Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT05205707 |
| Other study ID # |
2021/5 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
January 1, 2022 |
| Est. completion date |
January 21, 2022 |
Study information
| Verified date |
January 2022 |
| Source |
Jordan University Hospital |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
COVID-19 cases are rising substantially in Jordan. Since this is a novel virus, there is
still much to be investigated surrounding its pathophysiology in order to attempt to find
suitable treatments or better decision-making in the prognosis of the disease. This project
aims to identify if soluble angiotensin-converting enzyme (ACE2) can be used as a prognostic
factor for COVID-19 severity, which will allow clinicians to manage COVID-19 cases more
efficiently. ACE2 is of interest since the coronavirus enters host cells through ACE2
receptors. It can slo be hypothesized that the irus may also bind to soluble ACE2, but
without mediating its effects. It si, therefore, expected that those with higher levels of
ACE2 would more likely have milder disease. This can potentially help improve survival rate,
allowing clinicians to identify the higher-risk patients and monitoring them more closely.
Description:
SARS-CoV-2 is a new isolate of coronavirus that caused an epidemic in Wuhan, China in
December 2019. The virus has then spread to the rest of the world causing a pandemic, and the
disease the virus causes was designated the name COVID-19.
The presence of underlying medical condition increases a risk of severe disease course.
Diabetes and cardiovascular disease are amongst the conditions that are associated with the
worst COVID-19 prognosis . Renal failure is also associated with more severe illness On
another note, angiotensin-converting enzyme 2 (ACE2) is expressed in human airway epithelia,
lung parenchyma, small intestine cells as well as in the heart, kidneys and testis It
functions as both an enzyme and a receptor for viral entry as it is known that SARS-CoV-2
enters into human host cells mainly through the cellular receptor ACE2, . It is hypothesized
that with the damage and loss of cells induced by infection, enzymatic ACE2 activity would be
globally compromised, inducing a state of relative ACE2 deficiency. This leads to enhanced
and protracted tissue and vessel exposure to Ang II and therefore vasoconstriction, enhanced
thrombosis, increased tissue permeability and cytokine production resulting in inflammation
Chronic angiotensin 1 receptor (AT1R) blockade elevates ACE2 expression . Unlike ACE1,
however, ACE2 is insensitive to the actions mediated by ACE inhibitors . It might be
appealing to propose that chronic use of ACE inhibitors or AT1R antagonists puts patients at
particular high risk if they get infected with SARS-CoV-2, as ACE2 overexpression may
facilitate viral replication in the lung tissue . However, results of some studies performed
in healthy human subjects did not confirm such results. In vitro studies, on the other hand,
depict reduced concentrations of soluble ACE2 despite the increase in membrane expression and
tissue levels. Therefore, there is no current significant evidence regarding the effects of
ACE inhibitors and ARBs on COVID-19 infection .
In contrast, mild or moderate ACE2 deficiency is unlikely to be protective from viral
invasion either. This is due to the intrinsically high affinity of SARS-CoV-2 to ACE2
receptors The soluble form of ACE2 may be a biomarker of severity of COVID-19 progression in
patients . This could be due to the fact that COVID-19 binds to the soluble form, leaving
less to be bound to the ACE2 receptor and be taken up by host cells The aim of this project
is to identify any association between ACE2 levels with severity of COVID-19.
