Prevention and management of COVID-19 among patients with diabetes: an appraisal of the literature

Abstract

The coronavirus disease 2019 (COVID-19) pandemic has emerged as one of the greatest challenges faced by humankind in the recent past. People with diabetes and related comorbidities are at increased risk of its complications and of COVID-19-related death. Older age, multi-morbidity, hyperglycaemia, cardiac injury and severe inflammatory response are predictors of poor outcome. The complex interplay between COVID-19, diabetes and the effects of related therapies is being explored. Most patients experience a mild illness with COVID-19, while people with diabetes are at increased risk of severe disease. Optimising glycaemic control and adopting measures to prevent disease spread are critical aspects. The management of mild disease is supportive, while very many immunomodulatory and antiviral therapies are being investigated for the treatment of severe disease. Several of these agents have specific considerations for use in people with diabetes. Since mass population lockdowns are considered a key step in controlling disease spread, it follows that, in addition to the direct vulnerability to severe COVID-19, people with diabetes can be affected by limited access to healthcare, insulin, other medications and blood glucose monitoring equipment. Measures to prevent disease spread at the individual and community level are the key to mitigating the rapidly escalating pandemic, while agents for chemoprophylaxis and vaccines are being explored. People with diabetes should be recognised as a vulnerable group for complicated disease and are at risk during times of disturbed social systems. Strategies are needed to safeguard the health of patients with diabetes during the pandemic. This review summarises the current knowledge and perceived challenges for prevention and management of COVID-19 in people with diabetes.

Keywords: COVID-19; Coronavirus; Diabetes; SARS-CoV-2.

Fig. 1

Role of ACE2 in the pathogenesis of coronavirus diseases. ACE2 converts angiotensin I and angiotensin II to angiotensin-(1–9) and angiotensin-(1–7), respectively. ACE2 is also expressed in the lung, kidney, heart and pancreas and acts as a facilitator for CoV entry into cells. Use of ACEI/ARBs increases angiotensin I levels and upregulates ACE2 gene expression. This facilitates excess viral entry into host cells causing organ injury and insulin deficiency, contributing to hyperglycaemia. Upregulated ACE2 may convert angiotensin II to angiotensin-(1–7). The latter acts on the Mas1 receptor to trigger anti-inflammatory effects and inhibits the AT1 receptor to cause vasodilation. However, at least in ACEI users, angiotensin II levels will be low and the net benefit of ACE2 upregulation is uncertain. CoV infection downregulates ACE2 expression, thereby reducing angiotensin-(1–7) levels, which reduces its anti-inflammatory effects and potentially worsens organ vulnerability to infection. AT, angiotensin; RBD, receptor binding domain. This figure is available as part of a downloadable slideset

Fig. 2

COVID-19 preventive and management considerations for people with diabetes at an individual level and from a healthcare service perspective. ^aOwing to limited evidence, and risk of dehydration and euglycaemic ketoacidosis, it may be advisable to discontinue SGLT2 inhibitors until recovering from acute illness and/or until further evidence is available. Insulin is safe, provided glycaemic status is regularly monitored and treatment is adjusted. Other agents should be used with caution, particularly in hospitalised patients. IVI, intravenous infusion; MDI, multiple daily injections. This figure is available as part of a downloadable slideset