Szakirodalom

Levothyroxine (L-T4) monotherapy is the standard of care for the treatment of hypothyroidism. A minority of L-T4-treated patients remain symptomatic and report better outcomes with combination therapy that contains liothyronine (L-T3) or with desiccated thyroid extract (DTE).

The disturbances in thyroid hormones lead to altered brain metabolism, function, and cognition. Neuroimaging studies have shown structural and functional changes in hypothyroidism. Present study investigates the neuro-metabolite changes in dorsolateral prefrontal cortex (DLPFC) and posterior parietal cortex (PPC) and associated decline cognitive function in hypothyroid patients before and after thyroxine treatment. We performed neuropsychological test and H MRS in hypothyroid patients (n = 25) and controls (n = 30). In addition, follow-up data was also collected from 19 patients treated with levo-thyroxine for 32 weeks. The concentration of the neurometabolites were calculated using LCModel. MRS data were analyzed using analysis of covariance (ANCOVA), with age and gender as covariates. A paired t-test was conducted to compare the baseline hypothyroid with the follow-up. Partial correlations were utilised to assess possible associations between neuropsychological scores and neurometabolites with age and gender as covariates. Spearman correlation was performed between thyroid hormone levels and neurometabolites. Hypothyroid patients showed an impairment in delayed recall, immediate recall of semantic, visual retention, recognition of objects memory, attention, and motor function at baseline, which improved significantly after thyroxine therapy. At baseline, patients with hypothyroidism exhibited significantly higher levels of choline compounds (GPC + PCh) [Cho]. No significant normalization of Cho levels was observed, despite achieving euthyroidism with thyroxine treatment. Cho levels showed a positive correlation with TSH in PPC and a negative correlation with T4 in DLPFC and PCC. Cho levels also showed negative correlations with delayed recall, immediate recall of semantic, visual retention memory and MMSE scores. The MRS findings show increased levels of Cho in hypothyroid patients compared to healthy controls. These Cho levels are not reversible within 32 weeks of treatment, suggesting that a longer follow-up may be needed to see if levels can be normalized.

Depression and anxiety are the main disorders in patients suffering from hypothyroidism. These disorders can lead to increased patient suffering. Since hypothyroidism is one of the most prevalent endocrine diseases, controlling the metabolic variables that increase the severity of anxiety and depression is important. This study aimed to assess the prevalence of anxiety and depression and to identify their associated factors, including metabolic variables, among people with hypothyroidism.

This study aimed to evaluate the impact of combined levothyroxine (LT4) and triiodothyronine (LT3) therapy on quality of life in patients with primary hypothyroidism.

Between 10% and 15% of people with hypothyroidism experience persistent symptoms, despite achieving biochemical euthyroidism. The underlying causes are unclear. Type D personality (a vulnerability factor for general psychological distress) is associated with poor health status and symptom burden but has not been studied in people with hypothyroidism.

Perinatal depression has been suggested to adversely impact child neurodevelopment. However, the complexity of the early childhood environment challenges conclusive findings.

We sought to explore the risk factors for anxiety and depression in patients with coronary heart disease and subclinical hypothyroidism through logistic regression analysis. A retrospective analysis was conducted on 168 patients with coronary heart disease and subclinical hypothyroidism admitted to the Department of Cardiology of our hospital from February 2020 to November 2022. Patients were categorized into the control group, anxiety group, and depression group based on the Hamilton Anxiety Scale (HAMA) and Hamilton Depression Rating Scale (HAMD) scores. All participants were informed about the protocol and provided signed informed consent upon inclusion. The study examined influencing factors for anxiety and depression in patients with coronary heart disease and subclinical hypothyroidism. Collect patients’ gender, age, presence or absence of chronic diseases (including Diabetes, hypertension and hyperthyroidism), sleep quality, dietary habits, psychosocial stress, living environment, social support, education level, and blood TSH levels. The linear relationship between anxiety, depression, and each influencing factor was quantified using the Pearson correlation coefficient. Blood level of TSH and free T4 were detected by chemiluminescence immunoassay. Multiple logistic regression was applied to analyze the factors influencing anxiety and depression in these patients. Various factors were identified as significant influencers of anxiety and depression in patients with coronary heart disease and subclinical hypothyroidism. For anxiety, presence or absence of chronic diseases, sleep quality, dietary habits, psychosocial pressure, living environment, and blood TSH levels were found to be influential (P < 0.05). Similarly, for depression, presence or absence of chronic diseases, sleep quality, social support, quality of life, social support, education level, and blood TSH levels were identified as significant factors (P < 0.05). The study revealed positive correlations between presence or absence of chronic diseases, psychosocial stress, and TSH levels with anxiety symptoms in patients with coronary heart disease and subclinical hypothyroidism (P < 0.05). Conversely, sleep quality, dietary patterns, and living environment showed negative correlations with anxiety symptoms (P < 0.05).Gender and age had no correlation with anxiety levels (P > 0.05). Presence or absence of chronic diseases and TSH levels were positively correlated with depressive symptoms in patients with coronary heart diseaseand subclinical hypothyroidism (P < 0.05). On the other hand, sleep quality, social support, quality of life, and educational level were negatively correlated with anxiety symptoms (P < 0.05). Gender and age had no correlation with depression (P > 0.05). Notably, TSH levels in both the anxiety and depression groups were higher than those in the control group (P < 0.05), with no significant difference in free T4 levels among the groups (P > 0.05). The combination of chronic illness types, living habits (sleep quality, dietary habits), psychosocial pressure, living environment, and TSH levels emerged as risk factors for anxiety in patients with coronary heart disease and subclinical hypothyroidism (P < 0.05). Similarly, the combination of chronic illness types, sleep quality, social support, quality of life, education level, and TSH levels were identified as risk factors for depression in these patients (P < 0.05). This logistic regression analysis underscores the significant impact of factors such as types of chronic illness, sleep quality, social support, living environment, education level, and TSH levels on anxiety and depression symptoms in patients with coronary heart disease and subclinical hypothyroidism. These findings highlight the importance of considering these multiple risk factors collectively when devising treatment and management strategies to reduce the risk of mental health issues in this patient population.

Patients treated for hypothyroidism with levothyroxine (LT4) monotherapy may present with persistent hypothyroidism symptoms, including cognitive symptoms, despite having a normal thyroid stimulating hormone (TSH) level. It remains unclear whether LT4 monotherapy is sufficient to normalize cognitive function outcomes over time. This is a multisite longitudinal study of a diverse group of women during midlife representing 5 ethnic/racial groups from 7 enrollment sites across the United States in the Study of Women’s Health Across the Nation. Women were screened for a history of thyroid disease and the use of LT4. The study consisted of two primary groups: women with LT4-treated hypothyroidism and control women without thyroid disease. Each participant completed up to 9 cognitive assessments over the study period testing processing speed, working memory, and episodic memory (immediate and delayed recall). Multivariable generalized linear mixed models of scores for each cognitive assessment were developed to determine the association between LT4-treated hypothyroidism and cognitive function trajectories. Covariates included sociodemographic, clinical characteristics, and menopausal status (pre/early peri, late peri, and surgical/post). Sensitivity analyses were conducted to assess the impact of abnormal TSH levels and practice effects (i.e., improvements in scoring after repeated testing). Of the 2033 women who were included in the study, 227 (11.2%) met criteria for LT4-treated hypothyroidism. At baseline, both processing speed and working memory scores were higher in LT4-treated women (mean processing speed scores: 56.5 vs 54.4; value = 0.006; mean working memory scores: 6.8 vs 6.4; value = 0.018). However, when considering the effect of LT4-treated hypothyroidism over time, there were no significant differences in the rate of cognitive decline (in any measure) between the hypothyroidism and control groups with or without covariate adjustment. The results were similar when considering LT4-treated women with abnormal TSH levels or after minimizing practice effects. We observed no difference in cognitive decline between women with LT4-treated hypothyroidism and women without thyroid disease. For similar aged patients with cognitive complaints, if thyroid function testing is normal, clinicians should consider causes other than inadequate thyroid hormone treatment to explain these symptoms.

Maternal depression and anxiety during pregnancy are significant public health concerns commonly reported worldwide among pregnant women. This study aimed to investigate the impact of anxiety and depression on thyroid function, pregnancy outcomes, and sleep quality among pregnant women with hypothyroidism in the later stages of pregnancy.

Recently, research into the link between thyroid dysfunction and Alzheimer’s disease (AD) remains a current topic of interest. Previous research has primarily concentrated on examining the impact of thyroid dysfunction on the risk of developing AD, or solely explored the mechanisms of interaction between hypothyroidism and AD, a comprehensive analysis of the mechanisms linking thyroid dysfunction, including hyperthyroidism and hypothyroidism, to Alzheimer’s disease (AD) still require further elucidation. Therefore, the aim of this review is to offer a thorough and comprehensive explanation of the potential mechanisms underlying the causal relationship between thyroid dysfunction and AD, highlighting the existence of a vicious circle. The effect of thyroid dysfunction on AD includes neuron death, impaired synaptic plasticity and memory, misfolded protein deposition, oxidative stress, and diffuse and global neurochemical disturbances. Conversely, AD can also contribute to thyroid dysfunction by affecting the stress repair response and disrupting pathways involved in thyroid hormone (TH) production, transport, and activation. Furthermore, this review briefly discusses the role and significance of utilizing the thyroid as a therapeutic target for cognitive recovery in AD. By exploring potential mechanisms and therapeutic avenues, this research contributes to our understanding and management of this devastating neurodegenerative disease.