NEUROENDOCRINE RESPONSES OF THE THYROID AND PARATHYROID GLANDS DURING ACUTE CEREBRAL ISCHEMIA
Keywords:
acute ischemic stroke, thyroid hormones, non-thyroidal illness syndrome (NTIS), parathyroid hormone (PTH), neuroendocrine, prognosisAbstract
Acute cerebral ischemia (ischemic stroke) triggers systemic neuroendocrine
responses that commonly alter thyroid and parathyroid physiology. The most
consistent thyroid pattern is the “non-thyroidal illness syndrome” (NTIS, or low-T3
syndrome) characterized by reduced peripheral T3, variable T4, raised reverse T3
(rT3), and typically normal or low-normal TSH. These changes correlate with stroke
severity and worse outcomes in many studies. Changes in parathyroid function and
mineral metabolism—principally altered parathyroid hormone (PTH), vitamin D
status, and calcium—have also been reported; elevated PTH and low 25-OH vitamin
D associate with increased stroke risk and with particular stroke subtypes in some
cohorts. This article reviews the physiology, proposed mechanisms, human and
animal evidence, clinical significance, and potential implications for management
and research.
References
1.
Wajner SM, et al. New insights toward the acute non-thyroidal illness
syndrome. (Review). — discusses NTIS mechanisms and peripheral deiodinase
changes.
2.
Jiang X, et al. Prognostic value of thyroid hormones in acute ischemic stroke.
Sci Rep. 2017 — meta-analysis showing associations between low T3 and poorer
stroke outcomes.
3.
Huang S, et al. Research progress on the role of hormones in ischemic stroke.
(Review) 2022 — overview linking multiple endocrine axes (including PTH/vitamin
D) to stroke.
4.
Çelik G, et al. Parathyroid Hormone Levels in the Prediction of Ischemic
Stroke. 2017 — study examining PTH and 25(OH)D as predictors.
