Thyroid hormones antibodies

The assessment of patients for thyroid disorders entails a history and physical examination. In many patients with subclinical or mild thyroid disease, there may be an absence of specific signs and symptoms, and the physical examination may be normal. Various diagnostic tests can be used, including serum thyroid hormone(s), TSH, and thyroid antibody levels and imaging techniques to evaluate patients for thyroid disorders. Normal values for selected laboratory tests are given in Table 41-1. 

Thyroid Hormone Receptor (TR) can bind to the LTR in vivo independently of its ligand and regulates promoter activity. ChIP assays with anti-acetylated-histone antibodies revealed that unliganded TR reduce the local histone acetylation levels at the HIV-1 LTR, while thyroid hormone treatment reverses this induction (Hsia and Shi, 2002). Accordingly, unliganded TR recruits co repressors and at least one HDAC (Hsia and Shi, 2002). 

While they are often prescribed, the lower costs of codeine, ACE inhibitors, beta-blockers, thyroid hormones, calcium blockers, and benzodiazepines keep them off the list of top sales. Conversely, the higher cost of erythropoietins, antineo monoclonal antibodies, angiotensin II antagonists, antiarthritis drugs, and bisphosphonates put them on the list of top sales but not top prescriptions. 

Thyroid Effects. Limited information is available on thyroid effects in PBDE-exposed humans. There are suggestive occupational data as shown by effects that included increased serum FSH, low or borderline low serum T4, and increased thyroid antimicrosomal antibody titers in workers exposed to decaBDE and/or unspecified PBBs. There was no clear association between plasma levels of 2,2, 4,4-tetraBDE and thyroid hormone levels (free and total T3 and T4, TSH, free testosterone, follicle-stimulating hormone, lutenizing hormone, and prolactin) in men who consumed varying amounts of fatty fish from the Baltic Sea. Based on consistent evidence in animals, as summarized below, the thyroid is particularly sensitive to PBDEs and is a likely target of toxicity in exposed humans. 

While this pattern of biochemistry does not exclude transient relapse of Graves hyperthyroidism (despite the finding of negative TSH receptor antibodies), or a transient thyroiditis, the authors speculated that indinavir (prescribed in this patient together with stavudine and lamivudine) had inhibited the glucuronidation of thyroxine and hence caused a rise in serum thyroid hormone concentrations. 

The spectrum of interferon alfa-induced thyroid disorders ranges from asymptomatic appearance or increase in antithyroid autoantibody titers to moderate or severe clinical features of hypothyroidism, hyperthyroidism, and acute biphasic thyroiditis. Antithyroid hormone antibodies have also been found in one patient, and this could have been the cause of erroneously raised thyroid hormone concentrations (504). 

The leading cause of Graves disease occurs when there is a defect in the immune system that causes the production of autoantibodies to TSH receptors located on the surface of thyroid cells. These antibodies act as agonists to stimulate the thyroid, causing it to enlarge (goiter formation), with the overproduction of thyroid hormones... 

The concept that plasma membrane transport plays a key role in the regulation of intracellular thyroid hormone levels is supported by studies with a monoclonal antibody against an antigen exposed on rat liver cells [107], This antibody inhibited the uptake of different iodothyronines by rat hepatocytes under initial rate conditions as well as the metabolism of these compounds during prolonged incubations [107]. Uptake and metabolism of T4, T3 and rT3 were affected to the same extent, suggesting that a single system operates in the transport of different iodothyronines, which is opposite to the view advanced above. However, it is not excluded that the antibody interacts with a component of the plasma membrane and thereby affects multiple transport systems. 

Immunoassays of various designs for estimating free thyroid hormones using antibody extraction techniques have been developed. These assays are subdivided as either sequential two-step assays or simultaneous one-step Canalogue ) assays. Each procedure involves the direct incubation of serum with a specific anti-T4 or anti-T3 antibody, during which thyroid hormones reach a new equilibrium with all of the binders present. A slight decrease in free hormone concentration occurs, but is insignificant if the antibody sequesters less than 5% of the total amount of hormone present in the specimen. Thus the amount of immunoex-tracted T4 or T3 closely approximates the undisturbed free hormone concentration that preexists in serum at equilibrium. 

The key feature of this two-step method is that the labeled hormone is physically prevented from interacting with serum binding proteins. This ensures that antibody binding of tracer is governed solely by the free hormone concentration and not by changes in thyroid hormone-binding proteins. Test results obtained with two-step methods correlate well with those obtained by reference methods across a wide range of clinical disorders. 

Thyrotoxicosis is most commonly caused by Graves disease, which is an autoimmune disorder in which thyroid-stimulating antibody (TSAb) directed against the thyrotropin receptor elicits the same biologic response as thyroid-stimulating hormone (TSH). 

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