Responding to this news article which is responding to Bornstein et al on the subject of diabetes as a complication of COVID-19 infection.
The paper is primarily about management of COVID19 in patients with existing diabetes, rather than the risk of new-onset diabetes as a result of COVID infection, so it’s on shakier ground than you might expect given the news article. The relevant arguments given are: (1) pancreatic beta cells express ACE2 in a mouse model, (2) SARS1 was known to directly damage pancreatic beta cells, and (3) Italian physicians anecdotally report a high rate of DKA in new-onset COVID19 patients (no percentage or citation).
This is strong enough to convince me that this is a thing that happens, for at least a non-negligible (but not necessarily large) subset of the patients who are admitted to ICU.
Some background for people less familiar with diabetes. Pancreatic beta cells produce insulin, which is a hormone that signals to the rest of the body that they should eat the sugar that’s in the blood. Under normal circumstances, this keeps blood sugar within a narrow range (70-110mg/dL). However, if the pancreas is damaged or if the pancreatic-function-to-body-size ratio is too low, it can’t produce enough insulin, so blood sugar rises higher than it’s supposed to. Very high blood sugar is toxic to pancreatic beta cells themselves, causing a feedback loop which leads to a state called diabetic ketoacidosis (DKA), which is reliably fatal if left untreated.
Twenty of the 39 followed-up patients were diabetic during hospitalization. After 3 years, only two of these patients had diabetes.
Unfortunately the paper didn’t say how many of those patients had gotten as far as DKA, as opposed to developing diabetes short of DKA in a hospital setting and having it treated promptly. I haven’t verified this yet, but my prior belief was that anyone who enters DKA is probably going to be diabetic forever.
This is all separate from the question of whether there’s a lasting risk of diabetes in patients who were not hospitalized, or who survived their hospitalization without obvious blood sugar complications. This is a hard question; it seems plausible, but we don’t yet have empirical evidence either way. My guess is probably some increased risk, but not a very large one, and decreasing over time.
Responding to this news article which is responding to Bornstein et al on the subject of diabetes as a complication of COVID-19 infection.
The paper is primarily about management of COVID19 in patients with existing diabetes, rather than the risk of new-onset diabetes as a result of COVID infection, so it’s on shakier ground than you might expect given the news article. The relevant arguments given are: (1) pancreatic beta cells express ACE2 in a mouse model, (2) SARS1 was known to directly damage pancreatic beta cells, and (3) Italian physicians anecdotally report a high rate of DKA in new-onset COVID19 patients (no percentage or citation).
This is strong enough to convince me that this is a thing that happens, for at least a non-negligible (but not necessarily large) subset of the patients who are admitted to ICU.
Some background for people less familiar with diabetes. Pancreatic beta cells produce insulin, which is a hormone that signals to the rest of the body that they should eat the sugar that’s in the blood. Under normal circumstances, this keeps blood sugar within a narrow range (70-110mg/dL). However, if the pancreas is damaged or if the pancreatic-function-to-body-size ratio is too low, it can’t produce enough insulin, so blood sugar rises higher than it’s supposed to. Very high blood sugar is toxic to pancreatic beta cells themselves, causing a feedback loop which leads to a state called diabetic ketoacidosis (DKA), which is reliably fatal if left untreated.
For SARS1, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7088164/ says:
Unfortunately the paper didn’t say how many of those patients had gotten as far as DKA, as opposed to developing diabetes short of DKA in a hospital setting and having it treated promptly. I haven’t verified this yet, but my prior belief was that anyone who enters DKA is probably going to be diabetic forever.
This is all separate from the question of whether there’s a lasting risk of diabetes in patients who were not hospitalized, or who survived their hospitalization without obvious blood sugar complications. This is a hard question; it seems plausible, but we don’t yet have empirical evidence either way. My guess is probably some increased risk, but not a very large one, and decreasing over time.