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.
51. Thyroid hormone and cardiovascular functions
Thyroid hormone is well known for its direct effects in regulating cardiovascular
function and metabolism. In the recent meta-analyses of
population-based studies with long-term follow-up have clarified the
risk of cardiovascular disorders in patients with subclinical thyroid
dysfunction, researchers at the Inwendige Geneeskunde - Endocrinologie
en Metabolisme, showed that treatment of patients with TSH levels
between 0.1-0.4 mU/l or 4-10 mU/l
should depend on other risk factors and patient age, with no treatment
for persons with a TSH level of 4-10 mU/l who are older than 65
years(51).
52. Thyroid dysfunction are not associated with normocholesterolemia or hypercholesterolemia
In the study to assess in a clinically healthy, middle-aged population of employees the prevalence of thyroid function disorders and their relation to demographic variables and cardiovascular risk factors, found that the cardiovascular
risk profile of subjects with mild subclinical hypothyroidism was not
different from subjects with normal TSH levels. The prevalence of
subclinical hypothyroidism was 0.8% in normocholesterolemic (cholesterol
<5.2 mmol/l) and 1.4% in hypercholesterolemic subjects (n.s.). One
woman each with the subclinical form of the disease developed
hypothyroidism or hyperthyroidism after 21 and 11 months of follow-up,
respectively. Subclinical hypothyroidism and subclinical hyperthyroidism
were rarely observed in a target group for coronary heart disease
prevention. Mild subclinical hypothyroidism was not associated with any
adverse cardiovascular
risk profile. These results argue against indiscriminate measurements
of TSH concentrations in clinically healthy subjects either with
normocholesterolemia or hypercholesterolemia(52).
53. Subclinical hypothyroidism treatment?
Subclinical thyroid dysfunction is characterized by normal levels of thyroid hormones
but abnormal values of thyrotropin (TSH) in an asymptomatic individual.
It is a common disorder with a prevalence of
about 7 to 8% in women (most frequently in females over 50 years), and
about 3% in men. In the study of Is there a need for treatment in
subclinical hypo- and hyperthyroidism?, researchers indicated that most
frequently, this disorder is caused by exogenous L-thyroxine
treatment. The endogenous form of subclinical hyperthyroidism mainly
caused by nodular goiter has a prevalence of up to 20% in patients with
large goiters. In patients with subclinical hyperthyroidism, there is an
increased risk for development of atrial fibrillation and for a
decrease in bone mass in postmenopausal women. In the majority of
patients measurable TSH levels can be detected before or after
stimulation with TRH. This formally excludes overt hyperthyroidism in
such patients. Frequently, there is no need for treatment but follow-up
is important. However, in patients with subclinical hyperthyroidism
associated with atrial fibrillation a therapy with antithyroid drugs,
beta-blockers or radioiodine must be considered(53).
54. Thyroid function and postmenopause
The rate of thyroid cancer increases with age. The incidence of thyroid disease in a population of postmenopausal women is as follows: clinical thyroid disease, about 2.4%; subclinical thyroid disease, about 23.2%. Among the group with subclinical thyroid
disease, 73.8% are hypothyroid and 26.2% are hyperthyroid. According to
the Institute for Medical Research and Education (IMRE), Essen, It is
of importance that even mild thyroid
failure can have a number of clinical effects such as depression,
memory loss, cognitive impairment and a variety of neuromuscular
complaints. Myocardial function has been found to be subtly impaired.
There is also an increased cardiovascular
risk, caused by increased serum total cholesterol and low-density
lipoprotein cholesterol as well as reduced levels of high-density
lipoprotein. These adverse effects can be improved or corrected by
L-thyroxine replacement therapy(54).
55. Thyroid hormone levels and vegetative dysfunction and heart connective tissue dysplasia (HCTD)
Heart connective tissue dysplasia (HCTD) are known to be subject to
infectious and inflammatory diseases due to peculiarities of their
immune system. In the study of 181 patients with HCTD depending on thyroid hormone levels and vegetative dysfunction.
indicated that HCTD was shown to be associated with a significant decrease of IgM
levels and increase of circulating immune complexes. The IgG level in
patients with mitral valve prolapse (MVP), anomalous chord localization,
and combination of MPV and tricuspid valve prolapse was significantly
higher than in the absence of HCTD(55).
56. Thyroid physiology and common diseases in pregnancy
Thyroid diseases are common during
pregnancy and an adequate treatment is important to prevent adverse
maternal and fetal outcomes, such as neurodevelopment complications in
the fetus. According to the study by Artemisia Fetal-Maternal Medical
Center, found that large-scale intervention trials are urgently needed
to assess the efficacy of preconception or early pregnancy screening for
thyroid disorders. Accurate interpretation of both antepartum and postpartum levels of thyroid hormones is important in preventing pregnancy-related complication secondary to thyroid dysfunction(56).
57. Subclinical hypothyroidism in pregnancy
In the study to evaluate the intellectual development of children of
mothers who had M-SCH during the pregnancy for these children with 68
children were recruited, after excluding those age < 4 or age >
15, 44, found that IQ level and cognitive performance of children born
to LT4-treated
hypothyroid mothers is similar in those whose mothers have M-SCH during
pregnancy compared with those whose mothers have normal serum TSH
concentrations during pregnancy(57).
58. Thyroid disease in pregnancy and childhood
Thyroid function in pregnancy is
characterised by a T4 surge at 12 weeks declining thereafter. Fetal
brain development depends on T4 transport into the fetus which in turn
depends on sufficient maternal iodine supply. In the study to measure
free T4 using direct equilibrium dialysis, as well as total T4 and TSH
in 287 pregnant women at 27 weeks' gestation, found that Increasing
maternal TSH was related to better performance on tests of
cognition and language at 12 months but not at later ages. At 60 months,
there was inconsistent evidence that higher TSH was related to improved
attention. We found no convincing evidence that maternal TH during the
second half of pregnancy was related to impaired child
neurodevelopment(58).
59. Hereditary medullary thyroid carcinoma (HMTC)
In the study to investigate the role of germline inheritance of
polymorphisms in CYP1A2*F, CYP1A1m1, GSTP1, NAT2 and TP53 genes in
hereditary medullary thyroid
carcinoma (HMTC) patients of 132 patients with HMTC, 88 first-degree
relatives of HMTC patients and 575 control individuals, found that
the inheritance of specific genes determining the individual response to
environmental toxins may contribute to the risk and phenotypic
variability that exists in patients with HMTC(59).
60. Thyroid Nodule Size and Cancer
In the study to evaluate the association of nodule size upon cancer
risk in a retrospective cohort analysis at an academic hospital with
4955 consecutive patients evaluated between 1995 and 2009, found that
Increasing thyroid nodule size impacts cancer risk in a nonlinear fashion. A threshold is detected at 2.0 cm, beyond which cancer risk is unchanged. However, the risk of follicular carcinomas and other rare thyroid malignancies increases as nodules enlarge(60).
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Sources
(51) http://www.ncbi.nlm.nih.gov/pubmed/23218037
(52) http://www.ncbi.nlm.nih.gov/pubmed/10880781
(53) http://www.ncbi.nlm.nih.gov/pubmed/10434773
(54) http://www.ncbi.nlm.nih.gov/pubmed/12724022
(55) http://www.ncbi.nlm.nih.gov/pubmed/23285764
(56) http://www.ncbi.nlm.nih.gov/pubmed/22419883
(57) http://www.ncbi.nlm.nih.gov/pubmed/21943136
(58) http://www.ncbi.nlm.nih.gov/pubmed/22132346
(59) http://www.ncbi.nlm.nih.gov/pubmed/23278115
(60) http://www.ncbi.nlm.nih.gov/pubmed/23275525
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