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 Table of Contents  
REVIEW ARTICLE
Year : 2020  |  Volume : 5  |  Issue : 2  |  Page : 11-12

COVID-19 and diabetes mellitus


1 Department of Public Health Dentistry, A.C.P.M Dental College, Dhule, Maharashtra, India
2 Department of Public Health Dentistry, V.Y.W.S Dental College, Amravati, Maharashtra, India
3 Department of Public Health Dentistry, SMBT Institute of Dental Sciences and Research, Nashik, Maharashtra, India
4 Department of Prosthodontics, Crown and Bridge, A.C.P.M Dental College, Dhule, Maharashtra, India

Date of Submission14-Oct-2020
Date of Acceptance17-Nov-2020
Date of Web Publication29-Jan-2021

Correspondence Address:
Dr. Mayuri Nepale
Room No. 702, Building-Spectra C, Casa Bella Gold, Palava City, Dombivali - East, Mumbai - 421 204, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmo.ijmo_3_20

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  Abstract 


A novel coronavirus, SARS-CoV-2, was identified as the pathogen causing coronavirus disease 2019 (COVID-19) in Wuhan, China, in 2019. On March 11, 2020, COVID-19 was declared a pandemic by the World Health Organization. Individuals with diabetes mellitus (DM), hypertension, and severe obesity (body mass index, 40 kg/m2) are more likely to be infected and are at a higher risk for complications and death from COVID-19. Considering the high proportion of critically ill patients with diabetes or hyperglycemia, the difficulty for treatment, and high mortality rate, effective diabetes management under epidemic conditions is extremely important. In order to increase disease awareness and improve the prognosis and outcome of patients with diabetes, better understanding of the etiological associations between COVID-19 and diabetes is needed.

Keywords: ACE-2, COVID-19, diabetes mellitus, SARS CoV- 2


How to cite this article:
Nepale M, Vishwakarma PY, Dodamani AS, Ray PM, Khobragade VR, Deokar RN, Hai Khan RA. COVID-19 and diabetes mellitus. Int J Med Oral Res 2020;5:11-2

How to cite this URL:
Nepale M, Vishwakarma PY, Dodamani AS, Ray PM, Khobragade VR, Deokar RN, Hai Khan RA. COVID-19 and diabetes mellitus. Int J Med Oral Res [serial online] 2020 [cited 2021 Feb 25];5:11-2. Available from: http://www.ijmorweb.com/text.asp?2020/5/2/11/308275




  Introduction Top


At the end of 2019, a novel RNA betacoronavirus (currently named SARS-CoV-2) has emerged in Wuhan, China, causing coronavirus disease 2019 (COVID-19). The disease has rapidly spread in several countries, and by March 11, 2020, the Director-General of the World Health Organization has declared COVID-19 a pandemic disease. The case fatality ratio of COVID-19 has been initially described in China to be about 1%–2%, but higher percentage may also be estimated.[1] In general, in most immunocompetent individuals, human CoV infection leads to mild upper respiratory infection.[2] The COVID-19 pathogen triggers severe pneumonia and acute, even lethal, lung failure.[3] COVID-19 interacts with preexisting conditions. Individuals with diabetes mellitus (DM), hypertension, and severe obesity (body mass index, 40 kg/m2) are more likely to be infected and are at a higher risk for complications and death from COVID-19.[4] Type 2 DM is a chronic metabolic disorder in which the prevalence has been increasing steadily all over the world. From current clinical reports, COVID-19-affected patients with diabetes are at high risk of becoming critically ill. Research has demonstrated that in the intensive care unit (ICU), 17% of patients were reported to have chronic medical illnesses, including diabetes (17%), cerebrovascular diseases (13.5%), and chronic cardiac diseases (10%). During ICU treatment, 35% of patients were reported to have hyperglycemia as comorbidity. More strikingly, the mortality in diabetics was as high as 77.7% (7/9) among critically ill patients.[5],[6]


  Mechanism that Increases the Risk of COVID-19 in Diabetes Top


Augmented ACE2 expression in alveolar AT2 cells, myocardium, kidney, and pancreas may favor increased cellular binding of SARS-CoV-2. Increased expression of ACE2 has been demonstrated in the lung, kidney, heart, and pancreas in rodent models of DM. Rao et al.[6] explored diseases or traits that may be causally linked to increased ACE2 expression in the lung. Interestingly, they found that DM was causally associated with increased lung ACE2 expression. Plasma glucose levels and DM are independent predictors for mortality and morbidity in patients with SARS. Potential mechanisms that may increase the susceptibility for COVID-19 in patients with DM include:

  1. Higher affinity cellular binding and efficient virus entry
  2. Decreased viral clearance
  3. Diminished T cell function
  4. Increased susceptibility to hyperinflammation and cytokine storm syndrome, and
  5. Presence of CVD.


DM inhibits neutrophil chemotaxis, phagocytosis, and intracellular killing of microbes. Impairments in adaptive immunity characterized by an initial delay in the activation of Th1 cell-mediated immunity and a late hyperinflammatory response are often observed in patients with diabetes. In patients with COVID-19, peripheral counts of CD4 and CD8 T cells are low, but with a higher proportion of highly proinflammatory Th17 CD4 T cells, as well as elevated cytokine levels. Thus, it is likely that patients with DM may have blunted antiviral IFN responses, and the delayed activation of Th1/Th17 may contribute to accentuated inflammatory responses. Another potential mechanism was that hyperglycemia was a risk factor for mortality.[5],[6],[7] Hyperglycemia induced by diabetes was linked to aggressive glycosylation, which leads to overproduction of advanced glycation end products.


  Pharmacological Therapy for Diabetes Top


A patient-centered approach should be used to guide the choice of pharmacological agents. Considerations include age, severity of COVID-19, cardiovascular comorbidities, and hypoglycemia risk. For patients with mild COVID-19, previous medication regimens should be evaluated and followed as appropriate. For ordinary cases, subcutaneous insulin injections, including rapid-acting prandial/ basal insulin or premixed insulin regimens, are recommended. For severe and critically ill patients, intravenous insulin therapy may be the preferred treatment.[8],[9]


  Special Considerations for Patients with Diabetes During the Epidemic Top


During the outbreak of COVID-19, we recommend the “Seven Treasures” policy for diabetes management, including health education, balanced nutrition, physical activity, standardized medication, blood glucose monitoring, regular schedule, and care for mental health.

”Five No” (no going out, no gatherings, no sedentariness, no stop on medications, and no anxiety), “Five Keep” (keep wearing a face mask when you go out, keep hands clean, keep routine medical check if necessary, keep regular life, and keep scientific attitude to COVID-19), and “Five Refuse” (refuse to visit friends, refuse group dining, refuse to taste wild animals, refuse rumors, and refuse to shake hands or hug or kiss) should be advocated for patients with diabetes by endocrinologists, health-care providers, and public health administrators.[10]


  Conclusion Top


It is important to follow standard hospital management and treatment regimens for COVID-19-affected patients with diabetes. Meanwhile, we should pay attention to the lifestyle and glucose management of patients with diabetes outside the hospital and provide them precise medical services. We also suggest that, if possible, global cooperation is needed in medical research, to better understand the genetic, molecular, and immune mechanisms explaining the interplay between COVID-19 and diabetes, and the interplay between disease features, such as susceptibility, severity, and outcome of diabetic patients, with COVID-19 in different populations. We believe that all our efforts will finally overcome COVID-19.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Muniyappa R, Gubbi S. COVID-19 pandemic, coronaviruses, and diabetes mellitus. Am J Physiol Endocrinol Metab 2020;318:E736-41.  Back to cited text no. 1
    
2.
Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: A descriptive study. Lancet 2020;395:507-13.  Back to cited text no. 2
    
3.
Centers for Disease Control and Prevention. National Diabetes Statistics Report, 2020. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 2020.  Back to cited text no. 3
    
4.
Yang J, Zheng Y, Gou X, Pu K, Chen Z, Guo Q, et al. Prevalence of comorbidities in the novel Wuhan coronavirus (COVID-19) infection: a systematic review and meta-analysis. Int J Infect Dis 2020;S1201-9712:30136-3.  Back to cited text no. 4
    
5.
Yang X, Yu Y, Xu J, Shu H, Xia J, Liu H, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: A single-centered, retrospective, observational study. Lancet Respir Med 2020;8:475-81.  Back to cited text no. 5
    
6.
Rao S, Lau A, So HC. Exploring diseases/traits and blood proteins causally related to expression of ACE2, the putative receptor of SARS-CoV-2: A mendelian randomization analysis highlights tentative relevance of Diabetes-Related traits. Diabetes Care 2020;43:1416-26.  Back to cited text no. 6
    
7.
Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med 2020;8:420-2.  Back to cited text no. 7
    
8.
Wan Y, Shang J, Graham R, Baric RS, Li F. Receptor recognition by the novel coronavirus from Wuhan: An analysis based on decade-long structural Studies of SARS coronavirus. J Virol 2020;94:e00127-20.  Back to cited text no. 8
    
9.
Bindom SM, Lazartigues E. The sweeter side of ACE2: Physiological evidence for a role in diabetes. Mol Cell Endocrinol 2009;302:193-202.  Back to cited text no. 9
    
10.
Wang W, Lu J, Gu W, Zhang Y, Liu J, Ning G. Care for diabetes with COVID-19: Advice from China. J Diabetes 2020;12:417-9.  Back to cited text no. 10
    




 

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