key: cord-0769987-xqfyirxc
authors: Ceriello, Antonio
title: Diabetes, D-dimer and COVID-19: The possible role of glucose control
date: 2020-10-15
journal: Diabetes Metab Syndr
DOI: 10.1016/j.dsx.2020.10.011
sha: 4d39b140a65a7bbe55830d6265043d997dc083f8
doc_id: 769987
cord_uid: xqfyirxc

nan

Diabetes is accompanied by a thrombosis-prone status [1, 2] . Available evidence shows that an activation of the thrombosis may be generated by hyperglycemia [1, 2] . A pro-thrombotic status may be induced by hyperglycemia through two different pathways: oxidative stress and non-enzymatic glycation [1, 2] . Acute hyperglycemia, through oxidative stress, increases thrombin generation [3] , while the non-enzymatic glycation reduces the functionality of both antithrombin III and heparin co-factor II [4, 5] . In conclusion, evidence shows that hyperglycemia may produce a prothrombotic status, due to an imbalance between pro-coagulation, anti-coagulation and fibrinolysis [1,2,6].

Mishra et al. have recently reported in the case of COVID-19 an increase of D-dimer in people with diabetes compared to people without diabetes [7] . Evidence is showing that high blood glucose can condition the prognosis of COVID-19 [8, 9] . Interestingly, in people with hyperglycemia and COVID-19 increased D-dimer levels have been found [8, 9] . Moreover, it has been shown that reducing hyperglycemia is followed by a decrease of the D-dimer [9] . This evidence suggests that hyperglycemia might favor the generation of the thrombosis, a complication very often is present in the COVID-19 [10, 11] .

If confirmed in specific well-designed studies, this hypothesis may pay the way to possible useful interventions. A fast reduction of hyperglycemia, for its important implications on coagulation activation [1, 2] , might be very important, while non-enzymatic glycation is, at the beginning, a reversible phenomenon [12] . Furthermore, a fast use of heparin may also be very relevant and not only for its obvious anticoagulant property: heparin can spare antithrombin III and heparin co-factor II from being glycated [4, 5] .

In conclusion, because thrombosis affects the prognosis of people with COVID-19 [13] , understanding what contributes to increase the risk for a thrombotic event in this disease is highly relevant. Therefore, clarifying the possible link between hyperglycemia and thrombosis with specific studies might be very useful for a better management of COVID-19.

None. AC wrote, revised and approved the final version of the manuscript.

Antonio Ceriello does not have conflicts of interest to declare.

Coagulation activation in diabetes mellitus: the role of hyperglycaemia and therapeutic prospects

Hyperglycemia: a prothrombotic factor?

Hyperglycemia-induced thrombin formation in diabetes. The possible role of oxidative stress

Induced hyperglycemia alters antithrombin III activity but not its plasma concentration in healthy normal subjects

Non-enzymatic glycation reduces heparin cofactor II anti-thrombin activity

Impaired fibrinolytic response to increased thrombin activation in type 1 diabetes mellitus: effects of the glycosaminoglycan sulodexide

Relation of D-dimer levels of COVID-19 patients with diabetes mellitus

Association of blood glucose control and outcomes in patients with COVID-19 and pre-existing type 2 diabetes

Outcomes in patients with hyperglycemia affected by COVID-19: can we do more on glycemic control?

Why is hyperglycaemia worsening COVID-19 and its prognosis?

Diabetes and Cardiovascular Disease (D&CVD) EASD Study Group. Issues of cardiovascular risk management in people with diabetes in the COVID-19 era

Influence of labile glucose adducts on glycosylated protein assay by aminophenylboronic acid affinity chromatography: in vivo studies

Pulmonary embolism or pulmonary thrombosis in COVID-19? Is the recommendation to use high-dose heparin for thromboprophylaxis justified?

E-mail address: antonio.ceriello@hotmail.it

Contents lists available at ScienceDirect Diabetes & Metabolic Syndrome