New evidence of Diabetes as a consequence of COVID-19 infection


Researchers from the Università di Milano in Italy and the from the Nephrology Division, Boston Children’s Hospital,Harvard Medical School-USA are warning that there will be a huge surge of diabetes caseloads in individuals who had been infected with the COVID-19 disease despite being healthy prior to the SARS-CoV-2 infection.

COVID-19 patients who were otherwise healthy prior to infection were reported to have a greater prevalence of hyperglycaemia.
The study team says that cytokine release as a consequence of SARS-CoV-2 infection may precipitate the onset of metabolic alterations by affecting glucose homeostasis.
The study team describes abnormalities in glycometabolic control, insulin resistance and beta cell function in patients with COVID-19 without any pre-existing history or diagnosis of diabetes, and document glycaemic abnormalities in recovered patients 2 months after onset of disease.
Shockingly in a cohort of 551 patients hospitalized for COVID-19 in Italy, the study team found that 46% of patients were hyperglycaemic, whereas 27% were normoglycaemic.
Utilizing clinical assays and continuous glucose monitoring in a subset of patients, the team detected altered glycometabolic control, with insulin resistance and an abnormal cytokine profile, even in normoglycaemic patients.
Glycaemic abnormalities can be detected for at least 2 months in patients who recovered from COVID-19 and in some cases even much longer.
The study findings demonstrate that COVID-19 is associated with aberrant glycometabolic control, which can persist even after recovery, suggesting that further investigation of metabolic abnormalities in the context of long COVID is warranted.
The study findings were published in the peer reviewed journal: Nature Metabolism.

Many physicians worldwide are now observing a new long-term health concern in patients hospitalized with COVID-19 especially an increase in new-onset hyperglycemia lasting months after infection.
This study found that about half of the patients admitted to the hospital for COVID-19 during the start of the pandemic had new cases of hyperglycemia, or high levels of blood sugar. They also had poorer outcomes.
Lead author Dr Paolo Fiorina, MD, Ph.D., who is affiliated with the Division of Nephrology at Boston Children’s Hospital, told Thailand Medical News, “These individuals were not diabetic before. But during admission, about 46 percent of the patients were found to have new hyperglycemia. While most cases resolved, about 35 percent of the newly hyperglycemic patients remained so at least six months after the infection.”
The clinical study assessed the health of 551 people admitted to the hospital in Italy from March through May 2020. A follow-up period included six months after hospital admission.
Significantly when compared with patients with no signs of glucose abnormalities, the hyperglycemic patients also had worse clinical concerns ie :
-longer hospital ization stays
-far worse clinical symptoms
-an increased need of oxygen
-a much higher need of ventilation
-greater need of intensive care treatment
Dr Fiorina added, “We wanted to understand the mechanism why these patients did poorly compared to those who did not have hyperglycemia.”
In order to learn more, all patients were fitted with a glucose sensor at admission. Over the course of time, the study team detected many abnormalities in glucose metabolic control in the hyperglycemic patients.
The team also found that hyperglycemic patients had abnormal hormonal levels.
Dr Fiorina further added, “We discovered they were severely hyperinsulinemic; they produced too much insulin. They also had abnormal levels of pro-insulin, a precursor of insulin, and markers of impaired islet beta cell function. Islet beta cells make and secrete insulin. Basically, the hormonal profile suggests that the endocrine pancreatic function is abnormal in those patients with COVID-19 and it persists long after recovery.”
It was found that the hyperglycemic patients also had severe abnormalities in the amount of inflammatory cytokines, including IL-6 and others.
Dr Fiorina, whose theory was proven true added, “We thought that blocking IL-6, and potentially even other cytokines, would be a benefit for beta cell function.”
Interestingly patients treated with anti-IL-6 therapy (tocilizumab), had greater improvement in glycemic control higher compared with those who did not receive the medication.
Although the glucometabolic abnormalities declined over time in some patients-particularly after COVID-19 infection, other issues remained.
It was found that many patients had higher post-prandial (after eating) glucose levels and abnormal pancreatic hormones in the post-COVID-19 period.
Dr Fiorina added, “This study is one of the first to show that COVID-19 has a direct effect on the pancreas. It indicates that the pancreas is another target of the virus affecting not only the acute phase during hospitalization but potentially also the long-term health of these patients.”
The research findings points to the importance of evaluating pancreatic function in patients hospitalized for COVID-19 while in the hospital and over the long term.
Dr Fiorina explained, “This goes beyond fasting glucose testing because we observed glucose metabolic abnormalities during the day which were not always present in a normal fasting test.”
Importantly in terms of treatment, questions remain about how to care for patients with COVID-19-related glucose abnormalities. Should patients be treated just with an anti-diabetic drug like an insulin sensitizer, or should anti-inflammatory drugs like tocilizumab and other drugs be used?
Dr Fiorina, who suggests larger studies need to be done to test anti-diabetic and anti-inflammatory treatment, said, “If you keep targeting and blocking insulin, but you have a strong and chronic inflammation, it may lead to chronic damage, when you consider how many patients have been hospitalized with COVID-19, and continue to be worldwide, we may see a huge increase in the diabetic population.”

The prevalence of COVID-19-associated diabetes is not the result of a single event but of a combination of disease susceptibility associated with chronic illness and COVID-19-specific mechanisms affecting metabolism. Whether a separate entity of post-COVID-19 diabetes, possibly associated with lasting β-cell damage, also exists is not yet clear.

In this Comment, I draw on my experience in treating patients with COVID-19 at Columbia University’s New York Presbyterian Hospital starting in March of 2020, as the pandemic struck New York City. The first wave peaked in mid-April, when our hospital census reached 772 patients with COVID-19, ~280 of whom required invasive assisted mechanical ventilation or extracorporeal membrane oxygenation. From the early days of the pandemic, patients with diabetes were over-represented among the admissions and exhibited an unusually high prevalence of ketoacidosis. Our collective experience as medical faculty at Columbia/New York Presbyterian has been reviewed elsewhere1.

What we know

Recent meta-analyses have confirmed initial observations2 that diabetes is a risk factor for symptomatic SARS-CoV-2 infection and COVID-19-related hospitalization3, escalation of care4, invasive assisted mechanical ventilation5, renal replacement therapy6, cardiac injury7, thromboembolic events8 and death9. My service has reflected these findings: most patients presenting with hyperglycaemia and ketoacidosis had pre-existing, often poorly controlled diabetes (haemoglobin A1c ≥ 10%/13.3 mmol). Although type 2 diabetes prevailed, I saw occasional cases of type 1 diabetes, all in parlous states of control. Previously undiagnosed pre-existing diabetes, on the basis of haemoglobin A1c levels, was common.

Excluding pre-existing diabetes can be tricky, particularly in the fraught context of COVID-19 admissions. Patients may have near-normal haemoglobin A1c levels as a result of lifestyle modifications or may have been teetering on the brink of the diagnostic criteria and surpassed the threshold only in the context of SARS-CoV-2 infection. However, patients without clear evidence of pre-existing diabetes may present with stress hyperglycaemia and may not require long-term antidiabetic treatment.

Only long-term follow-up can clarify whether COVID-19 accelerates the onset of permanent diabetes to a greater extent than other precipitating factors. For example, community-acquired pneumonia is frequently associated with hyperglycaemia in patients without diabetes, but it can be a harbinger of diabetes, particularly in older people. Thus, hyperglycaemia per se is not unique to COVID-19 (Fig. 1).

Fig. 1: Mechanisms of COVID-associated hyperglycaemia and ketoacidosis.

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