1.1) ABSTRACT:
There is a great outcome on lipids and other cardiovascular risk factors as a result of thyroid disorders. Patients with overt hypothyroidism are most commonly benefited with substitution therapy to improve their lipid profile. Nevertheless, it is still matter of debate if subclinical hypothyroidism should be used for treatment or not. Contrarily, hyperthyroidism can be related with the acquirement of unexplained enhancement of lipid profile or hypocholesterolemia. Generally, thyroid dysfunction should be taken into consideration at the result of evaluation and treatment of dyslipidemia patients.
1.2) MECHANISMS:
In thyroid hormone, the first step is cholesterol biosynthesis, which produces 3- hydroxy-3-methylglutaryl-coenzyme-A reductase. Furthermore, triiodothyronine (T3) regulates LDL receptors by managing low-density lipoprotein receptor gene activation. Triiodothyronine (T3) gene mediation activation is finalized by direct binding of triiodothyronine (T3) to particular thyroid hormone receptive elements (TREs). Triiodothyronine (T3) regulates sterol regulatory binding element protien-2 (SREBP-), in response it regulates LDL receptor’s gene expression. Triiodothyronine (T3) is likewise related in guarding low-density lipoprotein from oxidation.
Due to activity surge in cholesterol ester transfer protein, thyroid hormones can impact high-density lipoprotein (HDL) metabolism. Thus, by interchanging cholesterol esters from high-density lipoprotein to Triglycerides and very-low-density lipoproteins to opposite direction opposite. In combination, thyroid hormones stimulate lipoprotein lipase (LPL), which breaks down the triglyceride (TG) rich lipoprotein and provides to the conversion of intermediate-density lipoproteins (IDL) to low-density lipoprotien (LDL) and in exchange low-density lipoprotein (LDL) to small-density low-density lipoprotien (sdLDL). One ore effect of Triiodothyroninensit (T3) is regulation of apolipoprotein AV (ApoAV), which plays significant part in triglyceride (TG) regulation. As expected increased levels of apolipoprotein (ApoAV) have been related with decrease in levels of triglycerides (TGs). Suggested mechanism for this effect include decrease of plasma lipoprotein lipase levels and its activity, consequently increasing of lipoprotein generation because of improved LPL-mediated lipolysis of very low-density lipoprotein -TG. Additionally, considerable clearance of lipoprotein central leftover fragments, effected by increase in hepatic uptake because of enhanced empathy for LDL receptors, has additionally been associated with apolipoprotein(ApoAV).
Other than the effect on lipid profile thyroid hormones can similarly affect many other metabolic parameters associated to cardiovascular disease (CVD) risk. In reality, the thyroid role can impact the production of adipokines and adipocyte metabolism. Hyperthyroidism has been related with increased amounts of adiponectin, in conjunction with hypothyroidism is not related with noticeable modification in adiponectin. Insulin resistance is additionally consistent with thyroid function thyroid stimulating hormone (TSH) is similarly related by postprandial insulin concentration and by fasting and negatively due to insulin responsiveness. Besides, low the normal levels of free thyroxine (FT4) levels are remarkably as related with soaring insulin resistance. Research indicate disputed results over oxidative stress caused by thyroid function. Moreover, endothelial and cardiac function and atherosclerosis have been unquestionably associated with thyroid hormone levels. A positive association with waist circumference or by body mass index and thyroid stimulating hormone (TSH) has been reported. (Bjoro T., 1999)
The effect of substitution therapy, risk factors of cardiovascular disease (CVD) and thyroid dysfunction on lipid have been illustrated in diagrammatic form as given below.
Figure 1.1
Thyroid hormones effects on lipid metabolism.
Source: Open Cardiovasc Med J, 2011
Chapter 2
2.1) HYPOTHYROIDISM
Hypothyroidism (underactive thyroid) is a typical metabolic disorder in the general public in which the thyroid gland is not able to produce enough desirable important hormones. Initially it can be because of initial form of thyroid gland disease or otherwise a secondary hypothalamic pituitary disease. Clinical findings have proven that women, particularly older than 60 years old are most venerable to have hypothyroidism (Shin DJ, 2003). Hypothyroidism disrupts normal balance of chemical reactions taking place in the body. During early stages of hypothyroidism symptoms are rarely detected. Depending upon severity for hypothyroidism signs and symptoms will differ from patient to patient. Symptoms get worst gradually if not noticed. Incase if hypothyroidism is untreated then it can lead to lots of health problems for example cardiac disease, infertility, obesity and joint pains. Severe form of Hypothyroidism is called Myxedema, although it is very rare disease, it can be deadly if it occurs to a patient. There can be a number of reasons patient to suffer from hypothyroidism, one of them being an autoimmune disease. Hyperthyroidism can be treated by radiation therapy, thyroid surgery and by certain prescribed medications.
Typical symptoms of hypothyroidism are as follows;
• Weak muscle
• Bradycardia
• Depression
• weight gain
• Constipation
• Raised blood cholesterol
• Puffy face
• Hoarseness
• Sensitivity to cold
• Fatigue
• Stiff muscles, aches and tenderness
• Stiff or swelled joints
• Weak vision
• Memory loss
• Hair loss
Figure 2.1
Thyroid gland location
Source: Mayo Foundation for medical education & research, 2012
2.1.1) OVERT HYPOTHRYDOISM
2.1.2) LIPID PROFILE
Regardless of diminished function of thyroid is afterwards decreased by activity of HMG-CoA lyase is a ketogenic enzyme reductase, is low density lipoprotein cholesterol and triglyceride levels are elevated in patients possessing overt hypothyroidism. Reason being decreased in low density lipoprotein-receptor activity, causing in decrease of catabolism of low density cholesterol. Furthermore, decrease in lipoprotein functional level is detected in overt hypothyroidism, decreasing the clearance of triglyceride rich lipoproteins (Canaris GJ., 2009). This is why, overt hypothyroid patients might also present increased triglyceride levels along with elevated levels of very-low-density lipoprotein (VLDL) and sometimes avoiding chylomicronemia. Very low-density lipoprotein and intermediate-density lipoprotein (IDL) particles in hypothyroidism are abundant with apolipoprotein E and cholesterol.
Decreased thyroid function is followed decreased functional capability of HMG-CoA reductase, patients with over hypothyroidism have higher levels of Total Cholesterol and Low-density lipoprotein cholesterol. This is because, LDL receptors activity is decreased, due to decreased breakdown of LDL and IDL. Moreover, in overt hypothyroidism there LPL activity is found to be decreased, lowering the clearance of triglyceride rich lipoproteins. Therefore, overt hypothyroid patients might represent elevated levels of TG related to high levels VLDL and occasionally fasting chylomicronemia (Friis T, 1977). Particles of VLDL and IDL in hypothyroidism have abundant with cholesterol and apolipoprotein E, therefore, resembling like VLDL particles of type 3 hyperlipoproteinemia. Patients of homozygous having homozygous apolipoprotein E2 could develop type 3 hyperlipoproteinemia (full-blown syndrome) if they ever become hypothyroid patients.
Hypothyroid patients could also show increased levels of high density lipoprotein cholesterol, mainly because of elevated HDL2 particles concentration. Definitely, because of reduction of HDL activity, a reduction in HDL2 catabolism has been detected. Furthermore, decreased activity of the CETP consequences in decreased relocation of cholesteryl esters from high-density lipoprotein to very low-density lipoprotein, and elevating HDL-C levels. Hypothyroid patients represent high levels of lipoprotein (a), which are related with surge of getting CVD risk.
Elevated sdLDL concentration elevated chances of getting CVD. Trials determining effects of overt hypothyroidism on LDL sub fractions have represented contradictory results. A new research has showed patients with newly diagnosed hypothyroid patients has shown hypothyroidism was shown higher prevalence of sdLDL. Contritely, studies have also represented with no suggestive differences between overt hypothyroid and healthy controls patients concerning sdLDL levels.
Another study calculated short term effects of overt hypothyroidism LDL sub fraction. Thyroidectomized patients were taken off from substitution therapy for about 3 weeks to make them ready for radioactive iodine ablation. These patients showed increased levels of LDL-C which was found primarily because of surge in large particles of LDL, at the same time there was not significant change in sdLDL.
The above mentioned abnormalities of lipid metabolism in relation to overt hypothyroidism influence the risk of developing atherosclerotic coronary artery disease. Also, hypothyroidism can badly affect other risk factors of CVD, further elevating increased risks for CAD. Besides the fact that LDL particles are increased when thyroid function is lowered but also it also encourages LDL voidability. Furthermore, hypothyroidism raises levels of plasma homocysteine, which could be attributed to the hypothyroidism induced decrease in kidney function along with reduced methylenetetrahydrofolate reductase activity. Thyroid failure is highly related to arterial hypertension (particularly diastolic) by adrenal activation and sympathetic and increased vascular stiffness. Overt hypothyroidism patients also represent reduced endothelial function, increased uric acid and phosphate levels, all of which are linked to increased CVD risk.
In addition, it has been also observed that there is an increase of carotid intima media thickness (CIMT) with hypothyroid patients. Hypothyroidism is also increases the prevalence of metabolic syndrome and as well as waist-to-hip ratio. Thyroid failure also increases Insulin resistance, when there is a decline in GLUT-4 glucose transporters (causing decrease d uptake of glucose and elevating insulin resistance is observed). Even though no studies have confirmed that in hypothyroidism there is surge in levels high-sensitivity C-reactive protein.
2.2) SUBSTITUTION THERAPY
Management of L-thyroxine with substitution therapy dramatically enhances abnormalities of lipid metabolism. To fix dyslipidemia in overt hypothyroidism, thyroxin replacement therapy is required for 4 to 6 weeks to correct dyslipidemia. Generally, people suffering from hypothyroidism, serum lipoproteins of these patients are associated with alternation in free T4. In a study showed after thyroxine therapy on newly diagnosed patients hypothyroid showed a decrease in low density of lipoprotein cholesterol and serum triglyceride (TC) levels. Upon examining the effects of substitution therapy on lipid profile, no change in particle size was determined for low density lipoprotein (LDL). Significant reduction of serum levels of triglyceride (TC) has been noticed in hypothyroid patients having elevated baseline levels of thyroid stimulating hormone (TSH).
With thyroid replacement, high density lipoprotein serum levels tend to shrink. Also, lipoprotein(a) serum levels also tend to diminish with euthyroidism restoration. Patients after getting thyroxine treatment, Carotid Intima-Media Thickness (CIMT) reduction has been observed.
It is not rare to see that patients suffering from dyslipidemia have overt hypothyroidism. After levothyroxine therapy rehabilitation of euthyroidism, noticeable decrease of serum levels of low-density lipoprotein cholesterol (LDL-C), Apolipoprotein B (ApoB), Triglyceride and Lipoprotein(a) was noticed, whereas levels of high density lipoprotein cholesterol, apolipoprotein A1 and triglycerides (TGs) were not noticeably changed.
Amongst the most common factors of secondary dyslipidemia is due to hypothyroidism. Therefore, elevation of thyroid function is required before giving hypolipidemic therapy. Failure of thyroid is related to elevated levels of creatinine kinase. Creatine Kinase levels might considerably elevated levels by Statin therapy. Study examined effects on patients with undiagnosed hypothyroidism being accidentally given statin therapy. Comparing untreated patients with hypothyroidism, these patients had dramatically high levels of Creatine Kinase levels, coordinate for free T4 levels.
2.3) SUBCLINICAL HYPOTHYROIDISM
Subclinical hypothyroidism has increased serum levels of TSH with normal levels of Free T3 and Free T4, is significantly more recurring disorder than overt hypothyroidism. Mostly subclinical hypothyroidism in the general population is estimated at 4.3% – 9%. Older people and women in particular have higher rate acquiring subclinical hypothyroidism. Subclinical hypothyroidism might also progress into overt hypothyroidism. Due to thyroid stimulating hormone (TSH) or thyroperoxidase antibodies (TPO-Ab), rate of development is higher with associated with the presence of higher levels of thyroperoxidase antibodies or greater levels of thyroid stimulating hormone TSH.
2.3.1) LIPID PROFILE
Statin therapy is related with increased levels of low density lipoprotein cholesterol and triglycerides. Some studies have indicated that increased levels of triglycerides and decreased high density lipoprotein cholesterol, may also be accompanied by subclinical hypothyroidism dyslipidemia. Also, patients with high normal thyroid stimulating levels, yet with positive antithyroid antibodies also indicated elevated levels of cholesterol. Patients who underwent statin therapy had noticeably elevated levels of low-density lipoprotein cholesterol, triglyceride and thyroperoxidase antibodies (TPO-Ab) did not change noticeably important as compared to euthyroid controls. (Asvold BO, 2007)
Lots of studies has indicated elevation of lipoprotein (a) levels associated to statin therapy (SH). A study examined serum of lipoprotein(a) levels equating with glycoprotein apolipoprotein(a) phenotypes, which are known to influence Lipoprotein(a) levels, in patients of statin therapy (SH). Patients gone through statin therapy (SH) had elevated levels of Lipoprotein (a). There, was no noticeable difference in frequencies of Apo(a) phenotypes between patients with statin therapy (SH) and controls.
Thyroid autoimmunity plays critical role in elevation of lipoprotein(a) levels. It has been recorded that postmenopausal females and euthyroid males with proof of thyroid autoimmunity has elevated levels of lipoprotein(a). Contrarily, study comparing levels of Lipoprotein(a) of euthyroid subjects (in postmenopausal female and with thyroid autoimmunity, with age of 64 years and matched gender controls without thyroid autoimmunity. There were no noticeable changes in lipid values.
Thyroid Dysfunction and Lipid Profile:
Considering relationship between two even groups parameters, lipoprotein(a) and phenotypes. No noticeable difference in lipoprotein (a) levels was discovered in euthyroid patients suffering with chronic renal failure regardless of thyroid autoimmunity, of thyroperoxidase (a) phenotype, renal failure stage and dialysis technique in last stage patients. Additionally, patients undergone through statin therapy, presence of thyroid autoimmunity has not shown to effect serum lipid parameters.
There is a dispute in relating with the presence or the severity of statin therapy (SH) induced dyslipidemia. Certainly, studies have shown no important difference in lipid profile between statin therapy (SH) patients and controls patients. But, no difference was noticed between when for race, gender and age was noticed when lipid-lowering drugs were used between statin therapy (SH) patients and individuals who used as controls relating to lipid profile. Some studies have challenged the effects of thyroid hormones upon lipoprotein-a levels. In comparison to levels of lipoprotein (a), most studies have not shown any difference between control subjects and stain therapy (SH). Comparison of patients representing the whole range of thyroid function; determined no discrepancies in Lipoprotein (a) between groups. Moreover, there is no relation between levels of thyroid stimulating hormone (STH), lipoprotein (a), thyroid stimulating hormone or free thyroxine FT4. On the other hand, statin therapy of patients has noticeable negative effect was recorded between Lipoprotein (a) and triiodothyronine (FT3) levels. (Duntas LH., 2003)
In relation amongst thyroid function, insulin resistance and lipids has been discovered. Analysis conducted by Fremantle Diabetes Study (FDS) for a subgroup indicated the relationship between lipid profile and of thyroid stimulating (TSH) level is important commonly in the availability of insulin resistance. Comparable results were revealed in study of euthyroid subjects.
Most fascinating part of statin therapy is qualitative outcomes of thyroid hormones upon lipids facilitation is dyslipidemia. A study of comparing women on statin therapy (SH) and placebo. Between the two groups, no difference was found discovered on lipid profile. But decreased ratio of triglycerides/cholesterol in Low density lipoprotein in stain therapy (SH) subjects comparing controls showed presence of higher plasma triglyceride (TG) enhanced low density lipoprotein (LDL) particles in those patients. Contrary, a study comparing statin therapy (SH) of patients did not indicate any significant particle size
2.4 ) CARDIOVASCULAR DISEASE RISKS
A part to lipids, Subclinical hypothyroidism can have many harmful cardiovascular disease (CVD) risk factors. Subclinical hypothyroidism has been related to hypercoagulable state. Also, Subclinical hypothyroidism threatens cardiovascular, ventricular function and also respiratory adaptation to contribute and decreases heart rate variation. Subclinical hypothyroidism reduces accessibility of nitric oxide and reduces flow of mediated vasodilation availability, who are markers for endothelial function. Surge in Carotid intima-media stiffness has been represented in Subclinical hypothyroidism patients compared with control patients. Nevertheless, research done on patients suffering from Subclinical hypothyroidism did not validate such a surge in Carotid intima-media thickness as analyzed with euthyroid subjects. Even though, patients suffering from Subclinical hypothyroidism along with Thyroid Autoantibodies (TPO-Ab) had elevated Carotid intima media thickness values as compared to patients without Subclinical hypothyroidism and Thyroid Autoantibodies (TPO-Ab), this difference was not noteworthy.
Study indicated a higher rate of multivessel disease with patients of angina with high vales of Thyroid Stimulating Hormone (TSH) went through Thyroid Stimulating Hormone (TSH) was not acknowledged as forecaster for coronary artery stenosis. Contrarily, study in hypothyroid patients, 90% of who were victim of Subclinical hypothyroidism did not prevail any change in relation to carotid atherosclerosis (severity, carotid plaques prevalence, and carotid intima-media thickness CIMT) in comparison with euthyroid subjects after aligning various cardiovascular (CVD) risk factors. Subclinical hypothyroidism has also been linked with other cardiovascular (CVD) risk factors, for example increase in insulin resistance.
Subclinical hypothyroidism patients are represented by having high levels of plasma lipoprotein related to phospholipase A2 (Lp-PLA2) (known marker for cardiovascular disease) and low-high density lipoprotein Lp-PLA2 related to antiatherogenic effects of high density lipoprotein (HDL) activity. Also, negative relation between hsCRP and free thyroxine levels have been represented. Also surge in hsCRP levels have been traced in Subclinical hypothyroidism patients. A study showed linear relation between Thyroid Stimulating Hormone (TSH) and blood pressure even in normal reference ranges. Nonetheless, study in Subclinical hypothyroidism patients did not encounter any relation between increased blood pressure and Subclinical hypothyroidism. Also, smoking may decay lipid profile in women having Subclinical hypothyroidism and worsen intensity of thyroid failure, therefore adding development of atherosclerosis.
As explained, Subclinical hypothyroidism is correlated related with elevation of few cardiovascular disease (CVD) risk factors. It is important to find out data available on the incidence of cardiovascular disease (CVD) and subclinical hypothyroidism patients. Analysis of 12 trials found elevated risk factors for cardiovascular disease with patients who suffered from Subclinical hypothyroidism. Fascinating study measured the association of Subclinical hypothyroidism with the congestive heart failure (CHF), stroke, Coronary artery disease (CAD), peripheral artery disease and cardiovascular disease (CVD) or worst case complete death. This was a longitudinal cohort study analysis of aged adults raging from 70 to 79 years from the Health, Body, and Aging Composition (HEALTH RELIANCE) study. Subclinical hypothyroidism subjects were further divided in groups according to levels of Thyroid Stimulating (TSH) hormones. Patients with Thyroid Stimulating (TSH) levels 8 mIU/L had a larger risk for congestive heart failure (CHF) (p=0.007). Subclinical hypothyroidism was not related with surge in stroke frequency, cardiovascular disease (CVD) and peripheral artery disease mortality. Subclinical hypothyroidism patients having Thyroid Stimulating (TSH) 9 mIU/L had a higher chance getting myocardial infarction (MI) and total mortality. Alike, latest meta-analysis found a 40% surge in all mortality cases in Subclinical hypothyroidism patients compared with euthyroid patients. Other study for Subclinical hypothyroidism patients found a positive relation between coronary artery disease and Subclinical hypothyroidism, and overall mortality which was subsequently only limited only to men.
The results from studies evaluating the effects of Subclinical hypothyroidism in elderly populations are important. The study in Holland has found a connection amongst myocardial infarction and subclinical hypothyroidism and aortic atherosclerosis in older population. Subclinical hypothyroidism women. Also, presence of thyroperoxide antibodies Ab (TPO- Ab) surged threat for together aortic atherosclerosis and myocardial infarction. Presence of thyroid autoantibodies Ab in total study of the people was not associated with a history of myocardial infarction. Oppositely, Cardiovascular Health Study did not discover relationship between cardiovascular disease (CVD) and Subclinical hypothyroidism (SH) mortality in an elderly population, but elevated atrial fibrillation incidents were recorded. Study measured relationship of thyrotropin.
2.5 ) TREATMENT
There can be a number of reasons patient to suffer from hypothyroidism, one of them being an autoimmune disease. Hyperthyroidism can be treated by substitution therapy, radiation therapy, thyroid surgery and by certain prescribed medications.
Thyroid is a small gland, butterfly-shaped and it is situated at the base of the neck, right below Adam's apple. Thyroxine and Triiodothyronine, are the two kinds of hormones made by thyroid gland which crucial role on the health by maintain all aspects of metabolism. Body temperature regulation of proteins, usage of fats and carbohydrates in the body, they play key role in protein production regulation and they influence heart rate. Hypothyroidism may be due to a number of factors, including:
2.5.1) SUBSTITUTION THERAPY
Valuable effects were observed in some patients with subclinical hypothyroidism who underwent through substitution therapy upon lipid parameters and especially on low-density lipoprotein cholesterol and total cholesterol. According to meta-analysis, there was a mean decrease of low-density lipoprotein cholesterol total serum cholesterol levels after thyroxine substitution was -8.0 mg/dL and -9.0 mg/dL, correspondingly. Deterioration was larger in people with bigger pre-treatment cholesterol levels and individuals with hypothyroid overseeing suboptimal T4 medications. Report estimated the outcomes of thyroxine compared with placebo in patients suffering from subclinical hypothyroidism. Thyroxine was given with a goal of Thyroid stimulating levels of 0.4-1.4 mIU/L. Outcome of thyroxine therapy upon lipid profile was a significant drop of only Apolipoprotein B (ApoB) levels (p<0.01). Yet, upon studying subgroup of patients after getting TSH treatement, the levels 0.2-2 mIU/L was substantial drop in Total cholesterol (p<0.04) and Low-density lipoprotein cholesterol (p<0.01) was additionally perceived. Certainly, a drop in carotid intima-media thickness and enhancement of endothelial task has been labelled in Subclinical hypothyroidism patients after thyroxine replacement. Furthermore, thyroxine therapy improved HDL-associated, Lipoprotein-Associated, and Phospholipase A2Lp-PLA2 activity in Subclinical hypothyroidism subjects. (Bindels AJ., 1998)
These results, are not systematically proven by other researches. Some studies indicated no remarkable influence of thyroxine therapy on patients with lipid profile and subclinical hypothyroidism patients. Fascinatingly results of study measuring effects of thyroxine in subclinical hypothyroidism (SH) patients. Lipid profile was not importantly changed with the exclusion of reduction in levels of high density lipoprotein cholesterol. Nevertheless, in subgroup it was noticed that patients with triglyceride 238 mg/dL a decreased amount of triglyceride and low-density lipoprotein cholesterol were noticed. Recent analysis confirmed no importance in cardiovascular disease (CVD) or death after substitution therapy in subclinical hypothyroidism patients. Furthermore, quality of life was not improved by thyroxine replacement, beneficial outcome was observed on some lipid parameters and on left ventricular function.
The beneficial outcome of thyroxine substitution therapy on Lipoprotein(a) levels in Subclinical hypothyroidism patients are also questionable. Many studies have revealed that thyroxine therapy is ineffective on levels of Lipoprotein-a in Subclinical hypothyroidism patients. Nevertheless, other studies have indicated by administering thyroxine treatment, remarkable decrease of Lipoprotein (a) levels. Research with Subclinical hypothyroidism women shown a decrease of Lipoprotein (a) by 23% (p=0.0004) in comparison to baseline afterwards substitution therapy. It has been exhibited that thyroxine treatment was useful in reducing Lipoprotein (a) levels in Subclinical hypothyroidism patients (p=0.007). Importantly was that the decrease of Lipoprotein (a) levels attained importance only in low molecular weight phenotypes of Apolipoprotein(a) isoforms group of patients.
2.5.2) Should we treat Subclinical Hypothroidism Patients?
Even though it a fact that thyroid replacement therapy has excellent outcomes on serum lipid profile, overt hypothyroid and Cardiovascular Disease (CVD) patients. No impact has been adapted in regards to the treatment of Subclinical hypothyroidism patients. One of the reason being, that there are is no data available from large trials on what level does Subclinical hypothyroidism affects lipid profile. Also, overall effect of substitution therapy data is also missing for substitution therapy effect on mortality and success in Subclinical hypothyroidism patients. Moreover, there is not enough proof relating to long-term effects of thyroid replacement in Subclinical hypothyroidism patients and this is why no recommendations can be made. (Ayala C., 2001)
It looks like that if thyroid substitution of thyroid is used, it will be most successful to patients with noticeable thyroid dysfunction (TSH) (levels greater than 10 mIU/L), smokers, patients with positive thyroperoxidase antibodies (TPO-Ab), elevated initial cholesterol levels. Furthermore, treatment could play a crucial role in other phase of cardiovascular disease CVD risk surpassing lipids. Consequencelly, the possible unlikely effects of levothyroxine therapy should also be taken into consideration. Replacing thyroid could lower high-density lipoprotein (HDL) concertation, hurting the beneficial effect of triglyceride (TC) and low-density lipoprotein cholesterol (LDL-C) reduction in the patients. Moreover, while treating people with heart disease or angina pectoris, caution should be executed due to thyroxin therapy might aggravate angina or lead cardiac arrhythmia.
Finally, calculation of serum thyroid stimulating (TSH) levels should incorporate for patients suffering through dyslipidemia. Thyroxin substitution therapy could be used for hypercholesterolemic patients with Subclinical hypothyroidism for treatment, because lipid levels can successfully improve and restore by euthyroidism, may also fight back progression to overt hypothyroidism and relieve certain symptoms.
2.5.3) Autoimmune disease:
People who develop a particular inflammatory disorder known as Hashimoto's thyroiditis have the most usual reason of hypothyroidism. Autoimmune sicknesses appears when immune system manufactures antibodies which attacks its own tissues. Occasionally this development comprises the thyroid gland. Researchers are not certain for the reason body manufactures antibodies versus itself. It is a weak opinion that a virus or bacteria may cause the response, while others believe a genetic flaw may be involved. Almost certainly, autoimmune disorders result due to several factors. But what occurs, is that these antibodies disturb thyroid’s capability to manufacture hormones.
2.5.4) Treatment for hyperthyroidism:
Generally, patients suffering hyperthyroidism are often treated with radioactive iodine or anti-thyroid medications to normalize their thyroid function. Sadly, there are reports of permanent hypothyroidism due to treatment of hyperthyroidism.
2.5.5) Thyroid surgery:
By surgically removing all or large part of the thyroid gland, the thyroid function can fade or stop completely. Patient will be put on thyroid hormone for the rest of life time.
2.5.6) Radiation therapy:
Hypothyroidism sometimes is lead due dysfunctional thyroid gland by undergoing radiation therapy to fight cancer of head and neck.
2.5.7) Medications:
A number of medications can contribute to hypothyroidism. Lithium being prime example, it can treat certain psychiatric disorders. Doctor should be consulted in case medication is taken to eliminated side-effects to the thyroid gland.
2.5.8) Congenital disease:
Some infants are born with a malfunctioning in thyroid gland or with no thyroid gland. A lot of times, lack of thyroid gland develops due to unknown reasons, or by inherited reasons. Generally, infants born with congenital hypothyroidism appear to be normal at the time of birth. This being reason, most countries have implemented mandatory thyroid screening for newborns.
2.5.9) Pituitary gland disorder:
Thyroid-stimulating hormones (TSH) are not manufactured sufficiently by pituitary gland. Most cases the reason for this complication is tumour in pituitary gland. In unhealthiest conditions, pituitary gland fails to manufacture acceptable thyroid-stimulating hormones (TSH) because of tumor in the pituitary gland.
2.6) Pregnancy:
Women occasionally progress hypothyroidism during or post pregnancy, this is recognized as postpartum hypothyroidism. If untouched, hypothyroidism might elevate chances of premature delivery, preeclampsia and miscarriage. In this situation there is significant rise in woman's blood pressure during last tri-semester of her pregnancy. Fetal development can be seriously affect.
2.6.1) Iodine deficiency:
Mainly located in seafood, plants grown up in iodine-rich soil, iodized salt. Iodine is important mineral for the building thyroid hormones. Extreme Iodine consumption should be observed since too much iodine in body can lead to hypothyroidism.