Coronavirus Disease 2019 (COVID-19) had struck the world with health and economic catastrophes and recently with unusual autoimmune presentations, including new-onset Type 1 Diabetes. Herein we present a 17-year-old male patient who presented to the outptient clinic with fever, palpitation, and cough of four-week duration; he was referred to the emergency room and was found to have DKA. CT of the chest showed ground-glass opacities suggestive of COVID-19 pneumonia, and abdominal cuts showed dilated intrahepatic biliary radicles with pancreatic loculations suggestive of pancreatitis. The patient was admitted to the ICU, started on intravenous fluids and insulin infusion then COVID-19 PCR returned positive. We hypothesize that SARS-CoV-2 has a vital role in eliciting an autoimmune response triggering type 1 diabetes, and further studies are needed to confirm this hypothesis. SARS-CoV-2 may cause pancreatitis, and the first presentation could be high blood sugar or DKA.
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http://dx.doi.org/10.1016/j.sciaf.2021.e00915 | DOI Listing |
J Microbiol Immunol Infect
January 2025
Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan; Department of Pediatrics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan. Electronic address:
Background: COVID-19 mRNA vaccines have demonstrated 95 % efficacy in the general population. However, their immunogenicity in adolescents with Type 1 Diabetes (T1D), who exhibit weaken immune responses, remains insufficiently explored.
Methods: Longitudinal analysis of innate immune responses following PRR-agonists and BNT162b2 vaccine stimulations, along with S-specific antibody responses, memory T cell recall responses, and RNA-sequencing were assessed in eight T1D adolescents and 16 healthy controls at six different timepoints.
Cell Signal
January 2025
Department of Endocrinology, The Third Xiangya Hospital, Central South University, 410007 Changsha, Hunan, China. Electronic address:
Type 1 diabetes (T1D) is an autoimmune disease characterized by hyperglycemia caused by the destruction of insulin-producing β cells. Viral infection is an important environmental factor which is associated with the islet autoimmunity in genetically susceptible individuals. Loss of β-cells and triggering of insulitis following viral infection could result from several non-exclusive mechanisms.
View Article and Find Full Text PDFContemp Clin Trials
January 2025
Kaiser Permanente Washington Health Research Institute, 1730 Minor Ave, Seattle, WA 98101, USA.
Ecotoxicol Environ Saf
January 2025
Department of Occupational and Environmental Health, School of Public Health, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, China; Global Health Research Center, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, China. Electronic address:
Sodium arsenite (NaAsO), the most common form of inorganic arsenic prevalent in the environment, has been closely linked to islet β-cell dysfunction, a critical pathological hallmark of type 2 diabetes (T2D). Even though apoptosis plays a pivotal role in arsenic-induced islet β-cell dysfunction, the explicit underlying mechanisms remain elusive. Here, we have identified that the SET-Rac1 signaling pathway is instrumental in the apoptosis and dysfunction of islet β-cells induced by NaAsO.
View Article and Find Full Text PDFColloids Surf B Biointerfaces
December 2024
Department of Plastic and Cosmetic Surgery, The Second Affiliated Hospital of Army Medical University, Chongqing 400038, China. Electronic address:
The chronic diabetic wounds represented by diabetes foot ulcers (DFUs) are a worldwide challenge. Excessive production of reactive oxygen species (ROS) and persistent inflammation caused by the impaired phenotype switch of macrophages from M1 to M2 during wound healing are the main culprits of non-healing diabetic wounds. Therefore, an injectable DMM/GelMA hydrogel as a promising wound dressing was designed to regulate the mitochondrial metabolism of macrophages via inhibiting succinate dehydrogenase (SDH) activity and to promote macrophage repolarization towards M2 type.
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