By: Clay Wirestone
Diabetic ketoacidosis poses enough of a threat on its own. But in a small number of cases, it leaves sufferers open to a potentially fatal infection called mucormycosis.
University of California Los Angeles researchers decided to look into the fungal infection (which has a 50 percent mortality rate) and its connection with DKA. They not only found a clear link, they also discovered an avenue that could lead to new, effective treatments.
In the June 1 issue of The Journal of Clinical Investigation, researchers connected both DKA and the life-threatening infection to a specific protein. The protein is produced, they found, when human cells are subjected to the glucose and iron levels of diabetic ketoacidosis. What’s more, that glucose-regulated protein 78 essentially opens the door to the fungus that causes mucormycosis.
That’s a door you don’t want open. A mucormycosis infection invades the body’s blood vessels, causing clots and killing living tissue. Treatment includes drugs and surgery, but doctors have struggled with the condition’s high mortality rates. Survivors often deal with disfigurement from both the infection and surgery to remove the infected tissue.
The research team, led by Ashraf Ibrahim, took the investigation further than connecting DKA and mucormycosis. Experimenting on mice with ketoacidosis, they re-confirmed the basic link. They then vaccinated the mice with an immune serum that targeted the door-opening protein.
The treatment worked. The mice were more likely to survive the infection than a control group given a non-immune serum. That suggests that more effective human treatments could be on the way, too.
“These results provide insight into why patients with DKA are uniquely susceptible to mucormycosis infections,” the researchers wrote in their conclusion, “and provide a foundation for therapeutic interventions against extremely lethal mucormycosis.”
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