NCT04519398: iGenes-COVID19

Investigating the Involvement of ACE and Angiotensinogen Genes' Polymorphism Along With Other Thrombophilic Genotypes in Severe Forms of COVID-19 With/Without Thrombotic Events

Status unknown Last updated 19 August 2020

What this trial tests

trial testing Complete thrombophilic profile testing by multiplex PCR in Covid19 in 60 participants. Status unknown.

Timeline

18 August 2020

Primary endpoint
17 February 2021

18 August 2021

Quick facts

Lead sponsor	Grigore T. Popa University of Medicine and Pharmacy
Status	Status unknown
Study type	OBSERVATIONAL
Enrollment	60
Start date	18 August 2020
Primary completion	17 February 2021
Estimated completion	18 August 2021
Sites	1 location across Romania

Drugs / interventions tested

• Complete thrombophilic profile testing by multiplex PCR

Conditions studied

• Covid19 — all drugs for Covid19 →
• Corona Virus Infection — all drugs for Corona Virus Infection →
• Thrombosis — all drugs for Thrombosis →
• ARDS — all drugs for ARDS →

Sponsor

Grigore T. Popa University of Medicine and Pharmacy

Who can join

18 and older, any sex, with Covid19 or Corona Virus Infection. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

An estimated 22% of the global population is at an increased risk of a severe form of COVID-19, while one in four coronavirus patients admitted to intensive care unit will develop a pulmonary embolism. A major public health question remains to be investigated: why COVID-19 is mild for some, critically severe for others and why only a percentage of COVID-19 patients develop thrombosis, despite the disease's proven hypercoagulable state? Patients' intrinsic characteristics might be responsible for the deep variety of disease forms.

Our study aims to assess the validity of the hypothesis according to which underlining genetic variations might be responsible for different degrees of severity and thrombotic events risks in the novel coronavirus disease.

Moreover, we suspect that prothrombotic genotypes occuring in the genes that encode angiotensin-converting enzyme (ACE-DEL/INS) and angiotensinogen (AGT M235T) are involved in the unpredictable evolution of COVID-19, both in terms of severity and thrombotic events, due to the strong interactions of SARS-CoV-2 with the renin-angiotensin-aldosterone system (RAAS). Therefore, we also aim to assess the validity of the theory according to which there is a pre-existing atypical modulation of RAAS in COVID-19 patients that develop severe forms and/or thrombosis.

Our hypothesis is based on various observations. Firstly, there is a substantial similarity with a reasonably related condition such as sepsis, for which there is a validated theory stating that thrombophilic mutations affect patients' clinical response. Secondly, racial and ethnic genetic differences are responsible for significant dissimilar thrombotic risks among various nations. Thirdly, an increase in stroke incidence has been reported in young patients with COVID-19, without essential thrombosis risk factors, favoring the idea that a genetic predisposition could contribute to increase the thrombotic and thromboembolic risk. Fourthly, the plasminogen activator inhibitor (PAI)-1 4G/5G inherited mutation was found to be responsible for a thrombotic state causing post-SARS osteonecrosis.

Publications & conference data

1 peer-reviewed publication reference this trial (live from Europe PMC):

1. Is Thrombophilic Genetic Profile Responsible for an Acute Ischemic Stroke in a COVID-19 Male Patient?
   Burlacu A, Artene B, Crisan-Dabija R, Popa IV, et al · · 2020 · cited 2× · PMID 33054360 · DOI 10.1177/1076029620967107