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Diabetic ketoacidosis precipitated by Covid-19 in apatient with newly diagnosed diabetes mellitus - Ying Jie Chee -Khoo Teck Puat Hospital, Singapore

Ying Jie Chee

There is scarce data on diabetic ketoacidosis (DKA) inCovid-19 infection. We report a case of DKA precipitated byCovid-19 in a patient with newly diagnosed diabetes mellitus.A 37 year-old, previously healthy man presented with1 week history of fever, vomiting, polydipsia and polyuria.On admission, his temperature was 38.5°C. He washaemodynamically stable but mildly tachycardic. He did notdisplay Kussmaul’s breathing and did not require supplemen-tal oxygen. His body mass index was 22.6 kg/m2with no evi-dence of insulin resistance.Given positive contact history, he was tested and con-firmed to be infected with severe acute respiratory syndromecoronavirus  2  (SARS-CoV-2).  Laboratory  investigations(Table 1) were significant for hyperglycemia, high anion gapmetabolic acidosis and ketonemia, confirming the diagnosisof DKA.He received 6 L of intravenous fluids and intravenous insu-lin infusion in the first 24 h. Serum electrolytes were closelymonitored. DKA resolved the following day and he was tran-sitioned to subcutaneous insulin therapy.DKA occurs as a result of insulin deficiency and increasedcounterregulatory responses, which favour the production ofketones. The interactions between SARS-CoV-2 and the renin-angiotensin-aldosterone  system  (RAAS)  might  provideanother mechanism in the pathophysiology of DKA.Angiotensin-converting enzyme 2 (ACE2), a key enzyme inthe RAAS, catalyzes the conversion of angiotensin II to angio-tensin (1–7)[1]. ACE2 is highly expressed in the lungs, pan-creas and serves as the entry point for SARS-CoV-2[1]. Afterendocytosis of the virus complex, ACE2 expression is down-regulated[2]. There are 2 implications of these interactions.Firstly, entry of SARS-CoV-2 into pancreatic islet cells maydirectly aggravate beta cell injury[3]. Secondly, downregula-tion of ACE2 after viral entry can lead to unopposed angioten-sin II, which may impede insulin secretion[4]. These 2 factorsmight have contributed to the acute worsening of pancreaticbeta cell function and precipitated DKA in this patient.In addition, the relationship between SARS-CoV-2 and theRAAS  can  complicate  DKA  management.  Excessivefluid resuscitation may potentiate acute respiratory distress syndrome as angiotensin II increases pulmonary vascularpermeability and worsens damage to lung parenchyma[5].Furthermore, angiotensin II stimulates aldosterone secretion,potentiating the risk of hypokalemia, which may necessitatemore potassium supplementation in order to continue intra-venous insulin to suppress ketogenesis.In conclusion, it is possible that SARS-CoV-2 may aggra-vate pancreatic beta cell function and precipitate DKA. Fur-ther studies will help delineate the pathophysiology. Wealso highlight the pertinent clinical considerations in the con-current management of two life-threatening conditions –DKA and Covid-19.

A 37 year-old, previously healthy man presented with1 week history of fever, vomiting, polydipsia and polyuria.On admission, his temperature was 38.5°C. He washaemodynamically stable but mildly tachycardic. He did notdisplay Kussmaul’s breathing and did not require supplemen-tal oxygen. His body mass index was 22.6 kg/m2with no evi-dence of insulin resistance.Given positive contact history, he was tested and con-firmed to be infected with severe acute respiratory syndromecoronavirus  2  (SARS-CoV-2).

The authors declare that they have no known competingfinancial interests or personal relationships that could haveappeared to influence the work reported in this paper.

There are 2 implications of these interactions.Firstly, entry of SARS-CoV-2 into pancreatic islet cells maydirectly aggravate beta cell injury[3]. Secondly, downregula-tion of ACE2 after viral entry can lead to unopposed angioten-sin II, which may impede insulin secretion[4]. These 2 factorsmight have contributed to the acute worsening of pancreaticbeta cell function and precipitated DKA in this patient.In addition, the relationship between SARS-CoV-2 and theRAAS  can  complicate  DKA  management.  Excessivefluid resuscitation may potentiate acute respiratory distress syndrome as angiotensin II increases pulmonary vascularpermeability and worsens damage to lung parenchyma[5].Furthermore, angiotensin II stimulates aldosterone secretion,potentiating the risk of hypokalemia, which may necessitatemore potassium supplementation in order to continue intra-venous insulin to suppress ketogenesis.In conclusion, it is possible that SARS-CoV-2 may aggra-vate pancreatic beta cell function and precipitate DKA. Fur-ther studies will help delineate the pathophysiology.

Excessivefluid resuscitation may potentiate acute respiratory distress syndrome as angiotensin II increases pulmonary vascularpermeability and worsens damage to lung parenchyma[5].Furthermore, angiotensin II stimulates aldosterone secretion,potentiating the risk of hypokalemia, which may necessitatemore potassium supplementation in order to continue intra-venous insulin to suppress ketogenesis.In conclusion, it is possible that SARS-CoV-2 may aggra-vate pancreatic beta cell function and precipitate DKA. Fur-ther studies will help delineate the pathophysiology. Wealso highlight the pertinent clinical considerations in the con-current management of two life-threatening conditions –DKA and Covid-19.

 

Laboratory  investigations(Table 1) were significant for hyperglycemia, high anion gapmetabolic acidosis and ketonemia, confirming the diagnosisof DKA.He received 6 L of intravenous fluids and intravenous insu-lin infusion in the first 24 h. Serum electrolytes were closelymonitored. DKA resolved the following day and he was tran-sitioned to subcutaneous insulin therapy.DKA occurs as a result of insulin deficiency and increasedcounterregulatory responses, which favour the production ofketones. The interactions between SARS-CoV-2 and the renin-angiotensin-aldosterone  system  (RAAS)  might  provideanother mechanism in the pathophysiology of DKA.Angiotensin-converting enzyme 2 (ACE2), a key enzyme inthe RAAS, catalyzes the conversion of angiotensin II to angio-tensin (1–7)[1].

Afterendocytosis of the virus complex, ACE2 expression is down-regulated[2]. There are 2 implications of these interactions.Firstly, entry of SARS-CoV-2 into pancreatic islet cells maydirectly aggravate beta cell injury[3]. Secondly, downregula-tion of ACE2 after viral entry can lead to unopposed angioten-sin II, which may impede insulin secretion[4]. These 2 factorsmight have contributed to the acute worsening of pancreaticbeta cell function and precipitated DKA in this patient.In addition, the relationship between SARS-CoV-2 and theRAAS  can  complicate  DKA  management.

The authors declare that they have no known competingfinancial interests or personal relationships that could haveappeared to influence the work reported in this paper.

There are 2 implications of these interactions.Firstly, entry of SARS-CoV-2 into pancreatic islet cells maydirectly aggravate beta cell injury[3]. Secondly, downregula-tion of ACE2 after viral entry can lead to unopposed angioten-sin II, which may impede insulin secretion[4]. These 2 factorsmight have contributed to the acute worsening of pancreaticbeta cell function and precipitated DKA in this patient.In addition, the relationship between SARS-CoV-2 and theRAAS  can  complicate  DKA  management.  Excessivefluid resuscitation may potentiate acute respiratory distress syndrome as angiotensin II increases pulmonary vascularpermeability and worsens damage to lung parenchyma[5].Furthermore, angiotensin II stimulates aldosterone secretion,potentiating the risk of hypokalemia, which may necessitatemore potassium supplementation in order to continue intra-venous insulin to suppress ketogenesis.In conclusion, it is possible that SARS-CoV-2 may aggra-vate pancreatic beta cell function and precipitate DKA. Fur-ther studies will help delineate the pathophysiology.