Background: SARS-CoV-2-infected subjects have been proven contagious in the symptomatic, pre-symptomatic and asymptomatic phase. The identification of these patients is crucial in order to prevent virus circulation. No reliable data on the sensitivity of nasopharyngeal swabs (NPS) are available because of the lack of a shared reference standard to identify SARS-CoV-2 infected patients. The aim of our study was to collect data on patients with a known diagnosis of COVID-19 who underwent serial testing to assess NPS sensitivity.Methods: The study was a multi-center, observational, retrospective clinical study with consecutive enrollment. We enrolled patients who met all of the following inclusion criteria: clinical recovery, documented SARS-CoV-2 infection (≥1 positive rRT-PCR result) and ≥1 positive NPS among the first two follow-up swabs. A positive NPS not preceded by a negative nasopharyngeal swab collected 24–48 h earlier was considered a true positive. A negative NPS followed by a positive NPS collected 24–48 h later was regarded as a false negative. The primary outcome was to define sensitivity of SARS-CoV-2 detection with NPS.Results: Three hundred and ninety three NPS were evaluated in 233 patients; the sensitivity was 77% (95% CI, 73 to 81%). Sensitivity of the first follow-up NPS (n = 233) was 79% (95% CI, 73 to 84%) with no significant variations over time. We found no statistically significant differences in the sensitivity of the first follow-up NPS according to time since symptom onset, age, sex, number of comorbidities, and onset symptoms.Conclusions: NPS utility in the diagnostic algorithm of COVID-19 should be reconsidered.

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Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a highly prothrombotic disorder caused by anti-PF4 antibodies that activate platelets and neutrophils, leading to thrombosis. Heparin-induced thrombocytopenia (HIT) is a related anti-PF4 mediated disorder, with similar pathophysiology and clinical manifestations but different triggers (i.e., heparin vs adenoviral vector vaccine). Clinically, both HIT and VITT typically present with thrombocytopenia and thrombosis, although the risk of thrombosis is significantly higher in VITT, and the thromboses occur in unusual anatomical sites (e.g., cerebral venous sinus thrombosis and hepatic vein thrombosis). The diagnostic accuracy of available laboratory testing differs between HIT and VITT; for VITT, ELISAs have better specificity compared to HIT and platelet activation assays require the addition of PF4. Treatment of VITT and HIT is anticoagulation non-heparin anticoagulants; however, heparin may be considered for VITT if no other option is available.

Aspirin inhibits platelet function by irreversibly inhibiting the synthesis of thromboxane A2 (TxA2). Aspirin, at low doses, is widely used for cardiovascular prevention. Gastrointestinal discomfort, mucosal erosions/ulcerations and bleeding are frequent complications of chronic treatment. To reduce these adverse effects, different formulations of aspirin have been developed, including enteric-coated (EC) aspirin, the most widely used aspirin formulation. However, EC aspirin is less effective than plain aspirin in inhibiting TxA2 production, especially in subjects with high body weight. The inadequate pharmacological efficacy of EC aspirin is mirrored by lower protection from cardiovascular events in subjects weighing >70 kg. Endoscopic studies showed that EC aspirin causes fewer erosions of the gastric mucosa compared to plain aspirin (which is absorbed in the stomach) but causes mucosal erosions in the small intestine, where it is absorbed. Several studies demonstrated that EC aspirin does not reduce the incidence of clinically relevant gastrointestinal ulceration and bleeding. Similar results were found for buffered aspirin. Although interesting, the results of experiments on the phospholipid-aspirin complex PL2200 are still preliminary. Considering its favorable pharmacological profile, plain aspirin should be the preferred formulation to be used for cardiovascular prevention.