甲状腺機能亢進症が造血器系に及ぼす影響

Patients with hyperthyroidism frequently present with hematological abnormalities; however, the underlying mechanisms remain incompletely understood. This study enrolled 166 treatment-naïve hyperthyroidism patients and 56 age- and sex-matched healthy controls, comparing their complete blood count parameters. Additionally, a murine model of hyperthyroidism was established, and flow cytometry was employed to assess the quantity, proportion, cell cycle status, and apoptosis of hematopoietic stem/progenitor cells (HSPCs) in the bone marrow. Clinical data analysis revealed that, compared to the healthy control group, hyperthyroidism patients exhibited significant reductions in peripheral white blood cell counts-particularly neutrophils, eosinophils, and basophils-as well as in red blood cell parameters, including hemoglobin (HGB), hematocrit (HCT), mean corpuscular volume (MCV), mean corpuscular hemoglobin (HCH), and mean corpuscular hemoglobin concentration (MCHC). These alterations were more pronounced in female patients. Animal experiments confirmed that hyperthyroid mice also developed leukopenia and neutropenia. Further investigation demonstrated a decreased number of HSPCs in the bone marrow of hyperthyroid mice. The primary cause was identified as cell cycle arrest rather than increased apoptosis. This study reveals that elevated thyroid hormone levels may lead to alterations in peripheral blood cell counts by inducing cell cycle arrest in bone marrow HSPCs, thereby impairing their proliferation and differentiation capabilities. These findings provide a novel cellular perspective for understanding the mechanisms underlying hematological abnormalities in hyperthyroidism and offer a theoretical foundation for potential clinical intervention strategies.