The Association Between FT4/FT3 Ratio and Prognosis in Ischemic Stroke: A Retrospective Cohort Study

 Are you that blitheringly stupid you think 'prognosis' gets survivors recovered? Unless there are EXACT PROTOCOLS delivered after the prognosis, it is TOTALLY FUCKING USELESS! No understanding of that is grounds for firing! I take no prisoners in trying to get stroke solved to 100% recovery

The Association Between FT4/FT3 Ratio and Prognosis in Ischemic Stroke: A Retrospective Cohort Study

Guiling Wan 1, Linhong Mo 1

Affiliations 

• PMID: 41376201
 
• PMCID: PMC12696331
 
• DOI: 10.1002/brb3.71128

Abstract

Background and aim: The FT4/FT3 ratio reflects thyroid hormone metabolism and has emerged as a prognostic marker in cardiovascular diseases. However, its role in ischemic stroke (IS) remains unclear. This study aimed to investigate the association between the FT4/FT3 ratio and 3-month functional outcomes in IS patients.

Methods: We conducted a retrospective cohort study of 199 first-episode IS patients admitted within 14 days of onset between June 2021 and June 2023. Serum thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) were evaluated upon admission. Neurological severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) at admission. Functional outcomes were evaluated using the modified Rankin Scale (mRS) at 3 months post-stroke. Poor outcome was defined as an mRS score of 3-5. Separate analyses were conducted according to FT4/FT3 ratio and outcome.

Results: Patients were stratified by median FT4/FT3 ratio (3.75) into low (≤ 3.75, n = 100) and high (> 3.75, n = 99) ratio groups. The high-ratio group had lower FT3 (4.14 ± 0.52 vs. 4.68 ± 0.52 pg/mL, p < 0.001), higher FT4 (17.83 ± 2.10 vs. 15.36 ± 1.69 pmol/L, p < 0.001), more diabetes (52.5% vs. 34%, p = 0.010), and higher proportion of poor outcomes (46.5% vs. 28%, p = 0.007). Receiver operating characteristic (ROC) analysis revealed that the FT4/FT3 ratio demonstrated the highest predictive ability (area under the curve [AUC] = 0.662) with an optimal cut-off of 3.845. After adjusting for NIHSS scores, age, sex, and vascular risks, the FT4/FT3 ratio remained an independent predictor of poor outcomes (odds ratio [OR] = 2.589, 95% confidence interval [CI]: 1.171 - 5.727, p = 0.019). FT4 was a risk factor (OR = 1.324, 95% CI: 1.045 - 1.678, p = 0.020), while FT3 showed a nonsignificant protective trend (OR = 0.551, 95% CI: 0.218 - 1.390, p = 0.207).

Conclusion: An elevated FT4/FT3 ratio may serve as a novel biomarker for predicting poor outcomes in ischemic stroke(Do we now tell patients they are going to have a poor outcome?), reflecting thyroid hormone metabolic dysfunction that potentially exacerbates inflammation and impairs neuronal repair.

Limitations: This study is limited by its small sample size, single-center design, and absence of serial hormone measurements.

Triiodothyronine modulates neuronal plasticity mechanisms to enhance functional outcome after stroke

 Yes, in mice.

Is  your doctor and stroke hospital going to followup on this with researchers to get this tested in humans? If not, incompetence reigns in your stroke hospital, beginning at the top with the stroke president and board of directors. Have them all fired.

Triiodothyronine modulates neuronal plasticity mechanisms to enhance functional outcome after stroke

• Daniela Talhada,
• Joana Feiteiro,
• Ana Raquel Costa,
• Tiago Talhada,
• Elisa Cairrão,
• Tadeusz Wieloch,
• Elisabet Englund,
• Cecília Reis Santos,
• Isabel Gonçalves &
• Karsten Ruscher 

Acta Neuropathologica Communications volume 7, Article number: 216 (2019) Cite this article

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The development of new therapeutic approaches for stroke patients requires a detailed understanding of the mechanisms that enhance recovery of lost neurological functions. The efficacy to enhance homeostatic mechanisms during the first weeks after stroke will influence functional outcome. Thyroid hormones (TH) are essential regulators of neuronal plasticity, however, their role in recovery related mechanisms of neuronal plasticity after stroke remains unknown. This study addresses important findings of 3,5,3′-triiodo-L-thyronine (T₃) in the regulation of homeostatic mechanisms that adjust excitability – inhibition ratio in the post-ischemic brain. This is valid during the first 2 weeks after experimental stroke induced by photothrombosis (PT) and in cultured neurons subjected to an in vitro model of acute cerebral ischemia. In the human post-stroke brain, we assessed the expression pattern of TH receptors (TR) protein levels, important for mediating T₃ actions.
Our results show that T₃ modulates several plasticity mechanisms that may operate on different temporal and spatial scales as compensatory mechanisms to assure appropriate synaptic neurotransmission. We have shown in vivo that long-term administration of T₃ after PT significantly (1) enhances lost sensorimotor function; (2) increases levels of synaptotagmin 1&2 and levels of the post-synaptic GluR2 subunit in AMPA receptors in the peri-infarct area; (3) increases dendritic spine density in the peri-infarct and contralateral region and (4) decreases tonic GABAergic signaling in the peri-infarct area by a reduced number of parvalbumin⁺ / c-fos⁺ neurons and glutamic acid decarboxylase 65/67 levels. In addition, we have shown that T₃ modulates in vitro neuron membrane properties with the balance of inward glutamate ligand-gated channels currents and decreases synaptotagmin levels in conditions of deprived oxygen and glucose. Interestingly, we found increased levels of TRβ1 in the infarct core of post-mortem human stroke patients, which mediate T₃ actions. Summarizing, our data identify T₃ as a potential key therapeutic agent to enhance recovery of lost neurological functions after ischemic stroke.

Thyroid hormone and the brain: Mechanisms of action in development and role in protection and promotion of recovery after brain injury

Does your doctor have any mechanism of action that will take place to contact researchers for followup studies in humans?  Or is your doctor complete dead wood? 
https://www.ncbi.nlm.nih.gov/pubmed/29378220

Liu YY¹, Brent GA².

Author information

Abstract

Thyroid hormone (TH) is essential for normal brain development and may also promote recovery and neuronal regeneration after brain injury. TH acts predominantly through the nuclear receptors, TH receptor alpha (THRA) and beta (THRB). Additional factors that impact TH action in the brain include metabolism, activation of thyroxine (T4) to triiodothyronine (T3) by the enzyme 5'-deiodinase Type 2 (Dio2), inactivation by the enzyme 5-deiodinase Type 3 (Dio3) to reverse T3 (rT3), which occurs in glial cells, and uptake by the Mct8 transporter in neurons. Traumatic brain injury (TBI) is associated with inflammation, metabolic alterations and neural death. In clinical studies, central hypothyroidism, due to hypothalamic and pituitary dysfunction, has been found in some individuals after brain injury. TH has been shown, in animal models, to be protective for the damage incurred from brain injury and may have a role to limit injury and promote recovery. Although clinical trials have not yet been reported, findings from in vitro and in vivo models inform potential treatment strategies utilizing TH for protection and promotion of recovery after brain injury.

KEYWORDS:

Deiodinase; Neuronal protection; Thyroid hormone; Thyroid hormone receptor; Thyroid hormone transport; Traumatic brain injury

PMID:

29378220

DOI:

10.1016/j.pharmthera.2018.01.007

Free thyroxine and TSH interact with secreted protein acidic and rich in cysteine-like 1 in ischemic stroke

Useless information, what should be done with this knowledge? 
https://www.sciencedirect.com/science/article/pii/S0028384317304760

• Wojciech Ambrosius^{a, ,} ,
• Justyna Rosinska^a,
• Slawomir Michalak^b,
• Maria Lukasik^a,
• Radoslaw Kazmierski^c,
• Wojciech Kozubski^a

 Show more

https://doi.org/10.1016/j.pjnns.2018.01.001

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Abstract

The role of the thyroid gland in ischemic stroke pathology is not well understood. As thyroid hormones modulate the extracellular matrix, we explored the possible link between them and secreted protein acidic and rich in cysteine like 1 (SC1) – one of the extracellular matrix molecules.

In the 81 patients with acute ischemic stroke, serum SC1 levels were much higher compared with 30 control subjects: 4.47 vs 2.43 ng/mL (p < 0.001). Serum levels of free thyroxine (fT4) were higher in stroke subjects compared to those of controls (p = 0.03). In stroke patients, TSH concentration was lower than in the control group (p = 0.03). SC1 levels positively correlated with fT4 levels (p = 0.02) and negatively with TSH (p = 0.03) in stroke patients.

Our results confirmed the association between thyroid hormones and SC1 – extracellular matrix protein.

Keywords

• Thyroxine;
• Thyroid-stimulating hormone;
• Stroke;
• Extracellular matrix

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Corresponding author at: Department of Neurology, Poznan University of Medical Sciences, ul. Przybyszewskiego 49, 60-355 Poznan, Poland.

© 2018 Polish Neurological Society. Published by Elsevier Sp. z o.o. All rights reserved.