APS [
13]. One of the diagnostic criteria for this syndrome is the presence of one or more clinical manifestations such as vascular thrombosis, platelet depletion, and heart valve disease, followed by observing abnormal levels of antiphospholipid antibodies over a period of time [
14]. However, patients with acute diseases or infections like COVID-19 may also temporarily show high levels of these antibodies [
15]. Upon detecting signs of thrombosis, we first tested the patient for antiphospholipid antibodies, and as presented in Table
2, this test returned positive. However, COVID-19 patients may also show elevated levels of some isotypes of antiphospholipid antibodies, which may follow a fluctuating course according to several studies. In some patients, antiphospholipid antibodies may disappear within a few weeks. In our patient, the antibody titer decreased and returned to the normal range over the next 15 days, which ruled out the diagnosis of APS. Therefore, COVID-19 patients with positive antiphospholipid antibodies (COVID-19-induced APS-like syndrome) should be monitored for at least 12 weeks (tested twice or more for antiphospholipid antibodies within 12 weeks) to confirm or reject the differential diagnosis of APS and provide appropriate treatment if necessary [
13]. By binding to the surface of monocytes, platelets, and endothelium, antiphospholipid antibodies can also cause higher expression of tissue factor and the release of clotting microparticles [
16]. As explained in the biography, thrombotic events in the brachial artery are indicative of this process. Therefore, it is recommended to use heparin or low-molecular-weight heparin (such as enoxaparin) to prevent thrombotic events following COVID-19 in patients who are not contraindicated [
15]. Plasma exchange can also help treat thrombotic microangiopathy and eliminate additional inflammatory mediators. In our case, the patient underwent plasmapheresis, which, as mentioned, reduced the level of antibodies and set him on the path to recovery. Another important point is to pay attention to the patient’s test results during hospitalization. Our patient showed increased erythrocyte sedimentation rate (ESR) and CRP, thrombocytopenia, and leukopenia after surgery. As research has shown, the laboratory findings that indicate COVID-19 are usually nonspecific and do not follow the same pattern in all patients. However, most studies agree that people infected with COVID-19 are likely to show increased levels of ESR and CRP, thrombocytopenia, and leukopenia [
17,
18], as was the case in our patient. Another important issue is the loss of time that could be spent on providing more effective treatment because of incorrect sampling for the COVID-19 PCR test. As explained, in the reported case, a chest X-ray indicated the presence of COVID-19, but the PCR test returned negative twice, leading to a delay in the treatment process.