**2. General aspects on COVID-19 diagnosis**

Among the biomarkers analyzed, one of the most important findings was the raised C-reactive protein (CRP) level of 41.4 mg/L (standard at 0–6 mg/L) whose circulating concentrations rise in response to inflammation. Followed by the higher CRP, the biochemistry cardiac panel also showed raised myocardial infarction markers, such as lactic dehydrogenase (LDH), aspartate aminotransferase (AST), and creatine kinase (CK). Taken together, these biomarkers strongly indicated a severe acute inflammatory phase with the ongoing cardiac effect to be controlled. Mild lymphopenia with less than 9 × 10e5 cells per mL with normal platelet counts completes the first patient's overview [2].

Pulmonary function and lung aspects were investigated in this patient in order to do the etiological diagnosis. Hypoxemia was observed according to oxygen levels of 67 mm Hg. Lungs' aspect was set by chest radiographs on day 1 of hospital admission, which was the 6th day of disease progression. The images showed abnormal features with focal and patchy consolidation in both lungs, beyond air-space shadowing such as ground-glass like opacities [2].

Image examination of the chest shows a consolidation pattern at computedtomography (CT) scans: bilateral focal consolidation, lobar consolidation, and patchy consolidation, especially in the lower lung. Five days after admission, at the 11th day of disease progression, a chest radiograph revealed a bilateral diffuse patchy and fuzzy shadow [2].

With the advancement of the pandemic, what was seen as a respiratory disease became a more complex disease and new studies were set up to list other complications and associated risk factors.

#### **3. Potential impact of thrombotic complications on COVID-19 prognosis**

Many factors can contribute to increasing the risk for severe COVID-19, in some cases followed to death. The main comorbidities described are high age, obesity, diabetes, and hypertension. Beyond the inflammation and impaired coagulation, focal damage in some tissues/organs is also related to the COVID-19 spectrum, such as liver, kidney, and heart [3].

Thrombotic complications seem to emerge as an important issue in patients infected with COVID-19. Preliminary reports on COVID-19 patients' clinical and laboratory findings include thrombocytopenia, elevated D-dimer, prolonged prothrombin time, and disseminated intravascular coagulation.

In the course of the COVID-19 studies, a clear association with coagulation dysfunction was pointed in many cases. Intra-alveolar clots were prominent findings in COVID-19 patients who developed severe respiratory disease. The same findings have been described in both clinical and animal model studies. Apparently, an impaired response in the prothrombotic pathway is in charge of diffuse alveolar hemorrhage since it is related to overt clot formation [4].

In the recent publication "Should COVID-19 be branded to Viral Thrombotic Fever?," the authors intended to frame COVID-19 in more clinical terminology, making an analogy to Viral Hemorrhagic Fever (VHF). In this article, the authors reported: "We found irrefutable evidence in the current literature that COVID-19 is the first viral disease that can be marketed as a viral thrombotic fever" [5]. Although this is a very categorical statement, considering the small number of studies exclusively dedicated to the characterization of COVID-19 as a thrombotic fever, it is very important to consider this designation. Categorizing COVID-19 as a febrile variant of thromboembolism adds a series of procedures to be adopted in

patients' care. This approach can advance the treatment adequacy by many steps, making it as more personalized as possible.
