A T3 immunoassay test helps to determine whether the thyroid is functioning properly. It is primarily done to diagnose hyperthyroidism. T3 is also done to monitor the progress of a patient with a known thyroid disorder. T3 test is also sometimes conducted along with thyroid antibodies test to diagnose diseases such as Graves' disease, which is an autoimmune disorder that is the most common cause of hypothyroidism. Most of the T3 in the blood is attached to the thyroxine binding globulin. Only less than 1% of the T3 remains unattached. A T3 blood test is used to measure both the bound and the free Triiodothyronine. Increased or decreased T3 test result indicates that there is an imbalance between the body's requirement and supply of the hormone. If a patient is being treated with anti-thyroid medication for hyperthyroidism and the T3 is normal, then it is likely that the medication is controlling the condition. If the T3 is elevated, then the medication is not sufficient and the patient may be experiencing symptoms associated with hyperthyroidism. The normal test value for T3 is 100 to 200 ng/dL (nanograms per deciliter).
The T4 immunoassay test helps measure the amount of Thyroxine or T4 in the blood. A T4 immunoassay test is primarily done in response to an abnormal TSH result. Sometimes T4 is done along with TSH blood test. Thyroid hormone screening is commonly performed in newborns in the US as part of newborn screening programs for congenital hypothyroidism which may cause mental retardation if left untreated. False positive results can occur when testing a newborn for congenital hypothyroidism. Therefore normally the test is repeated a few days after initial testing. If the results continue to be abnormal, then additional testing is done. The normal range of a T4 test for an adult is 5 - 11 ug/dL (nanograms per deciliter).
There are other thyroid tests that indicate a malfunction. One such test is the 'Thyroid antibodies' test. This test is used to measure the presence of antibodies against thyroid tissue. Antibodies mean that the person has autoimmune disease such as Hashimoto's Thyroiditis or Graves' disease ( a condition characterized by an enlarged thyroid gland, weight loss without loss of appetite, sweating, heart palpitations, nervousness and inability to tolerate heat).
Thyroxine-binding globulin (TBG) is another thyroid test which detects the TBG which is an important protein in the blood that carries the thyroid hormones T3 and T4. This is a rare test and not done very commonly. Other diagnostic tests that are used to investigate problems with thyroid gland are the thyroid scan, thyroid ultrasound and thyroid biopsy.
Acardia is a rare and serious malformation that occurs exclusively in monizygous twins - twins developing from a single egg. Acardia represents one of the most severe and rare congenital anomalies. It is characterized by the absence of functioning heart. Acardia results from the artery to artery connections in the placenta, thereby causing a physically normal fetus to circulate blood for itself as well as a severely malformed fetus suffering from heart regression. In other words, fetus acardius is a parasite and it receives blood supply from the donor twin. Because the pump twin heart has to pump for two, there is a high risk of going into heart failure and this would lead to the death of the normal twin.
The most common variety is the acardius acephalus where the head is lacking and so are the upper extremities. Other types are acardius anceps, acardius acormus and acardius amorphous. While in acardius anceps, the most highly developed form, a partly developed head with remnants of cranial bones and brain tissue are present with developed body and extremities, acardius acormus is the rarest form of acardia. The monster is a head without a body. Acardia amorphous is the least developed monster not recognizable as a human form, with minimally developed visceral organs. Since there is no gross human form, the name acardius amorphous.
As to the cause of acardia, the etiology of acardiac monster is still unknown. Genetic defects have been reported to be the cause. Some researchers suggest chromosomal abnormalities to be the reason. Krause and Bejdl suggest that compression of the cephalic pole of the embryo prohibiting curving and fusion of the primitive heart tube to be the basic cause of this anomaly. As a result, the dependant entodermal organs like thyroid, esophagus, trachea, lung, liver and others are also not formed.
A pregnant woman carrying an acardiac twin is unlikely to have any unusual symptoms. An acardiac twin is often found incidentally on prenatal ultrasound. As no two acardiac twins are formed exactly alike, they may present differently. Several improved imaging techniques like 2D ultrasonography, 3D ultrasonography and transvaginal Doppler ultrasonography have made diagnosis of acardia possible even in the first trimester of pregnancy. Such early diagnosis helps to reduce the risk of complications. Fetal echocardiography is also recommended to assist in early detection of heart failure in the normal twin. Chromosome studies are also done on both fetuses.
One line of treatment is watching for the earliest signs of heart failure in the pump twin with frequent ultrasounds. If heart failure is identified and the pregnancy is also far enough, then the pump twin should simply be delivered. Physicians recommend prenatal interruption of the blood vessel connections before heart failure develops in the pump twin, thus sacrificing the acardiac twin.
Specialists use laser, electrical cauterization and electrodes, serial amniocentesis, medications and other treatments successfully. If the acardiac twin is large enough and the amount of blood flow to it can cause heart failure in the healthy twin, then blood flow is stopped with Fetal Image-Guided Surgery. The acardiac or parasitic twin never survives, as it is severely malformed and does not have a functioning heart. The normal twin is at risk for heart failure and complications associated with premature birth. The normal twin is expected to have about 10% risk for malformations.
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Collection of Pages - Last revised Date: October 21, 2019