Skip to main content
ENDO 2026 Main banner

Diabetes and Vascular Disease

MON-618 - Extreme Insulin Resistance in A Young Woman with Autoimmune Disease: A Presumptive Case of Type B Insulin Resistance Syndrome

Monday, June 15, 2026
9:00 AM - 2:00 PM CT
Location: ENDOExpo; Poster Floor
Disclosure(s):
Adriana Franjul, M.D.: No financial relationships to disclose
Jadailine Bermúdez-Santos, MD: No financial relationships to disclose
David Lopez, MD: No financial relationships to disclose
Angelica Vazquez Colon, MD: No financial relationships to disclose
Type B insulin resistance syndrome (TBIRS) is a rare autoimmune disorder caused by antibodies against the insulin receptor, resulting in extreme insulin resistance, marked hyperinsulinemia, and poor response to conventional insulin therapy. It is most often associated with autoimmune diseases, particularly systemic lupus erythematosus (SLE). Due to its rarity, limited availability of insulin receptor antibody testing, and lack of standardized treatment, TBIRS poses major diagnostic and therapeutic challenges. Early recognition is essential, as immunosuppressive therapy may lead to clinical improvement.

A 31-year-old Puerto Rican woman with latent autoimmune diabetes in adults (LADA), SLE, rheumatoid arthritis, and anemia presented with severe hyperglycemia, edema, and abdominal pain. She had poor longitudinal follow-up and required escalating insulin doses despite home therapy with basal–bolus insulin and sulfonylurea. Examination revealed extensive acanthosis nigricans, hirsutism, and significant unintentional weight loss. Laboratory evaluation showed hemoglobin A1c 15% with preserved endogenous insulin secretion (C-peptide 3.30ng/mL) and inappropriately elevated glucagon (3pg/mL), supporting severe insulin resistance rather than insulin deficiency. Secondary causes of insulin resistance were excluded.

Despite intravenous insulin infusion with daily insulin requirements > 1,000 units, glycemic control remained poor. Given the presence of extreme insulin resistance in the context of active autoimmune disease, TBIRS was strongly suspected. Insulin receptor antibody testing was unavailable. Following a multidisciplinary discussion, immunosuppressive therapy was initiated with mycophenolate mofetil and hydroxychloroquine, with subsequent administration of rituximab. Improved glycemic control with reduced insulin requirements permitted discharge on U-500 insulin and adjunctive antihyperglycemic therapy, with close follow-up by endocrinology and rheumatology.

This case highlights the importance of considering TBIRS in patients with autoimmune disease and extreme insulin resistance. When antibody testing is unavailable, a presumptive diagnosis based on clinical and biochemical features may allow timely initiation of immunosuppressive therapy. B-cell–directed treatment with rituximab can result in meaningful improvement in glycemic control and should be considered in refractory cases.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*