Context: Insulin autoantibody syndrome (IAAS) is considered to be a rare cause of hyperinsulinaemic hypoglycaemia. Lack of familiarity with the varied clinical manifestations leads to underdiagnosis. Localization techniques aimed at insulin-secreting neoplasms and nesidioblastosis, which are expensive often are ordered when the correct diagnosis is not made.
Aims: We describe the myriad of clinical manifestations associated with IAAS based on single centre experience.
Settings And Design: Retrospective analysis of patients who got admitted with symptoms suggestive of hypoglycaemia and underwent mixed meal test and prolonged hypoglycaemic test from 2016 to 2019.
Subjects And Methods: Retrospective data of 12 patients with IAAS who were diagnosed in the threeyear time period between 2016 and 2019 are included in this analysis. Clinical details, biochemical parameters and imaging modalities were analysed.
Statistical Analysis: All analyses were performed with SPSS software (version 17).
Results: Total of twelve patients 12 (5 male and 7 females) were identified as IAAS. Median age of presentation was 57 years. Median insulin levels and median C-peptide levels were 300 miu/ml and 18.5 ng/ml respectively. Only 3 (25%) patients had spontaneous resolution. Steroid induced remission occurred by 3 months in the remaining patients. Intermittent hyperglycaemia was seen in 9 (75%) patients. Implicatable drug use preceding the occurrence of the clinical symptoms was observed in five patients.
Conclusion: IAAS is not uncommon in India. The diagnosis should be pursued in patients with hyperinsulinaemic hypoglycaemia especially when insulin levels are very high or when there is intermittent hyperglycaemia.
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http://dx.doi.org/10.4103/ijem.IJEM_335_19 | DOI Listing |
Front Immunol
January 2025
Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China.
Type 1 diabetes (T1D) is a metabolic disorder caused by a complete lack of insulin, primarily manifested by hyperglycemia. The mechanisms underlying the onset of T1D are complex, involving genetics, environment, and various unknown factors, leading to the infiltration of various immune components into the islets. Besides T cells, B cells are now considered important contributors to the pathogenesis of T1D, according to recent studies.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, United States.
During type 1 diabetes (T1D) progression, beta cells become dysfunctional and exhibit reduced first-phase insulin release. While this period of beta cell dysfunction is well established, its cause and underlying mechanism remain unknown. To address this knowledge gap, live human pancreas tissue slices were prepared from autoantibody-negative organ donors without diabetes (ND), donors positive for one or more islet autoantibodies (AAb+), and donors with T1D within 0-4 years of diagnosis (T1D+).
View Article and Find Full Text PDFBMJ Open
January 2025
Vibrant Sciences LLC, Santa Clara, California, USA.
Objective: To evaluate the association between thyroid disease and diabetes markers.
Design: Retrospective cohort study.
Setting: The study was conducted in a diagnostic setting where the primary care providers recommended the patients to test for thyroid and diabetes panels.
Diabetes Technol Ther
January 2025
University of Minnesota School of Medicine, Minneapolis, Minnesota, USA.
BMJ Open Diabetes Res Care
January 2025
Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, Florida, USA
Introduction: Altered serum levels of growth hormones, adipokines, and exocrine pancreas enzymes have been individually linked with type 1 diabetes (T1D). We collectively evaluated seven such biomarkers, combined with islet autoantibodies (AAb) and genetic risk score (GRS2), for their utility in predicting AAb/T1D status.
Research Design And Methods: Cross-sectional serum samples (n=154 T1D, n=56 1AAb+, n=77 ≥2AAb+, n=256 AAb-) were assessed for IGF1, IGF2, adiponectin, leptin, amylase, lipase, and trypsinogen (n=543, age range 2.
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