In recent years, the outbreak of COVID-19 caused by SARS-CoV-2 has been witnessed globally. However, the impact of SARS-CoV-2 infection on thyroid dysfunction and subclinical thyroid dysfunction remains unclear. Therefore, this meta-analysis aimed to assess the effects of SARS-CoV-2 infection on thyroid dysfunction and its relationship with the severity of COVID-19.

Perinatal hypothyroidism causes long-lasting effects on behavior, including hyperactivity, cognitive delays/deficits, and a reduction in anxiety. Although there is some evidence that hypothyroidism during fetal development in humans has been associated with later autism spectrum disorder diagnosis or autism-like traits, the relationships between early thyroid hormones and social behaviors are largely unknown. Previously, we found that a moderate dose of the hypothyroid-inducing drug methimazole during embryonic and postnatal development dramatically increased juvenile play in male and female rats. The goal of the current study was to determine the extent to which thyroid hormones act in prenatal or postnatal development to organize later social behaviors. Subjects were exposed to methimazole in the drinking water during prenatal (embryonic day 12 to birth), postnatal (birth to postnatal day 23), or pre- and postnatal development; control animals received regular drinking water throughout the experiment. They were tested for play behavior as juveniles (P30-32). We found an interaction between pre- and postnatal methimazole administration such that postnatal hypothyroidism decreased some play behaviors, whereas sustained pre- and postnatal hypothyroidism restored play to control levels. The effects were similar in males and females. To our knowledge, this is the first report of an interaction between pre- and postnatal hypothyroidism on later behavior. The complexity of the timing of these effects may help explain why epidemiological studies have not consistently found a relationship between gestational hypothyroidism and later behavior.

Brown bears hibernate throughout half of the year as a survival strategy to reduce energy consumption during prolonged periods with scarcity of food and water. Thyroid hormones are the major endocrine regulators of basal metabolic rate in humans. Therefore, we aimed to determine regulations in serum thyroid hormone levels in hibernation compared to the active state to investigate if these are involved in the adaptions for hibernation.We used electrochemiluminescence immunoassay to quantify total triiodothyronine (T3) and thyroxine (T4) levels in hibernation and active state in paired serum samples from six subadult Scandinavian brown bears. Additionally, we determined regulations in the liver mRNA levels of three major thyroid hormone-binding proteins; thyroxine-binding globulin (TBG), transthyretin (TTR), and albumin, by analysis of previously published grizzly bear RNA sequencing data.We found that bears were hypothyroid when hibernating with T4 levels reduced to less than 44% (P = 0.008) and T3 levels reduced to less than 36% (P = 0.016) of those measured in the active state. In hibernation, mRNA levels of TBG and albumin increased to 449% (P = 0.031) and 121% (P = 0.031), respectively, of those measured in the active state. TTR mRNA levels did not change.Hibernating bears are hypothyroid and share physiologic features with hypothyroid humans, including decreased basal metabolic rate, bradycardia, hypothermia, and fatigue. We speculate that decreased thyroid hormone signaling is a key mediator of hibernation physiology in bears. Our findings shed light on the translational potential of bear hibernation physiology to humans for whom a similar hypometabolic state could be of interest in specific conditions.

Diagnostic re-evaluation is important for all patients with congenital hypothyroidism (CH) for determining the etiology and identifying transient CH cases. Our study is a first thyroxine therapy withdrawal study conducted in Macedonian CH patients for a diagnostic re-evaluation. We aimed to evaluate the etiology of CH, the prevalence of transient CH and identify predictive factors for distinguishing between permanent (PCH) and transient CH (TCH).

The major cause of primary hypothyroidism is autoimmune mediated with progressive and permanent destruction of the thyroid gland resulting in life-long replacement therapy. Treatable and reversible hypothyroidism is unusual and here forth is such a case due to infection of the thyroid gland with Tropheryma whippleii, Whipple disease.

To examine whether hypothyroidism is an extrahepatic feature of ATPase, aminophospholipid transporter, class I, type 8B, member 1 (ATP8B1) deficiency.

In childhood cancer survivors, the most common late effect is thyroid dysfunction, most notably subclinical hypothyroidism (SCH). Our study evaluated the risk factors for persistent SCH in survivors.

Hypothyroidism (HO) can induce significant metabolic dysfunction and increase cardiovascular disease risk. In the present study, we investigated the relationship between homocysteine (Hcy) and insulin resistance (IR) in patients with HO or subclinical hypothyroidism (SHO).

The modulation of the host's metabolism to protect tissue from damage induces tolerance to infections increasing survival. Here, we examined the role of the thyroid hormones, key metabolic regulators, in the outcome of malaria. Hypothyroidism confers protection to experimental cerebral malaria by a disease tolerance mechanism. Hypothyroid mice display increased survival after infection with Plasmodium berghei ANKA, diminishing intracranial pressure and brain damage, without altering pathogen burden, blood-brain barrier disruption, or immune cell infiltration. This protection is reversed by treatment with a Sirtuin 1 inhibitor, while treatment of euthyroid mice with a Sirtuin 1 activator induces tolerance and reduces intracranial pressure and lethality. This indicates that thyroid hormones and Sirtuin 1 are previously unknown targets for cerebral malaria treatment, a major killer of children in endemic malaria areas.

We describe a patient with type 2 diabetes mellitus and autoimmune hypothyroidism who presented with elevated serum creatinine possibly due to subclinical rhabdomyolysis induced by hypolipidemic drug therapy in the background of diabetic nephropathy. Both hypothyroidism and rhabdomyolysis were asymptomatic in this case as evidenced by lack of classical clinical features of hypothyroidism despite elevated serum TSH and absent pigment cast in renal biopsy. The combination of diabetes mellitus and hypothyroidism is common in the general population and should not be forgotten in patients with diabetes and kidney disease.

To investigate the association between hypothyroidism and glaucomatous disease.

The objective of this study was to evaluate the relationship between subclinical hypothyroidism (SCH) and depression. We also analysed the effect of levothyroxine (L-T4) on depression in SCH patients. We found an insignificant difference for the composite endpoint: standard mean difference (SMD) of 0.23 (95% confidence interval (CI) -0.03, 0.48, P = 0.08, I2 = 73.6%). The odds ratio (OR) for depressive patients was 1.75 (95% CI 0.97, 3.17 P = 0.064, I2 = 64.6%). Furthermore, sub-group analysis according to age found that SCH was related to depression in younger patients (<60 years old), as defined by the diagnosis of depression: OR of 3.8 (95% CI 1.02, 14.18, P = 0.047, I2 = 0.0%) or an increase on the depressive scale: SMD of 0.42 (95% CI 0.03, 0.82, P = 0.036, I2 = 66.6%). Meanwhile, SCH did not associate with depression in older patients (≥60 years old), as defined by the diagnosis of depression: OR of 1.53 (95% CI 0.81, 2.90, P = 0.193, I2 = 71.3%) or an increase on the depressive scale: SMD of 0.03 (95%CI -0.31, 0.37, P = 0.857, I2 = 79.8%). We also found an insignificant difference in the composite endpoint between the L-T4 supplementation group and placebo group in SCH patients. The estimated SMD was 0.26 (95% CI -0.09, 0.62, P = 0.143, I2 = 52.9%). This meta-analysis demonstrates that SCH is not connected to depression. However, sub-group analysis according to age found that SCH is related to depression in younger patients, but not in older patients. Furthermore, we failed to find an effect of L-T4 supplementation treatment for SCH on depression.

Thyroid hormones (THs) are important in the development and maturation of the central nervous system (CNS). The significant actions of THs during CNS development occur at the time when TH levels are lower than those in the mother and the hypothalamic-thyroid (HPT) axis is not fully functional. In the developing rat nervous system, primarily the cerebellum, the first three postnatal weeks represent a period of significant sensitivity to thyroid hormones. This study presents a spontaneous, inherited recessive hypothyroidism in Sprague-Dawley rats with devastating functional consequences to the development of the CNS. The clinical signs develop around 14 day's postnatal (dpn) and are characterized by ataxia, spasticity, weight loss and hypercholesterolemia. The afflicted rats died at 30 days due to severe neurological deficits. The deterioration affects the entire CNS and is characterized by progressive neuronal morphological and biochemical changes, demyelination and astrogliosis. The cerebellum, brain stem, neocortex, hippocampus and adrenal gland medulla appear to be most affected. Thyroid Stimulating Hormone (TSH), T3 and T4 levels were significantly lower in hypothyroid rats than control. Immunohistochemistry and RT-PCR demonstrated a reduction of Thyrotropin Releasing Hormone (TRH) in the hypothalamus of hypothyroid rats. The weight of both thyroid and pituitary glands were significantly less in hypothyroid rats than the corresponding normal littermate controls. Transmission electron microscopy demonstrates consistent postsynaptic dendritic, synaptic and spine alterative changes in the brain of hypothyroid rats. These data suggest that we discovered a tertiary form of inherited hypothyroidism involving the hypothalamus.

We investigated the mutual effects of overt hypothyroidism and prolonged sunlight exposure on free radical accumulation and oxidative skin damage.

Hypothyroidism and subclinical hypothyroidism (SCH) are common metabolic diseases with severe psychological and physiological effects, which may be the risk factors of sexual dysfunction.

Whereas there is increasing evidence that loss of expression and/or function of the thyroid hormone receptors (TRs) could result in a selective advantage for tumor development, the relationship between thyroid hormone levels and human cancer is a controversial issue. It has been reported that hypothyroidism might be a possible risk factor for liver and breast cancer in humans, but a lower incidence of breast carcinoma has been also reported in hypothyroid patients

The liver and thyroid hormones interact at multiple levels to maintain homoeostasis. The liver requires large adequate amounts of thyroid hormones to execute its metabolic functions optimally, and deficiency of thyroid hormones may lead to liver dysfunction. Hypothyroidism has been associated with abnormal lipid metabolism, non-alcoholic fatty liver disease (NAFLD), hypothyroidism-induced myopathy, hypothyroidism-associated gallstones and occasionally, interferon-induced thyroid dysfunction. NAFLD remain an important association with hypothyroidism and further studies are needed that specifically compare the natural course of NAFLD secondary to hypothyroidism and primary NAFLD. Hepatic dysfunction associated with hypothyroidism is usually reverted by normalizing thyroid status. Large scale studies geared towards finding new and effective therapies, especially for NAFLD are needed. The clinician must be aware that there exists overlapping symptomatology between liver dysfunction and severe hypothyroidism which may make delay the diagnosis and treatment of hypothyroidism; this requires a high index of suspicion.

Juvenile hypothyroidism (JH) can have deleterious effects on growth, pubertal development, and scholastic performance of children. In India, there is a paucity of data on acquired hypothyroidism in children, in contrast to congenital hypothyroidism. Our objective was to assess the profile of JH in a referral clinic from eastern India.

The objective of this study was to assess the existing literature to determine if a relationship exists between hypothyroidism and periodontitis.

The cardiovascular effects of mild and overt thyroid disease include a vast array of pathological changes. As well, thyroid replacement therapy has been suggested for preserving cardiac function. However, the influence of thyroid hormones on cardiac remodeling has not been thoroughly investigated at the molecular and cellular levels. The purpose of this paper is to study the effect of hypothyroidism and thyroid replacement therapy on cardiac alterations. Thirty Wistar rats were divided into 2 groups: a control (n = 10) group and a group treated with 6-propyl-2-thiouracil (PTU) (n = 20) to induce hypothyroidism. Ten of the 20 rats in the PTU group were then treated with L-thyroxine to quickly re-establish euthyroidism. The serum levels of inflammatory markers, such as C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL6) and pro-fibrotic transforming growth factor beta 1 (TGF-β1), were significantly increased in hypothyroid rats; elevations in cardiac stress markers, brain natriuretic peptide (BNP) and cardiac troponin T (cTnT) were also noted. The expressions of cardiac remodeling genes were induced in hypothyroid rats in parallel with the development of fibrosis, and a decline in cardiac function with chamber dilation was measured by echocardiography. Rapidly reversing the hypothyroidism and restoring the euthyroid state improved cardiac function with a decrease in the levels of cardiac remodeling markers. However, this change further increased the levels of inflammatory and fibrotic markers in the plasma and heart and led to myocardial cellular infiltration. In conclusion, we showed that hypothyroidism is related to cardiac function decline, fibrosis and inflammation; most importantly, the rapid correction of hypothyroidism led to cardiac injuries. Our results might offer new insights for the management of hypothyroidism-induced heart disease.