scholarly journals Neuroprotection of reduced thyroid hormone with increased estrogen and progestogen in postpartum depression

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Dan Li ◽  
Yangyao Li ◽  
Yun Chen ◽  
Haiyan Li ◽  
Yuqi She ◽  
...  

Abstract Background: Postpartum depression (PPD) is a common serious mental health problem. Recent studies have demonstrated that hormone therapy serves as a promising therapeutic approach in managing PPD. The present study aims at exploring the role of thyroid hormone (TH), estrogen and progestogen in patients with PPD. Methods: Initially, PPD patients were enrolled and a PPD mouse model was established. The serum levels of estradiol (E2), progesterone (P), triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH) were subsequently measured. Next, in order to identify the effects of TH, estrogen and progestogen on PPD progression, mice were administrated with E2, P, contraceptives (CA), Euthyrox and methimazole (MMI). Besides, the body weight, activities, basolateral amygdala (BLA) neuron cell structure and the related gene expression of mice were analyzed. Results: The PPD patients and the mice showed elevated serum levels of T3, T4, FT3 and FT4 along with diminished E2, P and TSH levels. In the mice administered with a combination of E2, P, and MMI, decreased TH and increased estrogen and progestogen were detected, which resulted in increased body weight, normal activities, and BLA neuron cell structure. Moreover, brain-derived neurotrophic factor (BDNF) and cAMP-responsive element-binding protein (CREB) were both up-regulated in PPD mice administrated with a combination of E2, P, and MMI, which was accompanied by decreased TH and elevated estrogen and progestogen. Conclusion: Taken together, reduced TH combined with enhanced estrogen and progestogen confers neuroprotection in PPD, highlighting a potential target in prevention and treatment of PPD.

2021 ◽  
pp. 75-77
Author(s):  
Meiyappan Kavitha ◽  
Mallaiyan Manonmani

Objectives: Nephrotic syndrome is a common renal disorder seen in children, with proteinuria as the hallmark. Growth retardation is a known feature of nephrotic syndrome, either due to the disease or treatment with steroids. Thyroid hormone strongly inuences growth of the body. So, the present study was undertaken with the objective to assess the thyroid prole in children with nephrotic syndrome Methods: The study involved 41 cases of nephrotic syndrome and 41 age and sex matched controls. Serum total triiodothyronine (T3), total thyroxine (T4), free triiodothyronine (T3), free thyroxine (T4) and thyroid stimulating hormone (TSH) were assessed in these subjects. The thyroid hormones were correlated with urinary protein creatinine ratio. The cases were followed up after one month and the levels of thyroid hormones were reassessed. Results: Total T3, total T4, free T3 and free T4 are signicantly decreased and TSH signicantly increased among cases when compared to controls. TSH is positively correlating with urinary protein creatinine ratio in cases. After one month of treatment, total T3 and total T4 are signicantly increased in cases. Conclusions: The thyroid hormone levels are altered in children with nephrotic syndrome during the episode. A state of subclinical hypothyroidism exists during the nephrotic stage. The alteration is normalized with remission and does not require treatment.


2014 ◽  
Vol 171 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Mikkel G Mieritz ◽  
Kaspar Sorensen ◽  
Lise Aksglaede ◽  
Annette Mouritsen ◽  
Casper P Hagen ◽  
...  

ObjectivePubertal gynaecomastia is a frequent phenomenon occurring in 20–40% of otherwise healthy adolescent boys. Little is known about the aetiology of pubertal gynaecomastia. Markedly elevated thyroid hormone levels in adults with hyperthyroidism are associated with gynaecomastia.DesignA cross-sectional examination of 444 healthy boys with and without pubertal gynaecomastia.MethodsWe evaluated TSH, triiodothyronine (T3), thyroxine (T4), free T4 and free T3 in a cohort of healthy boys with and without pubertal gynaecomastia.ResultsBoys with gynaecomastia had significantly higher serum free T3, even after correction for age, BMI and pubertal stage. After inclusion of IGF1 in the model the differences disappeared. TSH, T4, free T4 and T3 did not differ between the groups.ConclusionsWe speculate that the GH/IGF1 axis and thyroid hormones interact and influence the development of pubertal gynaecomastia.


2021 ◽  
Vol 22 (12) ◽  
pp. 6611
Author(s):  
Kenji Ohba

Inappropriate secretion of thyroid-stimulating hormone (IST), also known as central hyperthyroidism, is a clinical condition characterized by elevated free thyroxine and triiodothyronine concentrations concurrent with detectable thyroid-stimulating hormone (TSH) concentrations. Similarly, the term syndrome of IST (SITSH) is widely used in Japan to refer to a closely related condition; however, unlike that for IST, an elevated serum free triiodothyronine concentration is not a requisite criterion for SITSH diagnosis. IST or SITSH is an important indicator of resistance to thyroid hormone β (RTHβ) caused by germline mutations in genes encoding thyroid hormone receptor β (TRβ) and TSH-secreting pituitary adenoma. Recent evidence has accumulated for several conditions associated with IST, including RTH without mutations in the TRβ gene (non-TR-RTH), the phenomenon of hysteresis involving the hypothalamus-pituitary-thyroid axis (HPT-axis), methodological interference, and Cushing’s syndrome after surgical resection. However, little information is available on the systematic pathophysiological aspects of IST in previous review articles. This report presents an overview of the recent advances in our understanding of the etiological aspects of IST that are relevant for diagnosis and treatment. Moreover, the report focuses on the potential mechanism of IST caused by hysteresis in the HPT-axis (lagging TSH recovery) in terms of epigenetic regulation.


Author(s):  
Ichiro Kobayashi ◽  
Masaki Shimomura ◽  
Masahiro Ueki ◽  
Shunichiro Takezaki ◽  
Yuka Okura ◽  
...  

ABSTRACT We report a Japanese boy with Graves’ disease (GD) which developed during drug-free remission of juvenile dermatomyositis (JDM). He had been diagnosed with JDM at the age of 6 years by typical skin rashes, muscle weakness, elevated serum transaminase levels, and typical findings of both magnetic resonance imaging and muscle biopsy. Although anti-melanoma differentiation antigen 5 autoantibody was positive, there was no complication of interstitial lung disease. He showed good response to methylprednisolone pulse therapy followed by oral prednisolone in combination with weekly methotrexate (MTX) and achieved drug-free remission after 3.5 years of treatment. Nevertheless, serum levels of soluble interleukin-2 receptor (sIL-2R) gradually elevated to 3185 U/ml despite no signs of relapse or malignancy. Hyperactivity and attention deficit was also noted. One year and 3 months after the cessation of MTX, he presented with abdominal pain, tachycardia, and apparent goitre. Laboratory tests showed elevated free triiodothyronine, undetectable thyroid stimulating hormone (TSH), and positive anti-TSH receptor antibodies. 99mTc scintigraphy showed high levels of thyroid uptake. He was diagnosed with GD and treated with 15 mg/day of thiamazole. Although transient drug eruption was observed, his thyroid functions are currently well-controlled on 5 mg/day of thiamazole. In conclusion, to our knowledge, this is the first report in English literature describing complication of GD with JDM. Unexpected elevation of sIL-2R could be a clue to the diagnosis of GD during the follow-up of JDM.


2020 ◽  
Vol 46 (1) ◽  
Author(s):  
Hongping Sun ◽  
Lin Cao ◽  
Rendong Zheng ◽  
Shaofeng Xie ◽  
Chao Liu

Abstract Resistance to thyroid hormone syndrome (RTH) is an autosomal dominant or recessive genetic disease caused by mutation of either the thyroid hormone receptorβ (THR-β) gene or the thyroid hormone receptorα (THR-α) gene. RTH due to mutations of the THR-β gene (hereafter, RTH-β) is characterized by a decreased response of the target tissue to thyroid hormone, increased serum levels of free triiodothyronine (FT3) and/or free thyroxine (FT4), and inappropriate secretion of thyroid-stimulating hormone (TSH, normal or elevated). Clinical manifestations of RTH-β vary from hyperthyroidism to hypothyroidism or simple goiter, and RTH-β is often misdiagnosed clinically. The present review was prepared for the purpose of expanding knowledge of RTH-β in order to reduce the rate of misdiagnosis.


2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Tai-Yuan Chuang ◽  
Chia-Ying Lien ◽  
Chih-Hsiang Hsu ◽  
Chen-Wen Lu ◽  
Chung-Hsin Wu

Hypothyroidism frequently causes cardiopulmonary dysfunction, such as heart failure and respiratory and metabolic deficiencies. This study investigated the effects of Chinese herbal formula B307 on thyroidectomy-induced cardiopulmonary exercise dysfunction in rats. Twenty male rats were equally divided into four groups: negative control with sham treatment, positive control with oral B307 treatment only, thyroidectomy treatment only, and thyroidectomy with B307 posttreatment groups. The feeding dose of B307 was 50 mg/kg per day for 14 days. We examined and then compared the thyroid-stimulating hormone (TSH), free triiodothyronine (T3), free thyroxine (T4), and reactive oxygen species (ROS) from the blood of these four groups. Also, we compared the body weight, neck subcutaneous blood flow, cardiac ejection function, cardiopulmonary exercise function of oxygen consumption (VO2), carbon dioxide production (VCO2), and respiratory quotient (RQ = VCO2/VO2) among the four groups. Our results indicated that thyroidectomized rats had significantly decreased body weight, neck subcutaneous blood flow, cardiac ejection function, serum T3 and T4, and VO2 and VCO2, but had significantly increased ROS and TSH levels and RQ values compared with sham rats (P<0.01–0.05). In addition, thyroidectomized rats receiving oral B307 treatment had significantly increased body weight, neck subcutaneous blood flow, cardiac ejection function, and VO2, but significantly decreased ROS and TSH levels and VCO2 and RQ values compared with thyroidectomized rats (P<0.01–0.05). We suggest that the B307 could be a protective and beneficial alternative treatment for thyroidectomy-induced cardiopulmonary exercise dysfunction.


2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Maurizio Nordio ◽  
Sabrina Basciani

Clinical evidences have highlighted the efficacy of myo-inositol and selenium in the treatment of autoimmune thyroiditis. Aim of this study was to further analyze the role of myo-inositol plus selenium (Myo-Ins-Se) in restoring a normal thyroid function of Hashimoto’s patients with subclinical hypothyroidism. Eighty-six patients with Hashimoto’s thyroiditis having thyroid-stimulating hormone (TSH) levels between 3 and 6 mIU/L, elevated serum antithyroid peroxidase (TPOAb) and/or antithyroglobulin (TgAb), and normal free thyroxine (fT4) and free triiodothyronine (fT3) levels were enrolled in the study: one hyperthyroid subject with TSH about 0.14 μU/ml was included in this trial as a single case. Patients were assigned to receive Myo-Ins-Se. TSH, TPOAb, and TgAb levels were significantly decreased in patients treated with combined Myo-Ins-Se after 6 months of treatment. In addition, a significant fT3and fT4increase, along with an amelioration of their quality of life, was observed. Remarkably, TSH values of the hyperthyroid patient increased from 0.14 μU/ml up to 1.02 μU/ml, showing a complete restoration of TSH values at a normal range. In conclusion, the administration of Myo-Ins-Se is significantly effective in decreasing TSH, TPOAb, and TgAb levels, as well as enhancing thyroid hormones and personal wellbeing, therefore restoring euthyroidism in patients diagnosed with autoimmune thyroiditis.


Author(s):  
Jayne A. Franklyn

Subclinical hypothyroidism is defined biochemically as the association of a raised serum thyroid-stimulating hormone (TSH) concentration with normal circulating concentrations of free thyroxine (T4) and free triiodothyronine (T3). The term subclinical hypothyroidism implies that patients should be asymptomatic, although symptoms are difficult to assess, especially in patients in whom thyroid function tests have been checked because of nonspecific complaints such as tiredness. An expert panel has recently classified individuals with subclinical hypothyroidism into two groups (1): (1) those with mildly elevated serum TSH (typically TSH in the range 4.5–10.0 mU/l) and (2) those with more marked TSH elevation (serum TSH >10.0 mU/l).


1997 ◽  
Vol 43 (6) ◽  
pp. 957-962 ◽  
Author(s):  
Anthony G W Norden ◽  
Rodwin A Jackson ◽  
Lorraine E Norden ◽  
A Jane Griffin ◽  
Margaret A Barnes ◽  
...  

Abstract A novel interference with measurements of serum free thyroxine (FT4) caused by rheumatoid factor (RhF) is described. We found misleading, sometimes gross, increases of FT4 results in 5 clinically euthyroid elderly female patients with high RhF concentrations. All 5 patients had high FT4 on Abbott AxSYM® or IMx® analyzers. “NETRIA” immunoassays gave misleading results in 4 of the 5 patients; Amerlex-MAB® in 2 of 4 patients; AutoDELFIA®in 2 of the 5; and Corning ACS-180® and Bayer Diagnostics Immuno 1® in 1 of the 5. BM-ES700® system results for FT4 in these women remained within the reference range. Results for serum T4, thyroid-stimulating hormone, free triiodothyronine, thyroid-hormone-binding globulin, and FT4 measured by equilibrium dialysis were normal in all 5 patients. Drugs, albumin-binding variants, and anti-thyroid-hormone antibodies were excluded as interferences. Addition to normal serum of the RhF isolated from each of the 5 patients increased the apparent FT4 (Abbott AxSYM). Screening of 83 unselected patients demonstrated a highly significant positive correlation between FT4 (Abbott AxSYM) and RhF concentrations. Discrepant, apparently increased FT4 with a normal result for thyroid-stimulating hormone should lead to measurement of the patient’s RhF concentration.


2002 ◽  
Vol 47 (8) ◽  
pp. 742-749 ◽  
Author(s):  
Trino Baptista ◽  
Serge Beaulieu

Objective: To critically review published literature on the causal association between leptin, cytokines, and excessive body weight gain (BWG) induced by antipsychotic drugs (APs). Methods: We completed a Medline search using the words leptin, cytokines, antipsychotic drugs, neuroleptics, psychotropic drugs, weight gain, and obesity. We also included our empirical research on this topic in the discussion. We examined the relation between leptin, cytokines (mainly tumour necrosis factor alpha [TNF-α] and its soluble receptors), and AP-induced BWG, using the biological sciences' current theories of causality. Results: In the general field of weight regulation, there is scarce experimental evidence that leptin or TNF-α by themselves can induce obesity. Serum levels of leptin and TNF-α rather increase simultaneously as BWG occurs. This has also been reported during AP-induced BWG, with the equivocal exception of a study with clozapine. Some researchers have suggested that the absence of the expected correlation between leptin and body mass index (BMI) or serum insulin levels, and the lack of sex-related differences in leptin levels in AP-treated patients, may point to a causal relation. This contention requires more experimental support. In addition, future clinical studies must carefully control for sex and BMI. Conclusions: No conclusive evidence has been provided that leptin or TNF-α may induce obesity either in drug-free subjects or in AP-treated patients. In most cases, the elevated serum levels of these hormones appear to be a consequence rather than a cause of obesity. That does not mean that such an elevation is innocuous, since it may impair blood pressure and also carbohydrate and lipid metabolism regulation. Hence, all efforts should be made to prevent or attenuate BWG during treatment with APs.


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