Background: Subclinical hypothyroidism (SCH) is postulated to increase stroke risk via atherogenic changes associated with abnormal thyroid function. However, the direct relationship of SCH with subsequent stroke is poorly studied.
Methods: In this nested case-cohort study, we prospectively evaluated the association between any SCH and severity of SCH in relation to incident ischemic stroke risk among postmenopausal women in the Women's Health Initiative Observational Study. Trained Women's Health Initiative staff, masked to thyroid status, adjudicated stroke cases. We assessed thyroid function using baseline blood specimens. Women with normal free thyroxine levels and thyrotropin (TSH) levels ≥4.69 mU/L were considered to have SCH. Primary analysis included 639 ischemic stroke cases and 2927 randomly selected subcohort members with an average of seven years of follow-up.
Results: The multivariable adjusted hazard ratios (HR) from weighted Cox models were 1.06 (95% confidence interval [CI]: 0.77, 1.46) and 0.99 (95% CI: 0.67, 1.47) for women with any SCH and with mild SCH (TSH 4.69 to 6.99 mU/L), when compared with women with normal thyroid function. The HR for moderate/severe SCH (TSH ≥7.00 mU/L) was modestly elevated (HR: 1.22; 95% CI: 0.73, 2.05).
Conclusions: We found no evidence to suggest an association between SCH and ischemic stroke among healthy postmenopausal women.
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http://dx.doi.org/10.1089/thy.2014.0106 | DOI Listing |
Transl Stroke Res
January 2025
Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
The role of chromatin biology and epigenetics in disease progression is gaining increasing recognition. Genes that escape X chromosome inactivation (XCI) can impact neuroinflammation through epigenetic mechanisms. Our previous study has suggested that the X escapee genes Kdm6a and Kdm5c are involved in microglial activation after stroke in aged mice.
View Article and Find Full Text PDFNeuromolecular Med
January 2025
Department of Rehabilitation Medicine, The Affiliated Jiangning Hospital of Nanjing Medical University, No. 168 Gushan Road, Dongshan Street, Jiangning District, Nanjing, 211199, Jiangsu, China.
Muscle atrophy in pathological or diseased muscles arises from an imbalance between protein synthesis and degradation. Elevated levels of interleukin-6 (IL-6) are a hallmark of ischemic stroke and have been associated with muscle atrophy in certain pathological contexts. However, the mechanisms by which IL-6 induces muscle atrophy in the context of stroke remain unclear.
View Article and Find Full Text PDFNeurol Sci
January 2025
Neuroradiology Unit, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, Via Amendola 2, Reggio Emilia, 42122, Italy.
Introduction: Large artery atherosclerosis is a relevant cause of ischemic stroke. Beyond carotid artery stenosis ≥ 50%, causative in etiological classification of stroke, non-stenosing plaques are an increasingly reported cause of stroke with embolic pattern.
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J Neurol
January 2025
Neurology, Cantonal Hospital of Baden, Baden, Switzerland.
Background: Correct identification of those patients presenting with an acute vestibular syndrome (AVS) or an acute imbalance syndrome (AIS) that have underlying posterior-circulation stroke (PCS) and thus may benefit from revascularization (intravenous thrombolysis (IVT), endovascular therapy (EVT)) is important. Treatment guidelines for AVS/AIS patients are lacking. We reviewed the evidence on acute treatment strategies in AVS/AIS focusing on predictors for IVT/EVT and outcome.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, USA.
Background: Levels of inflammatory components gradually rise in tissues and blood as we age. This "inflammageing" process is often debilitating and even fatal. Cognitive impairment is one example of inflammageing's incapacitating nature.
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