Insulin autoimmune syndrome (IAS) is characterized by hyperinsulinemic hypoglycemia and elevated anti-insulin antibodies. While thiol-containing drugs commonly induce IAS, cases induced by proton pump inhibitors are rare. We report a case of IAS induced by omeprazole in a 27-year-old Chinese man with the HLA-DRB1*0406 subtype. This patient presented with Whipple's triad after taking omeprazole without concurrent insulin use. The mixed-meal tolerance test (MMTT) and insulin-C-peptide release tests revealed a rapid surge in insulin levels within one hour, with a non-significant increase in C-peptide and a significant rise in insulin after precipitation. Further examination revealed high-titer positive insulin autoantibodies, leading to a diagnosis of insulin autoimmune syndrome (IAS). Symptoms resolved upon discontinuation of omeprazole and adherence to dietary recommendations, with insulin autoantibody levels decreasing after a 6-month follow-up. This case highlights omeprazole's potential to induce IAS, underscoring the need for vigilance due to widespread use of proton pump inhibitor.
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http://dx.doi.org/10.1016/j.diabres.2024.111906 | DOI Listing |
Methods Cell Biol
January 2025
School of Cardiovascular and Metabolic Medicine & Sciences, King's College London, London, United Kingdom. Electronic address:
Many rodent models are available for preclinical diabetes research making it a challenge for researchers to choose the most appropriate one for their experimental question. To aid in this, models have classically been categorized according to which type of diabetes they represent, and further into whether the model is induced, spontaneous or the result of genetic manipulation. This fails to capture the complexity of pathogenesis seen in diabetes in humans.
View Article and Find Full Text PDFJ Clin Med
January 2025
Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism (CHROMETA), KU Leuven, 3000 Leuven, Belgium.
Type 1 diabetes (T1D) is an autoimmune disorder characterized by the destruction of insulin-producing pancreatic beta-cells, leading to lifelong insulin dependence. This review explores the current understanding of T1D pathogenesis, clinical progression, and emerging therapeutic approaches. We examined the complex interplay between genetic predisposition and environmental factors that could trigger the autoimmune response as well as the immunological mechanisms involved in beta-cell destruction.
View Article and Find Full Text PDFJ Clin Med
January 2025
Young Leaders Advocacy Group, Diabetes Research Institute Foundation, Hollywood, FL 33021, USA.
Type 1 Diabetes (T1D) is a progressive autoimmune disease often identified in childhood or adolescence, with early stages detectable through pre-diabetic markers such as autoantibodies and subclinical beta-cell dysfunction. The identification of the pre-T1D stage is critical for preventing complications, such as diabetic ketoacidosis, and for enabling timely interventions that may alter disease progression. This review examines the multifaceted approach to managing T1D risk in adolescents and teens, emphasizing early detection, nutritional interventions, beta-cell preservation strategies, and psychosocial support.
View Article and Find Full Text PDFLife (Basel)
January 2025
Laboratory of Nervous System Development, Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution "Petrovsky National Research Centre of Surgery", Tsurupi Street, 3, 117418 Moscow, Russia.
Type 1 diabetes (T1D) is related to the autoimmune destruction of β-cells, leading to their almost complete absence in patients with longstanding T1D. However, endogenous insulin secretion persists in such patients as evidenced by the measurement of plasma C-peptide. Recently, a low level of insulin has been found in non-β islet cells of patients with longstanding T1D, indicating that other islet cell types may contribute to persistent insulin secretion.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Unidad de Investigación en Enfermedades Metabólicas, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
Diabetes Mellitus Type 1 (DM1) is an autoimmune disease characterized by the destruction of beta cells in the pancreas. Although amyloid formation has been well-studied in Diabetes Mellitus Type 2 (DM2), its role in DM1 remains unclear. Understanding how islet amyloid polypeptide (IAPP) contributes to beta cell dysfunction and death in DM1 could provide critical insights into disease mechanisms and pave the way for novel diagnostic and therapeutic strategies.
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