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COVID-19 and DKA of Type 2 Diabetes, Impact and Outcome
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Abstract
Background
Recent evidence suggests a potential link between COVID-19 infection and the development of insulin dependence in individuals with diabetes, particularly through direct damage to pancreatic insulin-producing beta-cells mediated by the virus's affinity for ACE2 receptors. This association bears similarities to the role of other viruses like enteroviruses and mumps in causing fulminant ketoacidosis. While it is feasible that the insulin dependence seen in diabetic ketoacidosis (DKA) during COVID-19 arises from SARS-CoV-2-induced beta cell dysfunction, stronger evidence supports an alternate pathway involving indirect factors like systemic hypoxia, sepsis, inflammatory responses, and cytokine storms resulting from the infection.
Aim of the Work
This study aimed to assess the risk factors and outcomes related to DKA in COVID-19-infected patients with type 2 diabetes.
Patients and Methods
The research analyzed data from 70 patients, comprising 35 with DKA and 35 without DKA, focusing on variables such as age, sex, comorbidities, laboratory results, and clinical symptoms. The mean age was found to be significantly higher in the DKA group, aligning with previous studies that linked older age to increased DKA susceptibility during COVID-19. Sex distribution did not show significant differences between the DKA and non-DKA groups.
Results
Notably, patients with DKA displayed longer diabetes duration and significantly higher hemoglobin A1c levels, suggesting a potential role of poor glucose control in precipitating DKA during COVID-19 infection. Furthermore, DKA patients exhibited more severe acid-base disturbances and electrolyte imbalances compared to their non-DKA counterparts. These imbalances, along with respiratory and cardiovascular symptoms, characterized the clinical presentation of DKA during COVID-19.
Conclusion
Ultimately, the mortality rate was found to be markedly higher among DKA patients than among non-DKA patients. These findings emphasize the importance of recognizing the complex interplay between COVID-19 infection, diabetes, and DKA, especially in older individuals with longer diabetes duration and poor glycemic control. This study provides valuable insights into the risk factors and clinical outcomes associated with DKA in COVID-19-infected patients with type 2 diabetes, contributing to our understanding of the multifaceted relationship between these medical conditions. Further research is needed to elucidate the underlying mechanisms and optimize management strategies for this vulnerable patient population.
Title: COVID-19 and DKA of Type 2 Diabetes, Impact and Outcome
Description:
Abstract
Background
Recent evidence suggests a potential link between COVID-19 infection and the development of insulin dependence in individuals with diabetes, particularly through direct damage to pancreatic insulin-producing beta-cells mediated by the virus's affinity for ACE2 receptors.
This association bears similarities to the role of other viruses like enteroviruses and mumps in causing fulminant ketoacidosis.
While it is feasible that the insulin dependence seen in diabetic ketoacidosis (DKA) during COVID-19 arises from SARS-CoV-2-induced beta cell dysfunction, stronger evidence supports an alternate pathway involving indirect factors like systemic hypoxia, sepsis, inflammatory responses, and cytokine storms resulting from the infection.
Aim of the Work
This study aimed to assess the risk factors and outcomes related to DKA in COVID-19-infected patients with type 2 diabetes.
Patients and Methods
The research analyzed data from 70 patients, comprising 35 with DKA and 35 without DKA, focusing on variables such as age, sex, comorbidities, laboratory results, and clinical symptoms.
The mean age was found to be significantly higher in the DKA group, aligning with previous studies that linked older age to increased DKA susceptibility during COVID-19.
Sex distribution did not show significant differences between the DKA and non-DKA groups.
Results
Notably, patients with DKA displayed longer diabetes duration and significantly higher hemoglobin A1c levels, suggesting a potential role of poor glucose control in precipitating DKA during COVID-19 infection.
Furthermore, DKA patients exhibited more severe acid-base disturbances and electrolyte imbalances compared to their non-DKA counterparts.
These imbalances, along with respiratory and cardiovascular symptoms, characterized the clinical presentation of DKA during COVID-19.
Conclusion
Ultimately, the mortality rate was found to be markedly higher among DKA patients than among non-DKA patients.
These findings emphasize the importance of recognizing the complex interplay between COVID-19 infection, diabetes, and DKA, especially in older individuals with longer diabetes duration and poor glycemic control.
This study provides valuable insights into the risk factors and clinical outcomes associated with DKA in COVID-19-infected patients with type 2 diabetes, contributing to our understanding of the multifaceted relationship between these medical conditions.
Further research is needed to elucidate the underlying mechanisms and optimize management strategies for this vulnerable patient population.
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