Donald asks…

i want informations about goiter disease?

it’s a disease which infect thyroid gland… i want to make presentation about it so i want detailed regulated infgormations about this disease

Helen answers:

A goiter is an enlargement of the thyroid gland. Persons with enlarged thyroids may have normal function of the gland (euthyroidism), thyroid deficiency (hypothyroidism), or overproduction of the hormones (hyperthyroidism). Goiter may be congenital or acquired, endemic or sporadic.
The goiter often results from increased pituitary secretion of thyrotropic hormone in response to decreased circulating levels of thyroid hormones. Thyroid enlargement may also result from infiltrative processes that may be inflammatory or neoplastic. Goiter in patients with thyrotoxicosis is caused by thyrotropin receptor-stimulating antibodies.

Figure 561-1 Congenital goiter in infancy. A, Large congenital goiter in an infant born to a mother with thyrotoxicosis who had been treated with iodides and methimazole during pregnancy. B, A 6-wk-old infant with increasing respiratory distress and cervical mass since birth. The operation revealed a large goiter that almost completely encircled the trachea. Notice the anterior deviation and posterior compression of the trachea. Partial thyroidectomy completely relieved the symptoms. It is apparent why a tracheostomy is not adequate treatment for these infants. The cause for the goiter was not found.
561.1 Congenital Goiter
Congenital goiter is usually sporadic and may result from a fetal thyroxine (T4 ) synthetic defect or the administration of antithyroid drugs or iodides during pregnancy for the treatment of thyrotoxicosis. Goitrogenic drugs and iodides cross the placenta and at high doses may interfere with synthesis of thyroid hormone, resulting in goiter and hypothyroidism in the fetus. The concomitant administration of thyroid hormone with the goitrogen does not prevent this effect, because insufficient amounts of T4 cross the placenta. Iodides are included in many proprietary preparations used to treat asthma; these preparations must be avoided during pregnancy because they have often been a cause of unexpected congenital goiter. Amiodarone, an antiarrhythmic drug with a 37% iodine content, has also caused congenital goiter with hypothyroidism. Even when the infant is clinically euthyroid, there may be retardation of osseous maturation, low levels of T4 , and elevated levels of thyroid-stimulating hormone (TSH). In women with Graves disease on antithyroid drugs, these effects can occur when the mother takes only 100–200?mg of propylthiouracil/24?hr; all such infants should undergo thyroid studies at birth. Administration of thyroid hormone to affected infants may be indicated to treat clinical hypothyroidism, to hasten the disappearance of the goiter, and to prevent brain damage. Because the condition is rarely permanent, thyroid hormone may be safely discontinued after the antithyroid drug has been excreted by the neonate, usually after a week.
Enlargement of the thyroid at birth may occasionally be sufficient to cause respiratory distress that interferes with nursing and may even cause death. The head may be maintained in extreme hyperextension. When respiratory obstruction is severe, partial thyroidectomy rather than tracheostomy is indicated ( Fig. 561–1 ).
Goiter is almost always present in the congenitally hyperthyroid infant. These goiters usually are not large; the infant manifests

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clinical symptoms of hyperthyroidism, and the mother often has a history of Graves disease (see Chapter 562.1 ). TSH receptor-activating mutations are also a recognized cause of congenital goiter.
When no causative factor is identifiable, a defect in synthesis of thyroid hormone should be suspected. Neonatal screening programs find congenital hypothyroidism caused by such a defect in 1/30,000–50,000 live births. If the infant is hypothyroid, it is advisable to treat immediately with thyroid hormone and to postpone more detailed studies for later in life. Because these defects are transmitted by recessive genes, a precise diagnosis is helpful for genetic counseling. Monitoring subsequent pregnancies with ultrasonography can be useful in detecting fetal goiters (see Chapters 85.2 ).
Iodine deficiency as a cause of congenital goiters is rare in developed countries, but persists in isolated endemic areas (see below). More important is the recent recognition that severe iodine deficiency early in pregnancy may cause neurologic damage during fetal development, even in the absence of goiter. The iodine deficiency may result in maternal and fetal hypothyroidism, preventing the partially protective transfer of maternal thyroid hormones.
When the “goiter” is lobulated, asymmetric, firm, or large to an unusual degree, a teratoma within or in the vicinity of the thyroid must be considered in the differential diagnosis (see Chapter 563 ).
561.2 Endemic Goiter and Cretinism
Etiology
IODINE DEFICIENCY.
The association between dietary deficiency of iodine and the prevalence of goiter or cretinism has been recognized for more than half a century. A moderate deficiency of iodine can be overcome by increased efficiency in the synthesis of thyroid hormone. Iodine liberated in the tissues is returned rapidly to the gland, which resynthesizes triiodothyronine (T3 ) preferentially at a higher rate than normal. This increased activity is achieved by compensatory hypertrophy and hyperplasia, which satisfy the demands of the tissues for thyroid hormone. In geographic areas where deficiency of iodine is severe, decompensation and hypothyroidism may result. It is estimated that 2 billion individuals in developing countries live in areas of iodine deficiency.
Seawater is rich in iodine, and the iodine content of fish and shellfish is also high. Endemic goiter is rare therefore in populations living along the sea. Iodine is deficient in the water and native foods in the Pacific West and the Great Lakes areas of the United States. Deficiency of dietary iodine is even greater in certain Alpine valleys, the Himalayas, the Andes, the Congo, and the highlands of Papua New Guinea. In areas such as the United States, where iodine is provided in foods from other areas and in iodized salt, endemic goiter has disappeared. Iodized salt in the United States contains potassium iodide (100?µg/g) and provides excellent prophylaxis. Further iodine intake in the United States is contributed by iodates used in baking, iodine-containing coloring agents, and iodine-containing disinfectants used in the dairy industry. The recommended daily allowance of iodine for infants is greater than 30?µg/kg/24?hr; this amount is exceeded fourfold in breast-fed infants and 10-fold in infants fed cow’s milk in the United States.
Clinical Manifestations.
If the deficiency of iodine is mild, thyroid enlargement does not become noticeable except when there is increased demand for the hormone during periods of rapid growth, as in adolescence and during pregnancy. In regions of moderate iodine deficiency, goiter observed in schoolchildren may disappear with maturity and reappear during pregnancy or lactation. Iodine-deficient goiters are more common in girls than in boys. In areas where iodine deficiency is severe, as in the hyperendemic highlands of Papua New Guinea, nearly half the population has large goiters, and endemic cretinism is common.
Serum T4 levels are often low in individuals with endemic goiter, although clinical hypothyroidism is rare. This is true in New Guinea, the Congo, the Himalayas, and South America. Despite low serum levels of thyroid hormone, serum TSH concentrations are often only moderately increased. In such patients, circulating levels of T3 are elevated. Moreover, T3 levels are also elevated in patients with normal T4 levels, indicating a preferential secretion of T3 by the thyroid in this disease.
Endemic cretinism is the most serious consequence of iodine deficiency; it occurs only in geographic association with endemic goiter. The term endemic cretinism includes two different but overlapping syndromes—a neurologic type and a myxedematous type. The frequency of the two types varies among different populations. In Papua New Guinea, the neurologic type occurs almost exclusively, but in Zaire, the myxedematous type predominates. Both types are found in all endemic areas, and some individuals have intermediate or mixed features.
The neurologic syndrome is characterized by mental retardation, deaf-mutism, disturbances in standing and gait, and pyramidal signs such as clonus of the foot, the Babinski sign, and patellar hyperreflexia. Affected individuals are goitrous but euthyroid, have normal pubertal development and adult stature, and have little or no impaired thyroid function. Individuals with the myxedematous syndrome also are mentally retarded and deaf and have neurologic symptoms, delayed sexual development and growth, myxedema, and absence of goiter; serum T4 levels are low, and TSH levels are markedly elevated. Delayed skeletal maturation may extend into the 3rd decade or later. Ultrasonographic examination shows thyroid atrophy.
Pathogenesis.
The pathogenesis of the neurologic syndrome has been attributed to iodine deficiency and hypothyroxinemia during pregnancy, leading to fetal and postnatal hypothyroidism. Although some investigators have attributed brain damage to a direct effect of elemental iodine deficiency in the fetus, most believe the neurologic symptoms are caused by fetal and maternal hypothyroxinemia. There is evidence that the human fetal brain has receptors for thyroid hormone before development of the fetal thyroid, and there is also evidence of transplacental passage of maternal thyroid hormone into the fetus, which normally might ameliorate the effects of fetal hypothyroidism on the developing nervous system. The pathogenesis of the myxedematous syndrome leading to thyroid atrophy is more bewildering. Searches for additional environmental factors that may provoke continuing postnatal hypothyroidism have led to incrimination of selenium deficiency, goitrogenic foods, thiocyanates, and Yersinia. Studies from Western China suggest that thyroid autoimmunity may play a role. Myxedematous cretins with thyroid atrophy, but not euthyroid cretins, were found to have thyroid growth-blocking immunoglobulins of the kind found in infants with sporadic congenital hypothyroidism. Others are skeptical about any role of thyroid growth-blocking immunoglobulins to explain these findings.
Treatment.
In many developing countries, administration of a single intramuscular injection of iodinated poppy seed oil to women prevents iodine deficiency during future pregnancies for about 5 yr. This form of therapy given to children younger than 4 yr of age with myxedematous cretinism results in a euthyroid state in 5 mo. However, older children respond poorly and adults not at all to iodized oil injections, indicating an inability of the thyroid gland to synthesize hormone; these patients require treatment with T4 . In the Xinjiang province of China, where the usual methods of iodine supplementation had failed, iodination of irrigation water has increased iodine levels in soil, animals, and human beings.

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561.3 Sporadic Goiter
The term sporadic goiter encompasses goiters developing from a variety of causes; patients are usually euthyroid but may be hypothyroid. The most common cause of sporadic goiter is lymphocytic thyroiditis (see Chapter 560 ). Intrinsic biochemical defects in the synthesis of thyroid hormone are almost always associated with goiter. The occurrence of the disorder in siblings, onset in early life, and possible association with hypothyroidism (goitrous hypothyroidism) are important clues to the diagnosis.
Iodide Goiter.
A small percentage of patients treated with iodide preparations for prolonged periods acquire goiters. Iodides are commonly included for their expectorant effect in cough medicines and in proprietary mixtures for asthma. Goiters resulting from iodine administration are firm and diffusely enlarged, and in some instances hypothyroidism may develop. In normal individuals, acute administration of large doses of iodine inhibits the organification of iodine and the synthesis of thyroid hormone (Wolff-Chaikoff effect). This effect is short-lived and does not lead to hypothyroidism. When iodide administration continues, an autoregulatory mechanism in normal persons limits iodine trapping and permits the level of iodide in the thyroid to decrease and organification to proceed normally. In patients with iodide-induced goiter, this escape does not occur because of an underlying abnormality of biosynthesis of thyroid hormone. The persons most susceptible to the development of iodide goiter are those with lymphocytic thyroiditis or with a subclinical inborn error in thyroid hormone synthesis and those who have had a partial thyroidectomy.
Lithium carbonate also causes goiters; it is currently widely used as a psychotropic drug. Lithium competes with iodide; the mechanism producing the goiter or hypothyroidism is similar to that described earlier for iodide goiter. Lithium and iodide also act synergistically to produce goiter; their combined use should be avoided.
Amiodarone, a drug used to treat cardiac arrhythmias, can cause thyroid dysfunction with goiter because it is rich in iodine. It is also a potent inhibitor of 5′-deiodinase, preventing conversion of T4 to T3 . It can cause hypothyroidism, particularly in patients with underlying autoimmune disease; in other patients, it may cause hyperthyroidism.
Simple Goiter (Colloid Goiter).
A few children with euthyroid nontoxic goiters have simple goiters, a condition of unknown cause not associated with hypothyroidism or hyperthyroidism and not caused by inflammation or neoplasia. The condition predominates in girls and has a peak incidence before and during the pubertal years. Histologic examination of the thyroid either is normal or reveals variable follicular size, dense colloid, and flattened epithelium. The goiter may be small or large. It is firm in half the patients and is occasionally asymmetric or nodular. Levels of TSH are normal or low, scintiscans are normal, and thyroid antibodies are absent. Differentiation from lymphocytic thyroiditis may not be possible without a biopsy, but biopsy ordinarily is not indicated. Therapy with thyroid hormone may help avoid progression to a large multinodular goiter, although it is difficult to separate any treatment effects from the natural history, which is for the goiter to decrease in size. Untreated patients should be re-evaluated periodically. This condition must be differentiated from lymphocytic thyroiditis (see Chapter 560 ).
Multinodular Goiter.
Rarely, a firm goiter with a lobulated surface and single or multiple palpable nodules is encountered. Areas of cystic change, hemorrhage, and fibrosis may be present. The incidence of this condition has decreased markedly with the use of iodine-enriched salt. A mild goitrogenic stimulus, acting over a long time, is thought to be the cause. Ultrasonographic examination may reveal multiple echo-free and echogenic lesions that are nonfunctioning on scintiscans. Thyroid studies are usually normal, but TSH may be elevated and thyroid antibodies may be present. The condition occurs in children with McCune-Albright syndrome (usually resulting in hyperthyroidism) and has been described in three children (including two siblings) with digital anomalies and cystic renal disease. Dominant nodules within a multinodular goiter, particularly those not suppressed by replacement therapy with T4 , may be an indication for evaluation by fine-needle aspiration because malignancy cannot readily be ruled out.
Toxic Goiter (Hyperthyroidism).
See Chapter 562 .
561.4 Intratracheal Goiter
One of the many ectopic locations of thyroid tissue is within the trachea. The intraluminal thyroid lies beneath the tracheal mucosa and is frequently continuous with the normally situated extratracheal thyroid. The thyroid tissue is susceptible to goitrous enlargement, which involves the normally situated and the ectopic thyroid. When there is obstruction of the airway associated with a goiter, it must be ascertained whether the obstruction is extratracheal or endotracheal. If obstructive manifestations are mild, administration of sodium-l-thyroxine usually causes the goiter to decrease in size. When symptoms are severe, surgical removal of the endotracheal goiter is indicated (also see Chapter 561.1

Donna asks…

I missed my period this month and I have Grave’s Disease, took several tests and they are all negative, could?

I missed my period this month and last, took several tests but a negative result could I still be pregnant? I

Helen answers:

Grave’s disease would not effect the result of a home pregnancy test. These tests determine whether you are pregnant by detecting human chorionic gonadotropin – or hCG. This hormone is found ONLY in pregnant women, and it doubles in amount about every two days for someone who is pregnant. Since you took several tests, it would be unlikely that, especially since you already missed your period, that the tests (which have 99.9% accuracy) would not detect the rapidly rising amounts of hCG in your system. You may just be having an irregular period, which can be caused by something as simple as stress.

Michael asks…

Thyroid – if my t4 level is 30, is this very high?

I know the standard levels are suppose to be between 12.0-22. It was 27 in jan, 28 in feb, 29 in march and 30 in June. I know my level is high but I am just wondering how high 30 is. My doctor hasn’t given me any medication to treat this directly. Help! I would also like to add that I think my t3 level is normal. Apparently this is very unusual.

Helen answers:

A typical normal range is 4.5 to 11.2 micrograms per deciliter (mcg/dL).
Greater than normal levels of T4 along with low levels of TSH may be due to conditions that involve an overactive thyroid, including:–
* Early Hashimoto’s disease
* Graves disease
* Germ cell tumors
* High levels of the protein that carries T4 in the blood (can occur with pregnancy, use of birth control pills or estrogen, liver disease, and as part of an inherited condition)
* Iodine-induced hyperthyroidism
* Subacute or chronic thyroiditis
* Toxic multinodular goiter
* Trophoblastic disease

Mandy asks…

will i have to see a high risk ob for hypothyroidism?

i will be ttc in 9 months and want to be prepared

Helen answers:

No, I have Hyperthyroidism/Graves Disease, My thyroid is really out of whack. I am 17 weeks pregnant. As soon as my OB found out, he sent me to an endocrinologist. I take regular pills to control my thyroid. (Safe pills to take while pregnant, and breastfeeding) I get blood drawn every 4 weeks by my endocrinologist just to make sure my thyroid is okay. My OB is not a high risk OB.

Just please let your OB know ahead of time, follow the orders from your OB and your endocrinologist, make sure if you are on medications that they are safe to take while pregnant. And your pregnancy will be fine.

Good Luck and LOTS OF BABY DUST!!!

Thomas asks…

does thyroid disease have any affect on hcg production when pregnant?

i know that during the first trimester, your hcg levels lower your tsh (thyroid) levels…but i am wondering if the fact that i have thyroid disease will cause a slower production of hcg (pregnancy hormone). where it may not be detectable until later than 5 weeks. i’ve used hpt’s and had a blood test done at what would be 5 weeks…a few days later i got a very very very faint positive line on an hpt…but it was definately blue. i would be 6 weeks now and i am only hanging onto this because i have EVERY possible pregnancy symptom and had spotting (not at all like a period, as it had more clear mucus in it than anything and was very pale pink/tan in color). i also have very viseable blue veins for the past week all over my chest and breasts/nipples, and on the rest of my body (thighs especially…they are much more viseable than usual). i know my body and i just feel pregnant as i already have two children and know what pregnancy feels like~just cannot explain the hcg levels.

Helen answers:

I have Graves’ Disease (overactive thyroid) and I took the test 5 days before my period was due and it came back positive.

What made me take the test was that I had implantation bleeding (didn’t have it with my first) so the day after the bleeding stopped I took the pregnancy test and it was a faint line as well.

I am now into my tenth week.

I can’t explain the HCG levels either, except all I know, with both pregnancies my results came back early.

Like you, I had the exact same symptoms.

My first pregnancy seemed to help correct and ease my thyroid condition, to the point where after my daughter was born they slowly decreased my neo-mercazole and beta blocker and for the last 12 months I have been on no medication at all.

However, I am aware that my remission may only be intermitent.

I think with the thyroid disorders we are all so different, so while my HCG may be strong from the start, your HCG level may not be as strong and may just become stronger as the weeks progress.

Congrats on your pregnancy and I hope all goes well for you.

Only other women with this disease can truly understand what we go through, not just with pregnancy, but with the day to day challenges that we are faced with thyroid disorders.

I am on email through yahoo, so feel free to email me anytime.

Hope this helps.

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