Purpose We aimed to investigate the clinical performance of edoxaban for the treatment of pulmonary embolism (PE) in hospitalized COVID-19 patients. Methods We conducted a retrospective analysis selecting hospitalized patients with COVID-19 admitted to our Institution from 20 May 2020 to 20 November 2020 with computer tomography (CT) detected PE at admission, treated with edoxaban after initial parenteral therapy. Clinical outcomes were compared between patients with and without ARDS at admission and between those with and without CT confirmed PE resolution. Results 50 patients were included. Mean follow-up was 42.5 ± 10 days. No baseline differences were found between patients with ARDS (30%) and those without ARDS at admission. Patients with PE resolution (84%) were younger ( P = 0.03 ), had a shorter duration of fondaparinux therapy (9.9 ± 3.8 vs 15.8 ± 7.5 days; P = 0.0015) and length of hospitalization (36 ± 8 vs 46 ± 9 days: P = 0.0023) compared with those without PE resolution. 2 patients experienced major bleedings. At multivariate analysis the time to edoxaban switch was the only predictor of the PE resolution (HR: 0.92; 95% C.I. 0.86 to 0.99 ) . Conclusion Edoxaban was an effective and safe treatment for acute PE in COVID-19 setting.

Type 2 diabetes mellitus (T2DM) is a chronic and progressive disease, characterized by persistent hyperglycemia, due to both a decline of b-pancreatic insulin production and an increased peripheral insulin resistance. The incidence of this pathology is increasing rapidly, indeed, it was estimated that the number of diabetics will arise from 371 million (2012) to 552 million (2030), representing one of the major challenge to health care worldwide. 1Traditional therapies can be still considered suboptimal, since there are no treatments able to guarantee a perfect glycemic control and a stable prevention of diabetic complications, without the risk of hypoglycemia.2 For these reasons, the finding that particular hormones, called glucon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide, are able to induce a greater secretion of insulin only in the presence of high level of glucose, has quickly attracted the attention of scientists. 3,4 GLP-1 is a polypeptide, secreted by endocrine cells of small intestine during the digestive phase; the glucose in the intestinal lumen acts as a trigger and induces the release of this hormone. Through the circulation, GLP-1 reaches its receptor on bpancreatic cells, stimulating the secretion of insulin in relation to the amount of glucose concentration. Physiologically, the half-life of endogenous GLP-1 is around 2 min; this hormone, indeed, is quickly degraded by a specific peptidase, the dipeptdylpeptidase 4 (DPP-4). 5In addition to the stimulus of insulin secretion, the hypoglycemic effect of this substance is enhanced by the inhibition of glucagon release. Moreover, this hormone stimulates the transcription of insulin and ABSTRACTSitagliptin and saxagliptin are oral hypoglycemic agents inhibitors of DPP-4, indicated in the treatment of type 2 diabetes mellitus in combination with metformin, in patients who have not achieved adequate glycemic control. In our study we enrolled 128 decompensated type 2 diabetes patients while on metformin maximum dosage. At time 0' we have detected, body mass index (BMI), total cholesterol, high-and low-density lipoproteins (HDL and LDL), triglycerides, transaminases and pancreatic amylase; patients were randomized to receive sitagliptin or saxagliptin; follow-up was performed after 4 months with the revaluation of the same variables and adverse events. In both sitagliptin and saxagliptin groups we observed a significant reduction in fasting glucose, glycated hemoglobin, weighing, BMI, triglycerides, while the reduction in total cholesterol, LDL cholesterol did not reach statistical significance. There was no suspension of therapy, adverse events appeared minor and temporary. In conclusion, our observations highlight the almost identical efficacy of sitagliptin and saxagliptin. These data reinforce even more the idea that we should think about this class of drugs as the next step in patients failing therapy with metformin.