We have described a case of insulin allergy and type B insulin resistance that was successfully controlled with liraglutide. An allergic reaction to insulin products or insulin itself is an important clinical problem in patients using insulin, as it influences glycemic control [
3]. In a case with anti-insulin antibodies or insulin allergy, modifying the insulin therapy is a common strategy, although there is no established method for doing so. Type B insulin resistance syndrome is an autoimmune disease caused by the production of antibodies to the insulin receptor, resulting in severe insulin resistance. It may be complicated by the presence of collagenous disease. The following treatment options have been suggested: insulin-like growth factor 1, rituximab, plasmapheresis, immunosuppressive agents (e.g., cyclosporine, cyclophosphamide, azathioprine, and steroids), and an intensive combination therapy incorporating some of these options [
4]. For the treatment of diabetic patients with heart failure, empagliflozin (a sodium-glucose co-transporter 2 inhibitor, SGLT2I) is a promising therapeutic option according to EMPA-REG OUTCOME [
5]. However, the present patient had severe heart failure treated with an implanted LVAD and a urinary tract infection. We did not choose SGLT2I because of his susceptibility to urinary infectious complications. In addition, altering the insulin therapy was not an effective approach in this patient due to a high titer of anti-insulin antibodies. Moreover, he had type B insulin resistance syndrome. Because his endogenous insulin secretion was preserved, we attempted to use a glucagon-like peptide-1 receptor (GLP-1R) agonist. Liraglutide therapy eventually resulted in good glycemic control with an insulin-free state via monotherapy. Although a few cases of the successful use of liraglutide therapy to control hyperglycemia in patients with insulin allergy and type B insulin resistance have been reported [
6,
7], the biological mechanism associated with the use of liraglutide to treat type B insulin resistance syndrome, anti-insulin antibodies, and insulin allergy is unclear. GLP-1 acts at multiple sites with both insulinotropic pancreatic and extrapancreatic effects, including the intestinal– and cephalic–pancreas axes [
8]. It may exert a glucagon-suppressive effect or increase the residence time of food in the stomach, thus contributing to the improvement in glycemic control. Hirai et al. reported a patient with anti-insulin antibodies to exogenously injected insulin and noted that liraglutide may decrease the amount of anti-insulin antibodies and suppress further production [
7]. However, after 1 year of follow-up, liraglutide did not affect the serum concentration of anti-insulin antibodies; spontaneous remission of type B insulin resistance syndrome reversed the insulin receptor signaling and partially improved the glucose profile. Indeed, this patient did not show any typical clinical features of type B insulin resistance syndrome: acanthosis nigricans, collagenous disease. The titer of anti-insulin receptor antibody was also not so high. It has been reported that there are some patients without these typical clinical features of type B insulin resistance syndrome [
4]. Further study is required to elucidate the mechanistic details associated with the potential benefit of liraglutide in the treatment of type B insulin resistance syndrome, anti-insulin antibodies, and insulin allergy.