Abstract


The type B insulin resistance syndrome is an autoimmune disease which is due to the presence of antibodies against the insulin receptor, although in some cases it manifests with hypoglycemia, it more often presents with severe hyperglycemia with high insulin requirements and exaggerated insulin resistance. The immunomodulatory treatment may be the best strategy to achieve metabolic control view more

The type B insulin resistance syndrome is an autoimmune disease which is due to the presence of antibodies against the insulin receptor, although in some cases it manifests with hypoglycemia, it more often presents with severe hyperglycemia with high insulin requirements and exaggerated insulin resistance. The immunomodulatory treatment may be the best strategy to achieve metabolic control
Clinical case: A 23 year old, female patient, with systemic lupus erythematosus who was diagnosed in 2010; in August 2013 presented diabetic ketoacidosis triggered by a soft tissue infection. Steroids were suspended and treatment with insulin was begun. During her stay at the hospital high insulin requirements due to poor metabolic control, prompting a change from basal-bolus scheme to an insulin pump plus additional bolus, requiring progressive increases in doses up to 300 units of insulin per day through infusion pump plus a basal-bolus insulin scheme of glargine and glulisine indicated by glucometry, with doses up to 600 units day. Due to clinical signs of insulin resistance, high glycemic variability and HbA1c14%, metformin and sulfonylurea were added showing partial improvement. Subsequent management with GLP-1 analogue was required and an evaluation of genetic or immunological origin of insulin resistance was initiated. During monitoring she presented lupus activation with renal impairment handled with immunomodulatory therapy, reset of an azathioprine and prednisolone, obtaining an adequate response. The results of anti-insulin antibodies were positive and complete sequencing of the INRS gen was inconclusive. A short time after beginning the immunomodulators the patient started to lower her glucose measurements allowing sequential reductions in insulin dosage until the withdrawal of the infusion pump and the reduction of the basal-bolus scheme. In March 2015, she received the last dose of insulin, since that time maintaining an adequate glucometric control with liraglutide. In September 2015, mycophenolate was initiated for the management of her renal impairment allowing further withdrawal of liraglutide. Since then the patient has been without any antidiabetic treatment showing good glycemic control.

The type B insulin resistance syndrome should be suspected in a patient with autoimmune disease presenting severe hyperglycemia with very high insuline requirements, the study should include anti insulin antibodies and anti insulin receptor. In this patient the positivity for anti-insulin antibodies was confirmed at levels only slightly above the normal upper limit; but the transition from needing exaggerated insulin and GLP-1 analogs to the withdrawal of all antidiabetic metication with complete resolution of severe hyperglycemia in response to immunomodulators allowed us to confirm the diagnosis and prevent severe complications of prolonged uncontrolled hyperglycemia.

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