Condition: Diabetes Mellitus, Type 1 · Sponsor: Pirogov Russian National Research Medical University
Type 1 diabetes (T1D) is caused by destruction of pancreatic islet beta-cells that produce insulin - the hormone required for glucose uptake by body tissues and organs. Since loss of beta-cells leads to insulin deficiency, blood glucose increases and the symptoms of T1D (thirst, hunger, excessive urination) appear. Inability of patient's tissues and organs to utilize glucose results in rapid weight loss and life-threatening acute T1D complications - ketosis and coma. To ensure glucose consumption by tissues and organs and to prevent acute complications, all patients with T1D need lifelong therapy with insulin. Insulin therapy is also necessary to prevent long-term T1D complications (eye, renal, nerve, and heart problems). By the time T1D is diagnosed, 80-90% of beta-cells have already been destroyed. However, 10-20% viable insulin-producing beta-cells remain in the pancreas over several months and even years after T1D diagnosis. The higher the percentage of the remaining beta-cells, the smaller the risk of long-term complications. Destruction of beta-cells in T1D has an autoimmune origin. It means that the patient's immune system, which is normally targeted at microbes, viruses, and other non-self substances, mistakenly destroys the beta-cells. The key role in this autoimmune reaction is played by specific cells of the immune system: T- and B-lymphocytes. T-lymphocytes directly damage the beta-cells, while B-lymphocytes support T-lymphocytes activity via antigen presentation…
This description comes directly from the study's public registry record.
Elena E Petryaykina, M.D. · +79039756179 · director@rdkb.ru
Alexei V Timofeev, Ph.D. · +79161608994 · alvaltim@gmail.com
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| I.M. Sechenov First Moscow State Medical University (Sechenov University) | Moscow, Russia | Recruiting |
| Russian Children's Clinical Hospital, Pirogov Russian National Research Medical University | Moscow, Russia | Recruiting |
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Source record: clinicaltrials.gov/study/NCT07041268