Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be harmful in patients with diabetes during COVID-19 pandemic
Identifieur interne : 000639 ( Pmc/Corpus ); précédent : 000638; suivant : 000640Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be harmful in patients with diabetes during COVID-19 pandemic
Auteurs : Erkan Cure ; Medine Cumhur CureSource :
- Diabetes & Metabolic Syndrome [ 1871-4021 ] ; 2020.
Abstract
The novel coronavirus disease 2019 (COVID-19) outbreak once again demonstrated the importance of the renin-angiotensin system (RAS) in patients with diabetes. Activation of the RAS increases in patients with diabetes. The virus attaches to the ACE2 enzyme at low cytosolic pH values and enters into the cell and causes infection. Especially in the presence of diabetes mellitus and accompanying comorbid conditions such as hypertension, obesity, old age, and smoking, cytosolic pH is low, thus the virus easily may enter the cell by attaching to ACE2. ACEIs and ARBs lead to a reduction in angiotensin II level by increasing the ACE2 level, thus they cause a low cytosolic pH. Increased cardiac ACE2 levels due to ACEIs and ARBs can trigger cardiac arrhythmias and myocarditis by causing the virus to easily enter the heart tissue. There is ACE2 activity in the rostral ventrolateral medulla in the brain stem. The release of angiotensin 1-7 in the brain stem leads to the activation of the sympathetic nervous system. This activation causes systemic vasoconstriction and the patient’s blood pressure increases. The most important event is the increased sympathetic activity via the central stimulation, this activity increases pulmonary capillary leaking, causing the ARDS. As the cytosolic pH, which is already low in patients with diabetes will decrease further with the mechanisms mentioned above, the viral load will increase and the infection will be exacerbated. As a result, the use of ACEIs and ARBs in patients with diabetes can lead to increased morbidity and mortality of COVID-19.
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DOI: 10.1016/j.dsx.2020.04.019
PubMed: 32311651
PubMed Central: 7159862
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be harmful in patients with diabetes during COVID-19 pandemic</title><author><name sortKey="Cure, Erkan" sort="Cure, Erkan" uniqKey="Cure E" first="Erkan" last="Cure">Erkan Cure</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Ota&Jinemed Hospital, Istanbul, Turkey</nlm:aff></affiliation></author><author><name sortKey="Cumhur Cure, Medine" sort="Cumhur Cure, Medine" uniqKey="Cumhur Cure M" first="Medine" last="Cumhur Cure">Medine Cumhur Cure</name><affiliation><nlm:aff id="aff2">Department of Biochemistry, Private Practice, Istanbul, Turkey</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32311651</idno><idno type="pmc">7159862</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7159862</idno><idno type="RBID">PMC:7159862</idno><idno type="doi">10.1016/j.dsx.2020.04.019</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000639</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000639</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be harmful in patients with diabetes during COVID-19 pandemic</title><author><name sortKey="Cure, Erkan" sort="Cure, Erkan" uniqKey="Cure E" first="Erkan" last="Cure">Erkan Cure</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Ota&Jinemed Hospital, Istanbul, Turkey</nlm:aff></affiliation></author><author><name sortKey="Cumhur Cure, Medine" sort="Cumhur Cure, Medine" uniqKey="Cumhur Cure M" first="Medine" last="Cumhur Cure">Medine Cumhur Cure</name><affiliation><nlm:aff id="aff2">Department of Biochemistry, Private Practice, Istanbul, Turkey</nlm:aff></affiliation></author></analytic><series><title level="j">Diabetes & Metabolic Syndrome</title><idno type="ISSN">1871-4021</idno><idno type="eISSN">1878-0334</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The novel coronavirus disease 2019 (COVID-19) outbreak once again demonstrated the importance of the renin-angiotensin system (RAS) in patients with diabetes. Activation of the RAS increases in patients with diabetes. The virus attaches to the ACE2 enzyme at low cytosolic pH values and enters into the cell and causes infection. Especially in the presence of diabetes mellitus and accompanying comorbid conditions such as hypertension, obesity, old age, and smoking, cytosolic pH is low, thus the virus easily may enter the cell by attaching to ACE2. ACEIs and ARBs lead to a reduction in angiotensin II level by increasing the ACE2 level, thus they cause a low cytosolic pH. Increased cardiac ACE2 levels due to ACEIs and ARBs can trigger cardiac arrhythmias and myocarditis by causing the virus to easily enter the heart tissue. There is ACE2 activity in the rostral ventrolateral medulla in the brain stem. The release of angiotensin 1-7 in the brain stem leads to the activation of the sympathetic nervous system. This activation causes systemic vasoconstriction and the patient’s blood pressure increases. The most important event is the increased sympathetic activity via the central stimulation, this activity increases pulmonary capillary leaking, causing the ARDS. As the cytosolic pH, which is already low in patients with diabetes will decrease further with the mechanisms mentioned above, the viral load will increase and the infection will be exacerbated. As a result, the use of ACEIs and ARBs in patients with diabetes can lead to increased morbidity and mortality of COVID-19.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ribeiro Oliveira, A" uniqKey="Ribeiro Oliveira A">A. Ribeiro-Oliveira</name></author><author><name sortKey="Nogueira, A I" uniqKey="Nogueira A">A.I. Nogueira</name></author><author><name sortKey="Pereira, R M" uniqKey="Pereira R">R.M. Pereira</name></author><author><name sortKey="Boas, W W" uniqKey="Boas W">W.W. Boas</name></author><author><name sortKey="Dos Santos, R A" uniqKey="Dos Santos R">R.A. 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Santos</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cure, E" uniqKey="Cure E">E. Cure</name></author><author><name sortKey="Cumhur Cure, M" uniqKey="Cumhur Cure M">M. Cumhur Cure</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cure, E" uniqKey="Cure E">E. Cure</name></author><author><name sortKey="Cumhur Cure, M" uniqKey="Cumhur Cure M">M. Cumhur Cure</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Resnick, L M" uniqKey="Resnick L">L.M. Resnick</name></author><author><name sortKey="Gupta, R K" uniqKey="Gupta R">R.K. Gupta</name></author><author><name sortKey="Sosa, R E" uniqKey="Sosa R">R.E. Sosa</name></author><author><name sortKey="Corbett, M L" uniqKey="Corbett M">M.L. Corbett</name></author><author><name sortKey="Laragh, J H" uniqKey="Laragh J">J.H. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Diabetes Metab Syndr</journal-id><journal-id journal-id-type="iso-abbrev">Diabetes Metab Syndr</journal-id><journal-title-group><journal-title>Diabetes & Metabolic Syndrome</journal-title></journal-title-group><issn pub-type="ppub">1871-4021</issn><issn pub-type="epub">1878-0334</issn><publisher><publisher-name>Diabetes India. Published by Elsevier Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32311651</article-id><article-id pub-id-type="pmc">7159862</article-id><article-id pub-id-type="publisher-id">S1871-4021(20)30085-0</article-id><article-id pub-id-type="doi">10.1016/j.dsx.2020.04.019</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be harmful in patients with diabetes during COVID-19 pandemic</article-title></title-group><contrib-group><contrib contrib-type="author" id="au1"><name><surname>Cure</surname><given-names>Erkan</given-names></name><email>erkancure@yahoo.com</email><xref rid="aff1" ref-type="aff">a</xref><xref rid="cor1" ref-type="corresp">∗</xref></contrib><contrib contrib-type="author" id="au2"><name><surname>Cumhur Cure</surname><given-names>Medine</given-names></name><email>medinecure@yahoo.com</email><xref rid="aff2" ref-type="aff">b</xref></contrib></contrib-group><aff id="aff1"><label>a</label>Department of Internal Medicine, Ota&Jinemed Hospital, Istanbul, Turkey</aff><aff id="aff2"><label>b</label>Department of Biochemistry, Private Practice, Istanbul, Turkey</aff><author-notes><corresp id="cor1"><label>∗</label>Corresponding author. Department of Internal medicine, Ota & Jinemed Hospital, Muradiye Mahallesi Nuzhetiye Cad, Deryadil Sokagi No:1, Istanbul, 34357, Turkey. <email>erkancure@yahoo.com</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>15</day><month>4</month><year>2020</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub" iso-8601-date="2020-08-01"><season>July-August</season><year>2020</year></pub-date><pub-date pub-type="epub"><day>15</day><month>4</month><year>2020</year></pub-date><volume>14</volume><issue>4</issue><fpage>349</fpage><lpage>350</lpage><history><date date-type="received"><day>12</day><month>4</month><year>2020</year></date><date date-type="rev-recd"><day>14</day><month>4</month><year>2020</year></date><date date-type="accepted"><day>14</day><month>4</month><year>2020</year></date></history><permissions><copyright-statement>© 2020 Diabetes India. Published by Elsevier Ltd. All rights reserved.</copyright-statement><copyright-year>2020</copyright-year><copyright-holder>Diabetes India</copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="abs0010"><p>The novel coronavirus disease 2019 (COVID-19) outbreak once again demonstrated the importance of the renin-angiotensin system (RAS) in patients with diabetes. Activation of the RAS increases in patients with diabetes. The virus attaches to the ACE2 enzyme at low cytosolic pH values and enters into the cell and causes infection. Especially in the presence of diabetes mellitus and accompanying comorbid conditions such as hypertension, obesity, old age, and smoking, cytosolic pH is low, thus the virus easily may enter the cell by attaching to ACE2. ACEIs and ARBs lead to a reduction in angiotensin II level by increasing the ACE2 level, thus they cause a low cytosolic pH. Increased cardiac ACE2 levels due to ACEIs and ARBs can trigger cardiac arrhythmias and myocarditis by causing the virus to easily enter the heart tissue. There is ACE2 activity in the rostral ventrolateral medulla in the brain stem. The release of angiotensin 1-7 in the brain stem leads to the activation of the sympathetic nervous system. This activation causes systemic vasoconstriction and the patient’s blood pressure increases. The most important event is the increased sympathetic activity via the central stimulation, this activity increases pulmonary capillary leaking, causing the ARDS. As the cytosolic pH, which is already low in patients with diabetes will decrease further with the mechanisms mentioned above, the viral load will increase and the infection will be exacerbated. As a result, the use of ACEIs and ARBs in patients with diabetes can lead to increased morbidity and mortality of COVID-19.</p></abstract><kwd-group id="kwrds0010"><title>Keywords</title><kwd>Diabetes mellitus</kwd><kwd>Novel coronavirus disease 2019 (COVID-19)</kwd><kwd>Angiotensin converting enzyme inhibitors</kwd><kwd>Angiotensin receptor antagonists</kwd><kwd>Renin-angiotensin system</kwd></kwd-group></article-meta></front><body><p content-type="salutation">Dear Sir,</p><p id="p0010">The novel coronavirus disease 2019 (COVID-19) outbreak once again demonstrated the importance of the renin-angiotensin system (RAS) in patients with diabetes. Activation of the RAS increases in patients with diabetes [<xref rid="bib1" ref-type="bibr">1</xref>]. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II is a powerful vasoconstrictor that triggers oxidative stress, causing increased reactive oxygen species. Raised angiotensin II level causes insulin resistance, endothelial dysfunction, proteinuria, and elevated blood pressure. ACE2 uses angiotensin II as a substrate and produces angiotensin 1-7 [<xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib2" ref-type="bibr">[2]</xref>, <xref rid="bib3" ref-type="bibr">[3]</xref>]. ACE inhibitors (ACEIs) inhibit the formation of angiotensin II from angiotensin I. This event leads to the conversion of angiotensin I to angiotensin 1-9 [<xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib2" ref-type="bibr">[2]</xref>, <xref rid="bib3" ref-type="bibr">[3]</xref>]. Angiotensin 1-9 is converted to angiotensin 1-7 by ACE2 [<xref rid="bib1" ref-type="bibr">1</xref>,<xref rid="bib2" ref-type="bibr">2</xref>]. Angiotensin receptor antagonists (ARBs) prevent angiotensin II from binding to the receptor, thus ARBs inhibit the effect of angiotensin II. ARBs, like ACEI, also increase the ACE2 level [<xref rid="bib4" ref-type="bibr">4</xref>]. Angiotensin II, which cannot bind to the receptor, is rapidly converted to angiotensin I-7 by increased ACE2 [<xref rid="bib5" ref-type="bibr">5</xref>]. The formation of angiotensin 1-7 is the desired event for patients with diabetes. Angiotensin 1-7 lowers glucose, causes vasodilation and reduces oxidative stress [<xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib2" ref-type="bibr">[2]</xref>, <xref rid="bib3" ref-type="bibr">[3]</xref>]. The vast majority of patients with diabetes use ACEIs and ARBs due to their renoprotective effects, even without hypertension.</p><p id="p0015">The COVID-19 outbreak continues to cause severe morbidity and mortality worldwide. The virus attaches to the ACE2 enzyme at low cytosolic pH values and enters into the cell and causes infection [<xref rid="bib5" ref-type="bibr">5</xref>]. Most patients with diabetes have comorbid conditions. The virus causes serious infections especially in elderly, hypertensive, diabetic and obese patients and smokers [<xref rid="bib5" ref-type="bibr">5</xref>]. Especially in the presence of diabetes mellitus and accompanying comorbid conditions such as hypertension, obesity, old age, and smoking, cytosolic pH is low, thus the virus easily may enter the cell by attaching to ACE2 [<xref rid="bib5" ref-type="bibr">5</xref>,<xref rid="bib6" ref-type="bibr">6</xref>]. The COVID-19 infection becomes more severe in these patients due to high viral load. Angiotensin II has a strong pH alkalizing effect. It alkalizes the pH even after strong acid loading [<xref rid="bib7" ref-type="bibr">7</xref>]. ACEIs and ARBs lead to a reduction in angiotensin II level by increasing the ACE2 level, thus they cause a low cytosolic pH [<xref rid="bib5" ref-type="bibr">5</xref>]. Unlike angiotensin II, angiotensin 1-7 does not affect on cytosolic pH [<xref rid="bib5" ref-type="bibr">5</xref>]. Therefore, increased angiotensin 1-7 levels may not reduce the viral load [<xref rid="bib5" ref-type="bibr">5</xref>]. RAS activity and angiotensin II levels decrease with aging [<xref rid="bib5" ref-type="bibr">5</xref>]. Especially in elderly patients with diabetes, COVID-19 infection will be more severe since cytosolic pH will be lower.</p><p id="p0020">Since angiotensin 1–7 has a vasodilator effect, it has been hypothesized that it may be protective against acute respiratory distress syndrome (ARDS) occurrence in COVID-19 infection [<xref rid="bib8" ref-type="bibr">8</xref>]. It is doubtful that the increment of angiotensin 1-7 level has a preventive effect on ARDS development. The evidence for the protective role of angiotensin 1-7 is limited at present. In an experimental model, continuous infusion of angiotensin 1–7 has been shown to have a vasodilator effect only in female rats [<xref rid="bib9" ref-type="bibr">9</xref>]. The reason why COVID-19 is less severe in women than men may be a protective effect of estrogen in premenopausal women [<xref rid="bib8" ref-type="bibr">8</xref>]. On the other hand, ACE2 is present in many tissues such as the brain, heart, kidney, testicle, veins. ACEIs and ARBs have been shown to increase the ACE2 level in the brain, heart, and kidney [<xref rid="bib8" ref-type="bibr">8</xref>]. There is no evidence in the lung tissue that these drugs increase the ACE2 level. Most patients with diabetes have coronary artery disease and carotid intima-media thickening even in the early stage due to hyperglycemia. Mortality is significantly higher in patients with cardiac involvement during COVID-19 infection compared to patients without cardiac involvement [<xref rid="bib8" ref-type="bibr">8</xref>]. Increased cardiac ACE2 levels due to ACEIs and ARBs can trigger cardiac arrhythmias and myocarditis by causing the virus to easily enter the heart tissue. The use of hydroxychloroquine and azithromycin may also increase the risk of QT prolongation and arrhythmia. As the attachment rate of the virus to cardiac ACE2 increases, patients with diabetes with COVID-19 may be more likely to die from cardiac arrhythmia. There is ACE2 activity in the rostral ventrolateral medulla in the brain stem [<xref rid="bib8" ref-type="bibr">8</xref>]. Interestingly, the release of angiotensin 1-7 in the brain stem leads to the activation of the sympathetic nervous system [<xref rid="bib10" ref-type="bibr">10</xref>,<xref rid="bib11" ref-type="bibr">11</xref>]. This activation causes systemic vasoconstriction and the patient’s blood pressure increases [<xref rid="bib10" ref-type="bibr">10</xref>,<xref rid="bib11" ref-type="bibr">11</xref>]. Increased blood pressure activates Na<sup>+</sup>/H<sup>+</sup> exchanger and lowers cytosolic pH [<xref rid="bib8" ref-type="bibr">8</xref>]. The ARBs and ACEIs-induced lower angiotensin II level in the diabetic patient, and the increased NHE activation, further reduce the already low cytosolic ph, leading to an increase of virus infection. Besides, increased sympathetic activity by the central pathway further increases virus-induced damage to the myocardium [<xref rid="bib8" ref-type="bibr">8</xref>,<xref rid="bib10" ref-type="bibr">10</xref>,<xref rid="bib11" ref-type="bibr">11</xref>]. The most important event is the increased sympathetic activity via the central stimulation, this activity increases pulmonary capillary leaking, causing the ARDS [<xref rid="bib8" ref-type="bibr">8</xref>,<xref rid="bib10" ref-type="bibr">10</xref>,<xref rid="bib11" ref-type="bibr">11</xref>]. It has not been demonstrated that angiotensin 1-7 inhibits ARDS. In an experimental study, as we mentioned above, angiotensin 1-7 did not cause vasodilation in male rats [<xref rid="bib9" ref-type="bibr">9</xref>]. Even if angiotensin 1–7 has a protective effect against ARDS, increased angiotensin 1-7 formation via ACE2 in the heart, kidneys, and vessels will not be protective against centrally induced ARDS and myocardial injuries. Patients with diabetes and associated comorbidities receive drugs like pioglitazone, glucagon-like peptide-1 agonists, statins, diuretics, and mineralocorticoid inhibitors. All these drugs cause an increase in ACE2 level [<xref rid="bib4" ref-type="bibr">4</xref>]. However, the combined use of ACEIs and ARBs and these drugs during the COVID-19 outbreak could lead to a markedly raised ACE2 level. As the cytosolic pH, which is already low in patients with diabetes, will decrease further with the mechanisms mentioned above, the viral load will increase and the infection will be exacerbated. As a result, the use of ACEIs and ARBs in patients with diabetes can lead to increased morbidity and mortality of COVID-19.</p><sec sec-type="COI-statement"><title>Declaration of competing interest</title><p id="p0025">This article is a letter to the editor. We confirm that the entire manuscript, or parts of it, have not been published previously or are not currently under consideration for publication elsewhere.</p><p id="p0030">We declare that have no financial relationships involved in this study.</p><p id="p0035">We declare that there is no conflict of interest.</p><p id="p0040">All authors confirm to have contributed substantially to the submission of this study.</p></sec></body><back><ref-list id="cebib0010"><title>References</title><ref id="bib1"><label>1</label><element-citation publication-type="journal" id="sref1"><person-group person-group-type="author"><name><surname>Ribeiro-Oliveira</surname><given-names>A.</given-names><suffix>Jr.</suffix></name><name><surname>Nogueira</surname><given-names>A.I.</given-names></name><name><surname>Pereira</surname><given-names>R.M.</given-names></name><name><surname>Boas</surname><given-names>W.W.</given-names></name><name><surname>Dos 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