Abstract

Preserved <scp>C</scp>‐peptide in survivors of <scp>COVID</scp>‐19: Post hoc analysis

Highlights

  • Hyperglycaemia[1] and new diagnoses of diabetes have been reported in patients with coronavirus disease 2019 (COVID-19).[1]

  • The receptor necessary for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular entry, angiotensin I-converting enzyme type 2 (ACE2), and its permissive protein, TMPRSS2, are present in the pancreatic microvasculature[4] and, at postmortem, SARS-CoV-2 viral RNA has been detected in pancreatic beta cells.[5]

  • Hyperglycaemia in patients with COVID-19 is associated with increased mortality rates,[12] and results from both impaired insulin secretion and increased peripheral insulin resistance.[13]

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Summary

| INTRODUCTION

Hyperglycaemia[1] and new diagnoses of diabetes (including autoantibody-negative type 1 diabetes2) have been reported in patients with coronavirus disease 2019 (COVID-19).[1]. It has been speculated that insulin secretory capacity may be curtailed by direct cytopathic action of SARS-CoV-2 on beta cells It is unknown whether such changes are of clinical relevance in survivors of COVID-19. Random non-fasting C-peptide (rCP) levels correlate with stimulated C-peptide levels derived during mixed meal tests,[7] and have high sensitivity and specificity compared with the gold standard threshold of 600 pmol/L considered to indicate insulin deficiency.[8]. It remains to be determined whether there is evidence for deficient insulin secretion, consistent with beta cell destruction, in survivors of COVID-19. We assessed rCP in patients at least 3 months after COVID-19 infection to assess longer term beta cell secretory capacity

| METHODS
| RESULTS
Findings
| DISCUSSION
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