Abstract
Abstract Disclosure: E. Chuki: None. M. Lightbourne: None. B. Abel: None. R.J. Brown: None. Bell’s palsy (BP) is associated with diabetic angiopathy and facial nerve ischemia and may be the first sign of diabetic mononeuropathy. Specific risk factors for diabetic mononeuropathy have not been well established. Rapid tightening of glycemic control has been associated with worsening diabetic retinopathy. However, this association has not been reported previously in the development of diabetic mononeuropathy or BP. We describe three patients with extreme insulin resistance, in whom rapid correction of hyperglycemia was temporally associated with development of BP. Case 1: A 63 year-old African American male with history of type 2 diabetes (T2D) and peripheral neuropathy was admitted with sudden onset severe insulin resistance and DKA, leading to a diagnosis of type B insulin resistance. Serum glucose was >600 mg/dl and A1c was 13.4%. He was treated with an insulin drip, then transitioned to subcutaneous insulin U-500 at a total daily dose of ∼3000 units, resulting in blood glucose between 140 and 180 mg/dl. On Day 5 after initiating U-500 and achieving tight control of glycemia, the patient developed bilateral Bell’s Palsy, which resolved after 4 years. Case 2: A 25 year-old African American female with history of T2D was admitted with sudden onset severe insulin resistance and DKA requiring an insulin drip of ∼3,000 units per day, leading to a diagnosis of type B insulin resistance. A1c on admission was 14%. After ∼5 days, she transitioned to U-500 that was titrated over 2 weeks to a total daily dose of 3,000 units with blood glucose between 98 and 177 mg/dL. She developed bilateral BP approximately 43 days from onset of DKA and 36 days after starting U-500 insulin with improved glycemic control. At last follow up 5 years later she still had residual facial weakness. Case 3: A 25 year-old Caucasian male with history of diabetes due to type A insulin resistance (Rabson-Mendenhall Syndrome) and recurrent ketosis on U500 insulin >1,000 units daily had poor adherence to insulin and diet with A1c of 14.3%. 3 weeks after A1c measurement he was started on a Continuous Glucose Monitor (CGM), leading to dramatic change in diet and medication adherence, with reduction in the estimated A1c based on glucose management indictor (GMI) to 7.7% within 3 weeks. 3 weeks after starting CGM use with improved compliance and glycemic control, he developed unilateral BP, which fully recovered after 1 month.We report 3 cases in which onset of BP was observed in rapid temporal correlation with massive increases in insulin dose and/or improvement in glycemia. Severe insulin resistance and rapid decrease of glycemic levels may lower intravascular volume and narrow vessels, leading to microvascular disruption of the vasa nervorum, ultimately causing mononeuropathy. A more gradual approach to glycemia management in patients with severe insulin resistance may be warranted to mitigate this risk. Presentation: Thursday, June 15, 2023
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