"But it’s not likely to replace a clinician’s expertise anytime soon, he says. For example, ChatGPT fabricates information sometimes when it can't find the answer." --so do doctors?
HGI reflects the effects of inflammation on HbA1c in a nondiabetic population of U.S. adults and may be a marker of risk associated with inflammation independent of FPG, race, and obesity.
Conditions that affect erythrocyte turnover influence HbA1c concentrations and the International Expert Committee has warned clinicians to be aware of any conditions that could affect the turnover of red blood cells. Although many forms of anemia are associated with lowering of HbA1c, iron deficiency has been shown to shift HbA1c slightly upward. The exact mechanism through which iron deficiency anemia affects HbA1c levels, however still remains unclear. The explanations provided above are merely speculations, warranting further studies to confirm and elucidate the role of these factors. As little work has been done in this field so future and large scale studies are required which may address HbA1c enhancing effect and the mechanism of increased HbA glycation in iron deficiency properly.
Plausible, need to reread.
June 2023
Inflammation can trigger lasting phenotypes in immune and non-immune cells. Whether and how human infections and associated inflammation can form innate immune memory in hematopoietic stem and progenitor cells (HSPC) has remained unclear. We found that circulating HSPC, enriched from peripheral blood, captured the diversity of bone marrow HSPC, enabling investigation of their epigenomic reprogramming following coronavirus disease 2019 (COVID-19). Alterations in innate immune phenotypes and epigenetic programs of HSPC persisted for months to 1 year following severe COVID-19 and were associated with distinct transcription factor (TF) activities, altered regulation of inflammatory programs, and durable increases in myelopoiesis. HSPC epigenomic alterations were conveyed, through differentiation, to progeny innate immune cells. Early activity of IL-6 contributed to these persistent phenotypes in human COVID-19 and a mouse coronavirus infection model. Epigenetic reprogramming of HSPC may underlie altered immune function following infection and be broadly relevant, especially for millions of COVID-19 survivors.