|
|
| (131 intermediate revisions by 3 users not shown) |
| Line 1: |
Line 1: |
| __NOTOC__
| | #Redirect [[Diabetes mellitus and COVID-19]] |
| {{SI}}
| |
| | |
| {{CMG}}; {{AE}}{{TAM}}
| |
| | |
| {{SK}} [[COVID-19-associated Diabetes Mellitus|New-onset Diabetes in COVID-19]] [[COVID-19-associated Diabetes Mellitus|Islet cell injury by SARS-CoV 2]]
| |
| ==Overview==
| |
| | |
| ==Historical Perspective==
| |
| * [[Diabetes mellitus]] is defined by insulin deficiency due to either diminished insulin release or end-organ insulin resistance.<ref name="KingAubert1998">{{cite journal|last1=King|first1=H.|last2=Aubert|first2=R. E.|last3=Herman|first3=W. H.|title=Global Burden of Diabetes, 1995-2025: Prevalence, numerical estimates, and projections|journal=Diabetes Care|volume=21|issue=9|year=1998|pages=1414–1431|issn=0149-5992|doi=10.2337/diacare.21.9.1414}}</ref>
| |
| * [[Diabetes]] is an umbrella term for conditions such as type I (T1DM) and type II (T2DM) [[diabetes mellitus]], [[gestational diabetes]], and [[maturity-onset diabetes of the young (MODY)]].<ref name="KingAubert1998">{{cite journal|last1=King|first1=H.|last2=Aubert|first2=R. E.|last3=Herman|first3=W. H.|title=Global Burden of Diabetes, 1995-2025: Prevalence, numerical estimates, and projections|journal=Diabetes Care|volume=21|issue=9|year=1998|pages=1414–1431|issn=0149-5992|doi=10.2337/diacare.21.9.1414}}</ref>
| |
| * Type 1 [[Diabetes Mellitus]] is caused by pancreatic β-cell failure or auto-immune destruction of the pancreatic β-cells. It generally presents in children and young adults.<ref name="KingAubert1998">{{cite journal|last1=King|first1=H.|last2=Aubert|first2=R. E.|last3=Herman|first3=W. H.|title=Global Burden of Diabetes, 1995-2025: Prevalence, numerical estimates, and projections|journal=Diabetes Care|volume=21|issue=9|year=1998|pages=1414–1431|issn=0149-5992|doi=10.2337/diacare.21.9.1414}}</ref>
| |
| * Type 2 [[Diabetes Mellitus]] (T2DM) is defined by [[insulin resistance]] and presents in adults. Family history, [[hypertension]], obesity, and [[dyslipidemia]] play a significant role in causing T2DM.<ref name="KingAubert1998">{{cite journal|last1=King|first1=H.|last2=Aubert|first2=R. E.|last3=Herman|first3=W. H.|title=Global Burden of Diabetes, 1995-2025: Prevalence, numerical estimates, and projections|journal=Diabetes Care|volume=21|issue=9|year=1998|pages=1414–1431|issn=0149-5992|doi=10.2337/diacare.21.9.1414}}</ref>
| |
| * Around 422 million individuals worldwide have diabetes, the dominant part living in low-and middle-income nations, and 1.6 million deaths are straightforwardly credited to diabetes every year. In the course of recent decades, a consistent rise has been observed in both the incidence and the prevalence.<ref>{{cite web |url=https://www.who.int/health-topics/diabetes#tab=tab_1 |title=Diabetes |format= |work= |accessdate=}}</ref>
| |
| * In China, in the year 2008, a study was done in which they compared 39 SARS-CoV patients with no previous history of diabetes, who never used steroids, with 39 matched healthy siblings.The results of the study revealed that 20 out of 39 SARS-CoV patients developed new-onset diabetes during the hospital stay. After 3 years of recovery from the SARS-CoV infection, only 5% of patients remained diabetic whereas blood sugar levels normalized in the rest of the patients with the infection recovery.<ref name="YangLin2009">{{cite journal|last1=Yang|first1=Jin-Kui|last2=Lin|first2=Shan-Shan|last3=Ji|first3=Xiu-Juan|last4=Guo|first4=Li-Min|title=Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes|journal=Acta Diabetologica|volume=47|issue=3|year=2009|pages=193–199|issn=0940-5429|doi=10.1007/s00592-009-0109-4}}</ref>
| |
| * ACE2 is the primary receptor For SARS-CoV spike protein. SARS-CoV causes infection by binding to ACE2 receptors on the target cells.<ref name="TurnerHiscox2004">{{cite journal|last1=Turner|first1=Anthony J|last2=Hiscox|first2=Julian A|last3=Hooper|first3=Nigel M|title=ACE2: from vasopeptidase to SARS virus receptor|journal=Trends in Pharmacological Sciences|volume=25|issue=6|year=2004|pages=291–294|issn=01656147|doi=10.1016/j.tips.2004.04.001}}</ref><ref name="LiMoore2003">{{cite journal|last1=Li|first1=Wenhui|last2=Moore|first2=Michael J.|last3=Vasilieva|first3=Natalya|last4=Sui|first4=Jianhua|last5=Wong|first5=Swee Kee|last6=Berne|first6=Michael A.|last7=Somasundaran|first7=Mohan|last8=Sullivan|first8=John L.|last9=Luzuriaga|first9=Katherine|last10=Greenough|first10=Thomas C.|last11=Choe|first11=Hyeryun|last12=Farzan|first12=Michael|title=Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus|journal=Nature|volume=426|issue=6965|year=2003|pages=450–454|issn=0028-0836|doi=10.1038/nature02145}}</ref> The study suggested, SARS-CoV may damage islets and cause acute insulin dependent diabetes mellitus.<ref name="YangLin2009">{{cite journal|last1=Yang|first1=Jin-Kui|last2=Lin|first2=Shan-Shan|last3=Ji|first3=Xiu-Juan|last4=Guo|first4=Li-Min|title=Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes|journal=Acta Diabetologica|volume=47|issue=3|year=2009|pages=193–199|issn=0940-5429|doi=10.1007/s00592-009-0109-4}}</ref>
| |
| | |
| ==Classification==
| |
| * There is no established system for the classification of COVID-19-associated Diabetes.
| |
| * Future research is needed to provide a better understanding of the type of Diabetes, SARS-CoV 2 causes. Whether SARS-CoV causes T1DM or T2DM or a new type of Diabetes.
| |
| | |
| ==Pathophysiology==
| |
| * [[Angiotensin-converting enzyme 2]] (ACE2) receptors expressed in the tissues that are highly involved in body metabolism. These tissues comprise of [[pancreatic beta cells]], [[adipose tissue]], [[small intestine]], and the [[kidneys]]. ACE2 receptors in the endocrine pancreas serve the entrance for Severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2), which causes Corononavirus Disease 2019 (COVID-19). <ref name="BornsteinDalan2020">{{cite journal|last1=Bornstein|first1=Stefan R.|last2=Dalan|first2=Rinkoo|last3=Hopkins|first3=David|last4=Mingrone|first4=Geltrude|last5=Boehm|first5=Bernhard O.|title=Endocrine and metabolic link to coronavirus infection|journal=Nature Reviews Endocrinology|volume=16|issue=6|year=2020|pages=297–298|issn=1759-5029|doi=10.1038/s41574-020-0353-9}}</ref>
| |
| * Expression of ACE2 receptors and effector protease TMPRSS2 in [[pancreas]] are associated with SARS-CoV 2 infection.<ref name="HoffmannKleine-Weber2020">{{cite journal|last1=Hoffmann|first1=Markus|last2=Kleine-Weber|first2=Hannah|last3=Schroeder|first3=Simon|last4=Krüger|first4=Nadine|last5=Herrler|first5=Tanja|last6=Erichsen|first6=Sandra|last7=Schiergens|first7=Tobias S.|last8=Herrler|first8=Georg|last9=Wu|first9=Nai-Huei|last10=Nitsche|first10=Andreas|last11=Müller|first11=Marcel A.|last12=Drosten|first12=Christian|last13=Pöhlmann|first13=Stefan|title=SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor|journal=Cell|volume=181|issue=2|year=2020|pages=271–280.e8|issn=00928674|doi=10.1016/j.cell.2020.02.052}}</ref>
| |
| * The pancreas consists of nine different cell types such as acinar cells, ductal cells, beta cells, alpha cells, mesenchymal cells, and endothelial cells. These pancreatic cells express both ACE2 and TMPRSS2. The expression of ACE2 in pancreatic alpha and beta cells is further proved by immunohistochemistry. Both beta cells that secrete insulin and alpha cells that secrete glucagon, stained positive for SARS-CoV 2 Spike protein and thus, it is postulated that SARS-CoV 2 can infect pancreatic islet cells.<ref name="HoffmannKleine-Weber2020">{{cite journal|last1=Hoffmann|first1=Markus|last2=Kleine-Weber|first2=Hannah|last3=Schroeder|first3=Simon|last4=Krüger|first4=Nadine|last5=Herrler|first5=Tanja|last6=Erichsen|first6=Sandra|last7=Schiergens|first7=Tobias S.|last8=Herrler|first8=Georg|last9=Wu|first9=Nai-Huei|last10=Nitsche|first10=Andreas|last11=Müller|first11=Marcel A.|last12=Drosten|first12=Christian|last13=Pöhlmann|first13=Stefan|title=SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor|journal=Cell|volume=181|issue=2|year=2020|pages=271–280.e8|issn=00928674|doi=10.1016/j.cell.2020.02.052}}</ref>
| |
| * A recent experiement was conducted to study SARS-CoV 2 tropism that is the cellular response to an external stimulus in human cells and organoids. Researchers infect human pluripotent stem cells (hPSC)-derived pancreatic endocrine cells with SARS-CoV 2.<ref name="YangHan2020">{{cite journal|last1=Yang|first1=Liuliu|last2=Han|first2=Yuling|last3=Nilsson-Payant|first3=Benjamin E.|last4=Gupta|first4=Vikas|last5=Wang|first5=Pengfei|last6=Duan|first6=Xiaohua|last7=Tang|first7=Xuming|last8=Zhu|first8=Jiajun|last9=Zhao|first9=Zeping|last10=Jaffré|first10=Fabrice|last11=Zhang|first11=Tuo|last12=Kim|first12=Tae Wan|last13=Harschnitz|first13=Oliver|last14=Redmond|first14=David|last15=Houghton|first15=Sean|last16=Liu|first16=Chengyang|last17=Naji|first17=Ali|last18=Ciceri|first18=Gabriele|last19=Guttikonda|first19=Sudha|last20=Bram|first20=Yaron|last21=Nguyen|first21=Duc-Huy T.|last22=Cioffi|first22=Michele|last23=Chandar|first23=Vasuretha|last24=Hoagland|first24=Daisy A.|last25=Huang|first25=Yaoxing|last26=Xiang|first26=Jenny|last27=Wang|first27=Hui|last28=Lyden|first28=David|last29=Borczuk|first29=Alain|last30=Chen|first30=Huanhuan Joyce|last31=Studer|first31=Lorenz|last32=Pan|first32=Fong Cheng|last33=Ho|first33=David D.|last34=tenOever|first34=Benjamin R.|last35=Evans|first35=Todd|last36=Schwartz|first36=Robert E.|last37=Chen|first37=Shuibing|title=A Human Pluripotent Stem Cell-based Platform to Study SARS-CoV-2 Tropism and Model Virus Infection in Human Cells and Organoids|journal=Cell Stem Cell|year=2020|issn=19345909|doi=10.1016/j.stem.2020.06.015}}</ref>
| |
| * Researchers found when SARS-CoV 2 infect pancreatic cells, it downregulates the pathways including calcium signaling pathways, glucagon signaling pathways of alpha cells, and metabolic pathways that assist in insulin secretion from pancreatic beta cells.<ref name="YangHan2020">{{cite journal|last1=Yang|first1=Liuliu|last2=Han|first2=Yuling|last3=Nilsson-Payant|first3=Benjamin E.|last4=Gupta|first4=Vikas|last5=Wang|first5=Pengfei|last6=Duan|first6=Xiaohua|last7=Tang|first7=Xuming|last8=Zhu|first8=Jiajun|last9=Zhao|first9=Zeping|last10=Jaffré|first10=Fabrice|last11=Zhang|first11=Tuo|last12=Kim|first12=Tae Wan|last13=Harschnitz|first13=Oliver|last14=Redmond|first14=David|last15=Houghton|first15=Sean|last16=Liu|first16=Chengyang|last17=Naji|first17=Ali|last18=Ciceri|first18=Gabriele|last19=Guttikonda|first19=Sudha|last20=Bram|first20=Yaron|last21=Nguyen|first21=Duc-Huy T.|last22=Cioffi|first22=Michele|last23=Chandar|first23=Vasuretha|last24=Hoagland|first24=Daisy A.|last25=Huang|first25=Yaoxing|last26=Xiang|first26=Jenny|last27=Wang|first27=Hui|last28=Lyden|first28=David|last29=Borczuk|first29=Alain|last30=Chen|first30=Huanhuan Joyce|last31=Studer|first31=Lorenz|last32=Pan|first32=Fong Cheng|last33=Ho|first33=David D.|last34=tenOever|first34=Benjamin R.|last35=Evans|first35=Todd|last36=Schwartz|first36=Robert E.|last37=Chen|first37=Shuibing|title=A Human Pluripotent Stem Cell-based Platform to Study SARS-CoV-2 Tropism and Model Virus Infection in Human Cells and Organoids|journal=Cell Stem Cell|year=2020|issn=19345909|doi=10.1016/j.stem.2020.06.015}}</ref>
| |
| * Researchers further stained SARS-CoV 2 infected hPSC-derived pancreatic endocrine cells with a cell apoptotic marker (CASP3). As a result of this staining, they found a large number of CASP3 cells in infected hPSC-derived pancreatic cells. This indicates that change in metabolic pathways of the pancreas is mainly due to cell apoptosis, trigger by SARS-CoV 2. This experiment suggest that when SARS-CoV 2 binds to ACE2 in Pancreas, this will upregulate the genes responsible for apoptosis and downregulate the genes responsible for the cell survival. <ref name="YangHan2020">{{cite journal|last1=Yang|first1=Liuliu|last2=Han|first2=Yuling|last3=Nilsson-Payant|first3=Benjamin E.|last4=Gupta|first4=Vikas|last5=Wang|first5=Pengfei|last6=Duan|first6=Xiaohua|last7=Tang|first7=Xuming|last8=Zhu|first8=Jiajun|last9=Zhao|first9=Zeping|last10=Jaffré|first10=Fabrice|last11=Zhang|first11=Tuo|last12=Kim|first12=Tae Wan|last13=Harschnitz|first13=Oliver|last14=Redmond|first14=David|last15=Houghton|first15=Sean|last16=Liu|first16=Chengyang|last17=Naji|first17=Ali|last18=Ciceri|first18=Gabriele|last19=Guttikonda|first19=Sudha|last20=Bram|first20=Yaron|last21=Nguyen|first21=Duc-Huy T.|last22=Cioffi|first22=Michele|last23=Chandar|first23=Vasuretha|last24=Hoagland|first24=Daisy A.|last25=Huang|first25=Yaoxing|last26=Xiang|first26=Jenny|last27=Wang|first27=Hui|last28=Lyden|first28=David|last29=Borczuk|first29=Alain|last30=Chen|first30=Huanhuan Joyce|last31=Studer|first31=Lorenz|last32=Pan|first32=Fong Cheng|last33=Ho|first33=David D.|last34=tenOever|first34=Benjamin R.|last35=Evans|first35=Todd|last36=Schwartz|first36=Robert E.|last37=Chen|first37=Shuibing|title=A Human Pluripotent Stem Cell-based Platform to Study SARS-CoV-2 Tropism and Model Virus Infection in Human Cells and Organoids|journal=Cell Stem Cell|year=2020|issn=19345909|doi=10.1016/j.stem.2020.06.015}}</ref>
| |
| * ACE2 is the target receptor for both SARS-CoV and SARS-CoV 2. Researchers in China observed new-onset diabetes among SARS-CoV patients. Therefore in agreement with this, the SARS-CoV 2 might enter pancreatic islets through binding to ACE2, and cause acute β-cell injury, leading to intense hyperglycemia and transient Type 2 Diabetes Mellitus.<ref name="YangLin2009">{{cite journal|last1=Yang|first1=Jin-Kui|last2=Lin|first2=Shan-Shan|last3=Ji|first3=Xiu-Juan|last4=Guo|first4=Li-Min|title=Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes|journal=Acta Diabetologica|volume=47|issue=3|year=2009|pages=193–199|issn=0940-5429|doi=10.1007/s00592-009-0109-4}}</ref>
| |
| * ACE2 serves as the negative regulator of the Renin-Angiotensin System (RAS) mainly by converting Ang (angiotensin) I and Ang II into Ang 1-9 and Ang 1-7, respectively.<ref name="PatelZhong2016">{{cite journal|last1=Patel|first1=Vaibhav B.|last2=Zhong|first2=Jiu-Chang|last3=Grant|first3=Maria B.|last4=Oudit|first4=Gavin Y.|title=Role of the ACE2/Angiotensin 1–7 Axis of the Renin–Angiotensin System in Heart Failure|journal=Circulation Research|volume=118|issue=8|year=2016|pages=1313–1326|issn=0009-7330|doi=10.1161/CIRCRESAHA.116.307708}}</ref><ref name="WangGheblawi2020">{{cite journal|last1=Wang|first1=Kaiming|last2=Gheblawi|first2=Mahmoud|last3=Oudit|first3=Gavin Y.|title=Angiotensin Converting Enzyme 2: A Double-Edged Sword|journal=Circulation|year=2020|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.120.047049}}</ref> When SARS-CoV and Sars-CoV 2 bind to ACE2 receptors, this will lead to the subsequent downregulation of surface ACE2 expression.<ref name="LiMoore2003">{{cite journal|last1=Li|first1=Wenhui|last2=Moore|first2=Michael J.|last3=Vasilieva|first3=Natalya|last4=Sui|first4=Jianhua|last5=Wong|first5=Swee Kee|last6=Berne|first6=Michael A.|last7=Somasundaran|first7=Mohan|last8=Sullivan|first8=John L.|last9=Luzuriaga|first9=Katherine|last10=Greenough|first10=Thomas C.|last11=Choe|first11=Hyeryun|last12=Farzan|first12=Michael|title=Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus|journal=Nature|volume=426|issue=6965|year=2003|pages=450–454|issn=0028-0836|doi=10.1038/nature02145}}</ref><ref name="WallsPark2020">{{cite journal|last1=Walls|first1=Alexandra C.|last2=Park|first2=Young-Jun|last3=Tortorici|first3=M. Alejandra|last4=Wall|first4=Abigail|last5=McGuire|first5=Andrew T.|last6=Veesler|first6=David|title=Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein|journal=Cell|volume=181|issue=2|year=2020|pages=281–292.e6|issn=00928674|doi=10.1016/j.cell.2020.02.058}}</ref><ref name="ZhouYang2020">{{cite journal|last1=Zhou|first1=Peng|last2=Yang|first2=Xing-Lou|last3=Wang|first3=Xian-Guang|last4=Hu|first4=Ben|last5=Zhang|first5=Lei|last6=Zhang|first6=Wei|last7=Si|first7=Hao-Rui|last8=Zhu|first8=Yan|last9=Li|first9=Bei|last10=Huang|first10=Chao-Lin|last11=Chen|first11=Hui-Dong|last12=Chen|first12=Jing|last13=Luo|first13=Yun|last14=Guo|first14=Hua|last15=Jiang|first15=Ren-Di|last16=Liu|first16=Mei-Qin|last17=Chen|first17=Ying|last18=Shen|first18=Xu-Rui|last19=Wang|first19=Xi|last20=Zheng|first20=Xiao-Shuang|last21=Zhao|first21=Kai|last22=Chen|first22=Quan-Jiao|last23=Deng|first23=Fei|last24=Liu|first24=Lin-Lin|last25=Yan|first25=Bing|last26=Zhan|first26=Fa-Xian|last27=Wang|first27=Yan-Yi|last28=Xiao|first28=Geng-Fu|last29=Shi|first29=Zheng-Li|title=A pneumonia outbreak associated with a new coronavirus of probable bat origin|journal=Nature|volume=579|issue=7798|year=2020|pages=270–273|issn=0028-0836|doi=10.1038/s41586-020-2012-7}}</ref>SARS-CoV 2 differs from SARS-CoV by 380 amino acid substitutions and thus has a stronger binding affinity than SARS-CoV, which explains the global impact of SARS-CoV 2 than the previous SARS-CoV outbreak.<ref name="YanZhang2020">{{cite journal|last1=Yan|first1=Renhong|last2=Zhang|first2=Yuanyuan|last3=Li|first3=Yaning|last4=Xia|first4=Lu|last5=Guo|first5=Yingying|last6=Zhou|first6=Qiang|title=Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2|journal=Science|volume=367|issue=6485|year=2020|pages=1444–1448|issn=0036-8075|doi=10.1126/science.abb2762}}</ref><ref name="ShangYe2020">{{cite journal|last1=Shang|first1=Jian|last2=Ye|first2=Gang|last3=Shi|first3=Ke|last4=Wan|first4=Yushun|last5=Luo|first5=Chuming|last6=Aihara|first6=Hideki|last7=Geng|first7=Qibin|last8=Auerbach|first8=Ashley|last9=Li|first9=Fang|title=Structural basis of receptor recognition by SARS-CoV-2|journal=Nature|volume=581|issue=7807|year=2020|pages=221–224|issn=0028-0836|doi=10.1038/s41586-020-2179-y}}</ref>
| |
| * ACE2 is the negative regulator of the Renin-Angiotensin system (RAS) and has protective benefits against many diseases and complications. SARS-CoV 2 binds to ACE2 receptors, this blocks all the protective benefits of the ACE2 pathway and shifts the cascade back to ACE/Ang II/AT1R-pathway, increasing Ang II, decreasing ACE2 and Ang-( 1-7)<ref name="GheblawiWang2020">{{cite journal|last1=Gheblawi|first1=Mahmoud|last2=Wang|first2=Kaiming|last3=Viveiros|first3=Anissa|last4=Nguyen|first4=Quynh|last5=Zhong|first5=Jiu-Chang|last6=Turner|first6=Anthony J.|last7=Raizada|first7=Mohan K.|last8=Grant|first8=Maria B.|last9=Oudit|first9=Gavin Y.|title=Angiotensin-Converting Enzyme 2: SARS-CoV-2 Receptor and Regulator of the Renin-Angiotensin System|journal=Circulation Research|volume=126|issue=10|year=2020|pages=1456–1474|issn=0009-7330|doi=10.1161/CIRCRESAHA.120.317015}}</ref> as shown in the figure.
| |
| | |
| [[File:COVID-19 associated Diabetes.PNG|600px|center]]
| |
| | |
| * Inhibition of '''RAS(Angiotensin→Ang1→Ang2→AT1R)''' protects pancreatic β-cells from oxidative stress-related tissue damage, therefore improves insulin synthesis and secretion.<ref name="GrankvistMarklund1981">{{cite journal|last1=Grankvist|first1=K|last2=Marklund|first2=S L|last3=Täljedal|first3=I B|title=CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in pancreatic islets and other tissues in the mouse|journal=Biochemical Journal|volume=199|issue=2|year=1981|pages=393–398|issn=0264-6021|doi=10.1042/bj1990393}}</ref>Hyperactivity of RAS works in contrast. In '''adipose tissue''', Ras decreases insulin sensitivity, decreases glucose uptake. In '''pancreatic tissue''', it decreases insulin secretion, increases islet oxidative stress and fibrosis, decrease perfusion.<ref name="BindomLazartigues2009">{{cite journal|last1=Bindom|first1=Sharell M.|last2=Lazartigues|first2=Eric|title=The sweeter side of ACE2: Physiological evidence for a role in diabetes|journal=Molecular and Cellular Endocrinology|volume=302|issue=2|year=2009|pages=193–202|issn=03037207|doi=10.1016/j.mce.2008.09.020}}</ref>
| |
| * In an experimental trial, pressor doses of Ang-II were given to healthy human subjects. As a result, researchers observed suppression of basal, pulsatile, and glucose-stimulated insulin release.<ref name="FliserSchaefer1997">{{cite journal|last1=Fliser|first1=Danilo|last2=Schaefer|first2=Franz|last3=Schmid|first3=Daniela|last4=Veldhuis|first4=Johannes D.|last5=Ritz|first5=Eberhard|title=Angiotensin II Affects Basal, Pulsatile, and Glucose-Stimulated Insulin Secretion in Humans|journal=Hypertension|volume=30|issue=5|year=1997|pages=1156–1161|issn=0194-911X|doi=10.1161/01.HYP.30.5.1156}}</ref>This loss of insulin release is supposed to be the contributing factor in the development of T2DM.<ref name="Gerich2002">{{cite journal|last1=Gerich|first1=J. E.|title=Is Reduced First-Phase Insulin Release the Earliest Detectable Abnormality in Individuals Destined to Develop Type 2 Diabetes?|journal=Diabetes|volume=51|issue=Supplement 1|year=2002|pages=S117–S121|issn=0012-1797|doi=10.2337/diabetes.51.2007.S117}}</ref>
| |
| * SARS-CoV 2 can cause hyperglycemia by direct injuring of pancreatic beta cells<ref name="YangLin2009">{{cite journal|last1=Yang|first1=Jin-Kui|last2=Lin|first2=Shan-Shan|last3=Ji|first3=Xiu-Juan|last4=Guo|first4=Li-Min|title=Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes|journal=Acta Diabetologica|volume=47|issue=3|year=2009|pages=193–199|issn=0940-5429|doi=10.1007/s00592-009-0109-4}}</ref> and by downregulating ACE2 receptors leading to unopposed angiotensin II, which may hinder insulin secretion.<ref name="CarlssonBerne1998">{{cite journal|last1=Carlsson|first1=P.-O.|last2=Berne|first2=C.|last3=Jansson|first3=L.|title=Angiotensin II and the endocrine pancreas: effects on islet blood flow and insulin secretion in rats|journal=Diabetologia|volume=41|issue=2|year=1998|pages=127–133|issn=0012-186X|doi=10.1007/s001250050880}}</ref>
| |
| | |
| ==Causes==
| |
| 1- Direst damage of pancreatic beta-cells by SARS-CoV 2 <ref name="YangLin2009">{{cite journal|last1=Yang|first1=Jin-Kui|last2=Lin|first2=Shan-Shan|last3=Ji|first3=Xiu-Juan|last4=Guo|first4=Li-Min|title=Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes|journal=Acta Diabetologica|volume=47|issue=3|year=2009|pages=193–199|issn=0940-5429|doi=10.1007/s00592-009-0109-4}}</ref>
| |
| | |
| 2- Downregulation of ACE2 by SARS-CoV 2 shift the cascade to the ACE/AngII/AT1R pathway which further leads to decrease insulin release and islet cell oxidative damage.<ref name="CarlssonBerne1998">{{cite journal|last1=Carlsson|first1=P.-O.|last2=Berne|first2=C.|last3=Jansson|first3=L.|title=Angiotensin II and the endocrine pancreas: effects on islet blood flow and insulin secretion in rats|journal=Diabetologia|volume=41|issue=2|year=1998|pages=127–133|issn=0012-186X|doi=10.1007/s001250050880}}</ref>
| |
| | |
| ==Risk Factors==
| |
| There are no established risk factors for COVID-19-associated Diabetes.
| |
| | |
| ==Screening==
| |
| There is insufficient evidence to recommend routine screening for COVID-19-associated Diabetes.
| |
| | |
| ==Diagnosis==
| |
| ===History and Symptoms===
| |
| According to a recent case report of Diabetic ketoacidoses precipitated by Covid-19 in a patient with newly diagnosed diabetes mellitus. He was a previously healthy man presented with 1-week history of:
| |
| *Fever (38.5 °C)
| |
| *Vomiting,
| |
| *Polydipsia (intense thirst)
| |
| *Polyuria (production of abnormally large volumes of dilute urine)<ref name="CheeNg2020">{{cite journal|last1=Chee|first1=Ying Jie|last2=Ng|first2=Shereen Jia Huey|last3=Yeoh|first3=Ester|title=Diabetic ketoacidosis precipitated by Covid-19 in a patient with newly diagnosed diabetes mellitus|journal=Diabetes Research and Clinical Practice|volume=164|year=2020|pages=108166|issn=01688227|doi=10.1016/j.diabres.2020.108166}}</ref>
| |
| | |
| ===Physical Examination===
| |
| * Mildly tachycardic
| |
| * Kusmmaul's breathing was not observed.<ref name="CheeNg2020">{{cite journal|last1=Chee|first1=Ying Jie|last2=Ng|first2=Shereen Jia Huey|last3=Yeoh|first3=Ester|title=Diabetic ketoacidosis precipitated by Covid-19 in a patient with newly diagnosed diabetes mellitus|journal=Diabetes Research and Clinical Practice|volume=164|year=2020|pages=108166|issn=01688227|doi=10.1016/j.diabres.2020.108166}}</ref>
| |
| | |
| ===Laboratory Findings===
| |
| * Hyperglycemia
| |
| * High anion gap metabolic acidosis
| |
| * Ketonemia <ref name="CheeNg2020">{{cite journal|last1=Chee|first1=Ying Jie|last2=Ng|first2=Shereen Jia Huey|last3=Yeoh|first3=Ester|title=Diabetic ketoacidosis precipitated by Covid-19 in a patient with newly diagnosed diabetes mellitus|journal=Diabetes Research and Clinical Practice|volume=164|year=2020|pages=108166|issn=01688227|doi=10.1016/j.diabres.2020.108166}}</ref>
| |
| | |
| ===X-ray===
| |
| There are no x-ray findings associated with [disease name].
| |
| | |
| OR
| |
| | |
| An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
| |
| | |
| OR
| |
| | |
| There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
| |
| | |
| ===Echocardiography or Ultrasound===
| |
| There are no echocardiography/ultrasound findings associated with [disease name].
| |
| | |
| OR
| |
| | |
| Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
| |
| | |
| OR
| |
| | |
| There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
| |
| | |
| ===CT scan===
| |
| There are no CT scan findings associated with [disease name].
| |
| | |
| OR
| |
| | |
| [Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
| |
| | |
| OR
| |
| | |
| There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
| |
| | |
| ===MRI===
| |
| There are no MRI findings associated with [disease name].
| |
| | |
| OR
| |
| | |
| [Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
| |
| | |
| OR
| |
| | |
| There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
| |
| | |
| ===Other Imaging Findings===
| |
| There are no other imaging findings associated with [disease name].
| |
| | |
| OR
| |
| | |
| [Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
| |
| | |
| ===Other Diagnostic Studies===
| |
| There are no other diagnostic studies associated with [disease name].
| |
| | |
| OR
| |
| | |
| [Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
| |
| | |
| OR
| |
| | |
| Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
| |
| | |
| ==Treatment==
| |
| ===Medical Therapy===
| |
| There is no treatment for [disease name]; the mainstay of therapy is supportive care.
| |
| | |
| OR
| |
| | |
| Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].
| |
| | |
| OR
| |
| | |
| The majority of cases of [disease name] are self-limited and require only supportive care.
| |
| | |
| OR
| |
| | |
| [Disease name] is a medical emergency and requires prompt treatment.
| |
| | |
| OR
| |
| | |
| The mainstay of treatment for [disease name] is [therapy].
| |
| | |
| OR
| |
|
| |
| The optimal therapy for [malignancy name] depends on the stage at diagnosis.
| |
| | |
| OR
| |
| | |
| [Therapy] is recommended among all patients who develop [disease name].
| |
| | |
| OR
| |
| | |
| Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
| |
| | |
| OR
| |
| | |
| Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
| |
| | |
| OR
| |
| | |
| Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
| |
| | |
| OR
| |
| | |
| Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
| |
| | |
| ===Surgery===
| |
| Surgical intervention is not recommended for the management of [disease name].
| |
| | |
| OR
| |
| | |
| Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]
| |
| | |
| OR
| |
| | |
| The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].
| |
| | |
| OR
| |
| | |
| The feasibility of surgery depends on the stage of [malignancy] at diagnosis.
| |
| | |
| OR
| |
| | |
| Surgery is the mainstay of treatment for [disease or malignancy].
| |
| | |
| ===Primary Prevention===
| |
| There are no established measures for the primary prevention of [disease name].
| |
| | |
| OR
| |
| | |
| There are no available vaccines against [disease name].
| |
| | |
| OR
| |
| | |
| Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
| |
| | |
| OR
| |
| | |
| [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].
| |
| | |
| ===Secondary Prevention===
| |
| There are no established measures for the secondary prevention of [disease name].
| |
| | |
| OR
| |
| | |
| Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].
| |
| | |
| ==References==
| |
| {{reflist|2}}
| |
| | |
| {{WikiDoc Help Menu}}
| |
| {{WikiDoc Sources}}
| |