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This is known as secondary or central hypothyroidism because of the negative feedback relationship between serum T 4 and T 3 levels and TSH secretion. As noted earlier and shown in Figure , people with primary hypothyroidism have high serum TSH levels. The concomitant finding of a high serum TSH concentration and a low free T 4 level confirms the diagnosis of primary hypothyroidism. People with a high serum TSH concentration and a normal or low-normal serum free T 4 level have, by definition, subclinical hypothyroidism.

The diagnosis of secondary hypothyroidism is based on the findings of a low serum free T 4 level and a serum TSH level that is normal or low. People with secondary hypothyroidism are unlikely to be detected by a screening program based on measurements of serum TSH, but the condition is much less common than primary hypothyroidism.

Hyperthyroidism is a hypermetabolic state that results from excess production of T 4 and T 3. Its major clinical manifestations are nervousness, anxiety, heart palpitations, rapid pulse, fatigability, tremor, muscle weakness, weight loss with increased appetite, heat intolerance, frequent bowel movements, increased perspiration, and often thyroid gland enlargement goiter. Most individuals with hyperthyroidism are women. Other caused of hyperthyroidism are a multinodular goiter, solitary thyroid adenoma, thyroiditis, iodide- or drug-induced hyperthyroidism, and, very rarely, a TSH secreting pituitary tumor.

The diagnosis of hyperthyroidism is based on the findings of a high serum free T 4 level and a low serum TSH concentration. Occasionally, people with hyperthyroidism have a normal serum free T 4 and high serum free T 3 concentrations. These patients have what is called T 3 -hyperthyroidism. An increase in serum thyroid hormone binding protein will raise the serum total T 4 level but not free T 4 concentrations. In these patients the serum TSH remains normal. Patients with a low serum TSH concentration and normal serum free T 4 and free T 3 levels have, by definition, subclinical hyperthyroidism.

Several medications have in vivo or in vitro effects on thyroid function tests that can create misleading results. Medications, notably estrogens, that raise serum TBG levels result in an increase in serum total T 4, but no change in serum free T 4 levels and no change in serum TSH concentrations. High doses of glucocorticoids adrenal hormones can lower the serum T 3 concentration by inhibiting the peripheral conversion of T 4 to T 3 and lower serum T 4 and T 3 by inhibiting TSH secretion. Iodide, contained in solutions used to sterilize the skin and in radiopaque contrast media used in coronary angiography and many other radiological.

The iodide-containing drug amiodarone, given to patients with cardiac arrhythmias, can also cause either hypothyroidism or hyperthyroidism in appropriately susceptible individuals. Other drugs have effects that alter thyroid function test results directly. For example, the anticoagulant heparin can raise serum free T 4 concentrations by stimulating release of free fatty acids from triglycerides in serum. Thyroid test methods that use fluorescence detection may be sensitive to the presence of fluorophore-containing drugs or diagnostics agents used in radiology.

Many people who are seriously ill have abnormal thyroid test results but no other evidence of thyroid dysfunction. These abnormalities occur in people with both acute and chronic illnesses and tend to be greater in those with more serious illnesses. Thus the laboratory diagnosis of thyroid disease can be extremely difficult to make in very sick people, especially those who need to be hospitalized. The effects of illness include decreased peripheral conversion of T 4 to T 3 , decreases in serum concentrations of thyroid hormone binding proteins, and decreases in TSH secretion.

These changes are reversible and do not seem to cause clinical manifestations of thyroid deficiency. Among healthier individuals, a few may have small changes in thyroid test results as a result of unrecognized nonthyroidal illness rather than thyroid dysfunction. In press. Laboratory support for the diagnosis and monitoring of thyroid disease.

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Laboratory Medicine Practice Guidelines. National Academy of Clinical Biochemistry. J Clin Endocrinol Metab 87 2 — Thyroid physiology and diagnostic evaluation of patients with thyroid disorders. Philadelphia: WB Saunders Company. When the Medicare program was established in , it was viewed as a form of financial protection for the elderly against catastrophic medical expenses, primarily those related to hospitalization for unexpected illnesses.

The first expansions to the program increased the eligible population from the retired to the disabled and to persons receiving chronic renal dialysis. It was not until that an expansion of services beyond those required "for the diagnosis or treatment of illness or injury or to improve the functioning of a malformed body member" was included in Medicare. These services, known as preventive services, are intended either to prevent disease by vaccination or to detect disease by diagnostic test before the symptoms of illness appear.

A Committee was formed "to conduct a study on the addition of coverage of routine thyroid screening using a thyroid stimulating hormone test as a preventive benefit provided to Medicare beneficiaries under Title XVIII of the Social Security Act for some or all Medicare beneficiaries. Based on feedback from you, our users, we've made some improvements that make it easier than ever to read thousands of publications on our website. Jump up to the previous page or down to the next one.


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Pathophysiology and Diagnosis of Thyroid Disease. Get This Book. Visit NAP. Looking for other ways to read this? No thanks. Introduction Page 14 Share Cite. Suggested Citation: "2.

Function of the thyroid

Page 15 Share Cite. Page 16 Share Cite. Page 17 Share Cite. Reference Intervals for Thyroid Function Tests. Page 18 Share Cite.

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Thyroid Function Testing in the Elderly. Diagnosis of Hypothyroidism. Page 19 Share Cite. Diagnosis of Hyperthyroidism. Pregnancy is characterised by immunosuppression to protect the foetus. This might trigger a graft-versus-host maternal immune response, leading to autoimmune diseases. Smoking is a well-known risk factor for GD. A meta-analysis showed an odds ratio OR of 3. This effect is more marked in women and appears to be dose dependent.

However, this risk is abolished a few years after smoking cessation, resulting in an insignificant OR of 1. On the other hand, current smoking protects against autoimmune hypothyroidism in a dose-dependent manner. This has been shown in several studies, including a population-based study by Pederson et al, where smoking was negatively associated with the presence of Tg-Abs more than TPO-Abs. Alcohol has been shown to protect against autoimmune hypothyroidism. Stress is known to be a triggering factor in the pathogenesis of GD, however, its effect on HT has been barely researched.

Hypothyroid cases were in fact found to suffer from a less depressed mood than controls at the point of diagnosis, and thus the authors concluded that stress is not implicated in the development of AITD.

Understanding Autoimmune Thyroid Disease

However, in a population-based case-control study, stress and negative life events within the previous 12 months were found to be associated with the onset of GD. Selenoproteins, mainly glutathione peroxidases, iodothyronine deiodinases and thioredoxin reductases are important enzymes involved with thyroid hormone metabolism, regulation of the redox state as well as protection of the thyroid gland from oxidative damage.

However, the results of clinical trials testing the effect of selenium supplementation on TAI are equivocal. Although Vitamin D deficiency is associated with various autoimmune diseases including type 1 diabetes T1D and rheumatoid arthritis, its association with AITD is still uncertain.

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Aetiology of thyroid autoimmunity

Several infections have been implicated in the development of AITD in genetically susceptible individuals including Yersinia enterocolitica , Hepatitis C virus, Coxsackie B virus, retroviruses, Borrelia Burgdorferi and Helicobacter pylori infection , particularly the cytotoxin-associated gene A strain. Hamilton et al investigated the effect of month of birth and seasonality on AITD onset in northern European Caucasian and United Kingdom populations and found no impact of month of birth on GD development.

Conversely, HT female birth rates peaked in winter, while males with HT were mostly born in winter and summer.


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In the general population births peaked in summer for both males and females. Instead of causing de novo TAI,lithium and amiodarone an iodine rich drug appear to be key risk factors for the development of hypothyroidism in patients with pre-existing TAI. It was found to be negatively correlated to TPO-Abs and was associated with a lower risk of subclinical or overt hyperthyroidism but not autoimmune hypothyroidism in a cross-sectional analysis of the Amsterdam AITD cohort. AITD is connected to therapeutic radiation including radioactive iodine, as well as occupational and environmental radiation exposure.

Increased AITD was initially seen in atomic bomb survivors in Japan and following the radioactive fallout in Chernobyl. Polyaromatic hydrocarbons including polychlorinated biphenyls PCB and polyhalogenated biphenyls PBB are organic compounds found in water and air and are made from coal. An increase in antimicrosomal and Tg-Abs together with a higher occurrence of hypothyroidism was noted in workers exposed to PBBs.

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Autoimmune hypothyroidism and thyroid antibodies tend to be more prevalent in iodine replete areas and in individuals with excessive iodine intake or following iodization programmes. The natural history of AITD involves four stages which are delineated in table 2. In a prospective study, progression to overt autoimmune hypothyroidism from euthyroidism took several years unlike the development of overt autoimmune hyperthyroidism which occurred after a few months.