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Discontinuation of ACEi/ARBWiki

Developed by Shray Alag
Clinical Trial MeSH HPO Drug Gene SNP Protein Mutation


Correlated Drug Terms (1)


Name (Synonyms) Correlation
drug217 Continuation of ACEi/ARB Wiki 1.00

Correlated MeSH Terms (5)


Name (Synonyms) Correlation
D008173 Lung Diseases, Obstructive NIH 0.50
D008171 Lung Diseases, NIH 0.50
D002318 Cardiovascular Diseases NIH 0.30
D011024 Pneumonia, Viral NIH 0.17
D011014 Pneumonia NIH 0.08

Correlated HPO Terms (0)


Name (Synonyms) Correlation

There is one clinical trial.

Clinical Trials


1 Effects of Discontinuing Renin-angiotensin System Inhibitors in Patients With COVID-19

Recent data from some of the earliest and worst affected countries of COVID-19 suggest a major overrepresentation of hypertension and diabetes among COVID-19-related deaths and among patients experiencing severe courses of the disease. The vast majority of patients with hypertension and/or diabetes are taking drugs targeting the renin-angiotensin system (RAS) because of their blood pressure-lowering and/or kidney-protective effects. Importantly, the virus causing COVID-19, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the transmembrane protein angiotensin converting enzyme 2 (ACE2) - an important component of RAS - for host cell entry and subsequent viral replication. ACE2 is normally considered to be an enzyme that limits airway inflammation via effects in RAS and increased ACE2 activity seems to alleviate acute respiratory distress syndrome (ARDS). Importantly, evidence from human studies as well as rodent studies suggests that the inhibition of RAS by angiotensin converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARB) leads to upregulation of ACE2, and treatment with ARB leads to attenuation of SARS-CoV-induced ARDS. This is of interest, as the vast majority of deaths from COVID-19 are due to ARDS and expression of ACE2 has previously been shown to be reduced by the binding of SARS-CoV to ACE2. Thus, ACE inhibitors and ARBs have been suggested to alleviate the COVID-19 pulmonary manifestations. In contrast to these notions, concern has been raised that ACE2 upregulation (by RAS-inhibiting drugs) will multiply the cellular access points for viral entry and might increase the risk of severe progression of COVID-19. The multiplied viral entry points could perhaps explain the alarmingly high morbidity and mortality among COVID-19 patients with diabetes and/or hypertension. Thus, a delineation of the role of RAS for the course of COVID-19 is of crucial importance for the management of COVID-19 patients. Aim: This randomised clinical trial will investigate whether to continue or discontinue treatment with ACE inhibitors or ARBs in hospitalised patients with COVID-19.

NCT04351581 Covid-19 Other: Discontinuation of ACEi/ARB Other: Continuation of ACEi/ARB

Primary Outcomes

Description: The primary endpoint is days alive and out of hospital within 14 days after recruitment

Measure: Days alive and out of hospital within 14 days after recruitment

Time: 14 days

Secondary Outcomes

Description: The key-secondary composite endpoint is the occurrence of worsening of COVID-19 as assessed by (whichever comes first): Severe respiratory insufficiency; defined by the occurrence of one of the following: PaO2/FiO2 ratio ≤40 kPa (300 mm Hg); PaO2, partial pressure of arterial oxygen; FiO2, percentage of inspired oxygen Commencement of non-invasive ventilation (NIV) Commencement of continuous CPAP (continuous positive airway pressure) treatment Commencement of high-flow oxygen therapy (HFOT); defined as an oxygen flow >16 l/min Referral to treatment in an intensive care unit Death

Measure: Key-secondary composite endpoint: Occurrence of worsening of COVID-19

Time: 30 days

Description: Occurrence and time to occurrence of each of the components of the key-secondary composite endpoint

Measure: Occurrence and time to occurrence of each of the components of the key-secondary composite endpoint

Time: 30 days

Description: Kidney function assessed by plasma creatinine

Measure: Kidney function assessed by plasma creatinine

Time: 30 days

Description: Duration of index hospitalisation

Measure: Duration of index hospitalisation

Time: 30 days

Description: 30-day mortality

Measure: 30-day mortality

Time: 30 days

Description: Number of days alive during the intervention period

Measure: Number of days alive during the intervention period

Time: 30 days

Description: Number of participants not yet discharged at day 30

Measure: Number of participants not yet discharged at day 30

Time: 30 days

Description: Number of readmissions after 30 days.

Measure: Number of readmissions after 30 days.

Time: 30 days

Description: Kidney function as assessed by eGFR

Measure: Kidney function as assessed by eGFR

Time: 30 days

Other Outcomes

Description: To support the clinical findings, blood samples will be analysed for ACE, ACE2, aldosterone, angiotensin II and renin, and expression of ACE, interferon signatures and T cell exhaustion markers.

Measure: Support for clinical findings via relevant blood markers

Time: 30 days


No related HPO nodes (Using clinical trials)