The Effects of Thyroid hormone (7)

Thyroid hormone (triiodothyronine (T3) and thyroxine (T4)), produced by the thyroid gland, plays an important role in regulation of metabolism, including directly boosts energy metabolism and triggers rapid protein synthesis and regulates mitochondrial gene transcription, etc. Iodine is necessary for the production of T₃ and T₄, deficiency of Iodine can lead to enlarge thyroid grand and goitre.
61. Analysis of patients with anaplastic thyroid cancer
In the study to to analyze the clinicopathologic characteristics of patients diagnosed with ATC expected to undergo curative thyroidectomy, with the goal of finding differences between patients surviving ≥6 months and <6 months, found that ATC showed female predominance. Patients initially presented with neck mass, and median age was 55 years. In patients with ATC who are expected to undergo curative thyroidectomy, surgery should actively be considered as primary therapy for patient survival when the size is <5 cm(61).

62. Treatment of patients with anaplastic thyroid cancer
Anaplastic thyroid cancer is known to have a poor prognosis due to its aggressive and rapid metastasis with median survival of less than 6 months. In a retrospectively reviewed medical records of 13 anaplastic thyroid cancer patients who received multidisciplinary treatment between 2006 and 2010, showed thatthe median patient age at diagnosis was 69 years, and six patients had stage IVc diseases. Eight patients received primary surgery followed by radiotherapy or concurrent chemoradiotherapy (CCRT). Five patients received weekly doxorubicin-based definitive CCRT, but only one patient's condition remained stable, while the rest experienced rapid disease progression. The median progression-free survival was 2.8 months (95% CI, 1.2-4.4 months), and the median overall survival was 3.8 months (95% CI, 3.0-4.6 months)(62).

63. Thyroid cancer and I-131 therapy
In the study in overview of the benefits of I-131 therapy for ablation, adjuvant treatment, and treatment of locoregional and/or metastasis of well-differentiated thyroid cancer and considers the risks of complications of I-131 therapy, showed that although there are never-ending controversies regarding I-131 therapy in well-differentiated thyroid cancer, the benefits and risks are becoming better understood. This in turn helps the treating physician and patient in making decisions regarding therapy(63).

64. Thyroid function in the nutritionally obese child and adolescent
In the study to evaluate the prevalence of disturbed thyroid hormone and TSH values in childhood obesity and the underlying pathophysiologic mechanisms linking obesity to thyroid function.l, showed that in the past 18 months, four studies demonstrated moderate elevation of TSH concentrations in 10-23% of obese children, which was associated with normal or slightly elevated thyroxine and triiodothyronine values. Two studies reported ultrasonographic hypoechogenicity of the thyroid in obese children with hyperthyrotropinemia, which was not caused by autoimmune thyroiditis; therefore, the authors hypothesized a link to chronic inflammation in obesity. Weight loss led to a normalization of elevated TSH levels in two studies. The adipokine leptin is the most promising link between obesity and hyperthyrotropinemia since leptin stimulates the hypothalamic-pituitary-thyroid(64).

65. Treating elevated thyroid stimulating hormone levels in obese children and adolescents?
In the differentiation to examine the prevalence of abnormal thyroid function tests among obese children and adolescents, and to study the effect of thyroid hormone supplementation on body weight, linear growth and lipid profiles in these children, showed that hyperthyrotropinemia is relatively common in obese children, but autoimmune thyroid disease accounts for a minority of the cases. TSH levels returned to normal in the majority of patients even without thyroid hormone administration. No beneficial effects on body weight, body mass index, linear growth and body lipids were found in treated subjects, suggesting that thyroid substitution is not necessary in most cases(65).

66. Thyroid disease in patients with vitiligo
In the study to summarize and critically appraise current evidence of the prevalence of thyroid diseases in vitiligo, found that There is an increased prevalence and an increased risk of (autoimmune) thyroid disease in patients with vitiligo compared with nonvitiligo. This risk seems to increase with age(66).

67. Thyroid antibodies and risk of preterm delivery
In a meta-analysis of prospective cohort studies to evaluate the associations between thyroid antibodies and risk of preterm delivery found that eleven prospective cohort studies involving 35 467 participants were included. The combined RR of preterm delivery for pregnant women with thyroid antibodies compared with the reference group was 1.41 (95% CI 1.08-1.84, P=0.011). Subgroup analysis yielded the combined RR of preterm delivery for pregnant women with TPO-Ab compared with the reference group was 1.69 (95% CI 1.19-2.41, P=0.003), whereas pregnant women with positive TG-Ab had no obvious risk of preterm delivery compared with the reference group (RR=0.88, 95% CI 0.60-1.29, P=0.513). Sensitivity analysis restricted to studies excluding women with thyroid dysfunction yielded similar results. Meta-regression analysis suggested that the status of exclusion or inclusion of women with thyroid dysfunction was the major source of heterogeneity in this meta-analysis(67).

68. Thyroid hormones in the skeleton
In the study to evaluate the cellular effects and molecular mechanisms of thyroid hormone action in the skeleton, showed that both thyroid hormone deficiency and excess are associated with an increased risk of fracture. Understanding the cellular and molecular basis of T3 action in skeletal cells will lead to the identification of new targets to regulate bone turnover and mineralization in the prevention and treatment of osteoporosis(68).



69. Skeletal responses to disruption of the hypothalamic-pituitary-thyroid axis
In the study to review the skeletal responses to disruption of the hypothalamic-pituitary-thyroid axis result from altered thyroid hormone (T(3)) action in bone of mice, showed that these mice must display opposing skeletal phenotypes if TSH has a major role in bone, whereas they would be similar if thyroid hormone actions predominate. Pax8(-/-) and hyt/hyt mice both displayed delayed ossification, reduced cortical bone, a trabecular bone remodeling defect, and reduced bone mineralization, thus indicating that the skeletal abnormalities of congenital hypothyroidism are independent of TSH. Treatment of primary osteoblasts and osteoclasts with TSH or a TSHR-stimulating antibody failed to induce a cAMP response. Furthermore, TSH did not affect the differentiation or function of osteoblasts or osteoclasts in vitro(69).

70. Congenital hypothyroidism (CH)
Congenital hypothyroidism (CH) is defined as thyroid hormone deficiency present at birth. According to the study by Department of Pediatrics, Dhahran Health Center, CH is classified into permanent and transient forms, which in turn can be divided into primary, secondary, or peripheral etiologies. Permanent CH refers to a persistent deficiency of thyroid hormone that requires life-long treatment. Transient CH refers to a temporary deficiency of thyroid hormone that is discovered at birth but recovers to normal in the first few months or years of life. Babies with CH who are not identified and treated promptly develop severe mental retardation. Most of the babies with CH do not manifest the typical known signs and symptoms of hypothyroidism, and this is most likely due to transplacental passage of some maternal thyroid hormone in addition to some residual neonatal thyroid function, as might be seen with thyroid hypoplasia, an ectopic gland, or mild dyshormonogenesis(70). 
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Sources
(61) http://www.ncbi.nlm.nih.gov/pubmed/22977757
(62) http://www.ncbi.nlm.nih.gov/pubmed/22318823
(63) http://www.ncbi.nlm.nih.gov/pubmed/20001720
(64) http://www.ncbi.nlm.nih.gov/pubmed/21430532
(65) http://www.ncbi.nlm.nih.gov/pubmed/17907328
(66) http://www.ncbi.nlm.nih.gov/pubmed/22860695
(67) http://www.ncbi.nlm.nih.gov/pubmed/22826476
(68) http://www.ncbi.nlm.nih.gov/pubmed/22634735
(69) http://www.ncbi.nlm.nih.gov/pubmed/17932107
(70) http://www.ncbi.nlm.nih.gov/pubmed/22570946