Neuroprotective actions of thyroid hormones and low-T3 syndrome as a biomarker in acute cerebrovascular disorders

Abstract

Acute cerebrovascular disorders are common causes of death and disability worldwide. Prognostication of stroke victims rests mainly on admission clinical and radiological indexes of disease severity. Preclinical studies strongly suggest that thyroid hormones have a capacity to exert neuroprotective actions in the central nervous system under ischemic conditions via genomic and nongenomic actions. Low triiodothyronine (T3) syndrome affects 32–62% of patients following acute cerebrovascular events. Lower serum T3 concentrations are associated with greater stroke severity, more complicated clinical course, greater mortality rates and elevated risk for poor functional outcomes at discharge and long term. Further studies should address whether T3 can improve clinical stroke prognostication models. Studies investigating the neuroprotective role of thyroid hormone administration in acute cerebrovascular disease victims are encouraged.

Keywords:

• biomarker
• hemorrhagic stroke
• ischemic stroke
• low T3 syndrome
• outcome
• subarachnoid hemorrhage
• triiodothyronine

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Acute cerebrovascular disorders, including ischemic stroke, hemorrhagic stroke and aneurysmal subarachnoid hemorrhage, remain the common causes of mortality and handicap worldwide.

• A substantial amount of research efforts are devoted toward improving risk stratification and prognostication of stroke victims to improve patient prognosis.

• Studies in animal stroke models strongly suggest that thyroid gland hormones, including triiodothyronine (T3) and thyroxin, exert numerous genomic and nongenomic neuroprotective actions under ischemic conditions and have a capacity to ameliorate neurological damage and reduce brain infarct volume.

• Low T3 syndrome is a common complication affecting 32 to 62% of patients with acute cerebrovascular disorders.

• A steadily growing literature strongly suggests that lower serum concentrations of T3 are associated with elevated mortality risk, worse functional outcome and greater cognitive impairment of acute cerebrovascular disease victims.

• Further studies should investigate whether evaluation of serum T3 concentrations in acute stroke victims can improve the prognostic value of currently used stroke prognostic models that encompass clinical impairment and radiological indexes of disease severity.

• Studies suggest that T3 administration is associated with improved outcomes of cardiovascular patients; however, the safety and efficacy of treatment of low T3 syndrome remains to be investigated in acute stroke patients.

• The association of T3 levels with more subtle patient-oriented outcomes, such as psychological distress and health-related quality of life, remains to be evaluated.