Assessment of the efficacy of spironolactone for COVID-19 ARDS patients

Yıl 2021, Cilt: 7 Sayı: 3, 191 - 209, 13.10.2021

Aysin Ersoy , Bülent Barış Güven , Tuna Ertürk , Fulya Yurtsever , Zöhre Karaman Temel Güner Özge Kömpe

Öz

INTRODUCTION AND AIM
The aim of our study is to compare patients monitored for ARDS diagnosis linked to COVID-19 treated with spironolactone with patients who did not use spironolactone and to retrospectively identify whether there was any positive effect on mortality using clinical and laboratory data from patients.
MATERIAL AND METHOD
Two groups were created of patients treated due to severe ARDS diagnosis linked to COVID-19 from one group administered spironolactone (Group S, n=30) and the other group not administered spironolactone (Group F, n=30). Groups were compared in terms of demographic characteristics, presence of comorbidity, inotropic agent requirements, days of admission, days of mechanical ventilation and mortality. Additionally, fever, PO2/FIO2 (Horowitz ratio), lymphocyte count, CRP value, SOFA scorer, and d-dimer levels on the day of admission, 1st day, 3rd day, 5th day, 8th day, 12th day, day of discharge or day of exitus were compared between the groups and statistically analyzed.
RESULTS
Group S were found to have higher days of admission and days of mechanical ventilation compared to Group F. Group F had significantly higher mortality rate compared to Group S. The final Horowitz value in Group F was found to be significantly lower compared to Group S. The lymphocyte values in Group F were significantly lower than Group S on the 1st, 3rd, 5th, 8th and 12th day and at the final measurement. The CRP values in Group F were significantly higher than Group S on the 3rd, 5th, 8th and 12th day and at the final measurement. The SOFA scores on the 8th and 12th days and at the final measurement in Group F were found to be significantly higher than GroupS.
CONCLUSION
In our study, parameters for disease severity regressed, patients survived for longer and mortality was identified to be lower in the group using spironolactone.

Anahtar Kelimeler

spironolactone, covid19, ARDS

Kaynakça

• 1- Alhazzani W, Møller MH, Arabi YM et al. Surviving Sepsis Campaign: guidelines on the management of critically ill adults with Coronavirus Disease 2019 (COVID-19). Intensive Care Med 2020; 1-4.
• 2- Guan WJ, Ni ZY, Hu Y, et al China Medical Treatment Expert Group for Covid-19. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med NEJMoa2002032, 2020. doi:10.1056/NEJMoa2002032.
• 3- He F., Deng Y., Li W. Coronavirus disease 2019 (COVID-19): what we know? J Med Virol. 2020 Mar 14. PubMed PMID: 32170865. Epub 2020/03/15. eng.
• 4- Lu H . Drug treatment options for the 2019-new coronavirus (2019-nCoV). Biosci Trends 2020; 14 (March 16(1)):69–71 PubMed PMID: 31996494. Epub 2020/01/31. eng
• 5- Murthy S, Gomersall CD, Fowler RA. Care for critically ill patients with COVID-19. JAMA. 2020. [Epub ahead of print].
• 6- Busse LW, Chow JH, McCurdy MT, Khanna AK. COVID-19 and the RAAS-a potential role for angiotensin II? Crit Care 2020; 24: 136.
• 7- Butler J, Anstrom KJ, Felker GM, Givertz MM, et al. Efficacy and Safety of Spironolactone in Acute Heart Failure: The ATHENA-HF Randomized Clinical Trial. JAMA Cardiol 2017; 2: 950-8.
• 8- Gattinoni L, Chiumello D, Caironi P, Busana M, et al. COVID-19 pneumonia: different respiratory treatment for different phenotypes? Intensive Care Med 2020; 1-4.
• 9- Stockman LJ, Bellamy R, Garner P. SARS: systematic review of treatment effects. PLoSMed 2006;3:e343. 10.1371/journal.pmed.0030343 16968120
• 10- Ferrario CM, Jessup J, Chappell MC, etal . Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2. Circulation 2005;111:2605-10. 10.1161/CIRCULATIONAHA.104.510461 1589734
• 11- Hoffmann M, Kleine-Weber H, Schroeder S, etal . SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 2020;S0092-8674(20)30229-4. 10.1016/j.cell.2020.02.052. 32142651
• 12- Heneghan C, Brassey J. NSAIDs in acute respiratory infection. 24 Mar 2020. https://www. cebm.net/oxford-covid-19/nsaids-in-acute-respiratory-infection.
• 13- Aronson J, Ferner R. Drugs and the renin-angiotensin system in covid-19. BMJ 2020;369:m1313 doi: 10.1136/bmj.m1313 (Published 2 April 2020)
• 14- Zhang H, Penninger JM, Li Y, Zhong N, Slutsky AS. Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target [published online March 3, 2020].Intensive Care Med. doi: 10.1007/s00134-020-05985-9 15- South AM, Tomlinson L, Edmonston D, Hiremath S, Sparks MA. Controversies of renin-angiotensin system inhibition during the COVID-19 pandemic. Nat Rev Nephrol. 2020;16:305–7.
• 16- Sodhi CP, Wohlford-Lenane C, Yamaguchi Y, et al. Attenuation of pulmonary ACE2 activity impairs inactivation of des-Arg9 bradykinin/BKB1R axis and facilitates LPS-induced neutrophil infiltration. Am J Physiol Lung Cell Mol Physiol 2018; 314: L17-L31.
• 17- Xu L, Xiaochun M. Acute respiratory failure in COVID-19: is it “typical” ARDS? Critical Care (2020) 24:198 https://doi.org/10.1186/s13054-020-02911-9
• 18- Chung M, Bernheim A, Mei XY, et al. CT imaging features of 2019 novel coronavirus (2019-nCoV). Radiology. 2020;295(1):202–7.
• 19- Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020. https://doi.org/10.1016/S0140-6736(20)30566-3.
• 20- Thille AW, Esteban A, Fernández-Segoviano P, et al. Comparison of the Berlin definition for acute respiratory distress syndrome with autopsy. Am J Respir Crit Care Med. 2013;187:761–7.
• 21- Zheng R, Hu M, Li R, et al. Respiratory treatment procedures in patients with severe novel coronavirus infected pneumonia: an expert opinion. Chin J CritCare Intensive Care Med. 2020. https://doi.org/10.3877/cma.j.issn.2096-1537.2020.0004.
• 22- Wang X, Dhindsa R, Povysil G, Zoghbi A, Motelow J, Hostyk J, Nickols N, Rettig M, Goldstein DB. TMPRSS2 Transcriptional Inhibition as a Therapeutic Strategy for COVID-19. 2020. p. 2020030360. https://doi.org/10.20944/ preprints202003.0360.v2
• 23- Liaduet L, Szabo C. Blocking mineralocorticoid receptor with spironolactone may have a wide range of therapeutic actions in severe COVID-19 disease. Critical Care (2020) 24:318 https://doi.org/10.1186/s13054-020-03055-6