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My Physicians.com |
There have been many claims for giving all children with DS thyroid hormone replacement, regardless of their blood tests. Dr. Turkel included thyroid hormone in his "U" series, Harrell's paper in 1981 on vitamin and mineral replacement included thyroid hormone therapy, and one researcher, Clemens Benda, advocated giving all children with DS a mixture of thyroid and pituitary gland. However, there is no known benefit from giving thyroid hormone to children with DS who have normal thyroid function, and could be detrimental.
Some researchers have claimed that there is a "low-borderline" thyroid state, and the thyroid tests could be normal as the body is able to partially compensate. However, research shows that giving thyroid replacement to individuals with DS and low-normal thyroid tests had no cognitive improvement.
Other people have latched on to a condition called Wilson's syndrome, called after the Dr. Wilson who first described it. Dr. Wilson believes that thyroid disease can be present with normal blood test, and evidenced by a low blood temperature and a collection of signs and symptoms, and then treated with a special thyroid replacement product. This has little to do with Down syndrome, except that some people have recently come forward claiming that hypothyroidism in people with DS may not be picked up with routine blood tests. In reality, there is no scientific evidence supporting these claims. For more information on this topic, see the American Thyroid Association's statement on Wilson's syndrome.
On December 10, 2001 the United States Food and Drug Administration (FDA) renewed its call for the widespread stockpiling of a thyroid-blocking medicine that prevents the absorption of radioactive iodine. Following the FDA announcement the United States Nuclear Regulatory Commission (NRC) ended its long-standing debate over the civilian stockpiling of potassium iodide (KI). The NRC declared that it will fund civilian supplies for one to two doses per individual for persons within the current 10-mile emergency planning zone of every nuclear power station in the US. The American Thyroid Association had also urged the federal government to distribute KI with a particular focus on the vulnerability of children뭩 thyroid glands caught downwind of a radioactive iodine release from a nuclear power plant accident or sabotage. The nuclear industry and the NRC had previously argued against KI distribution saying it would be too hard to administrate and hinder more practical civilian evacuations in the event of an accident. In the wake of the September 11 attacks on the World Trade Center and the Pentagon, the Federal Emergency Management Agency (FEMA) and NRC revised their policy directing states to consider KI stockpiling and distribution
Research reported on at the May 2005 Endocrine Society annual meeting summarized some of the key knowledge regarding hypothyroidism and pregnancy.
Historically, hypothyroidism has been thought to interfere with fertility.
Among women who were known to have thyroid deficiency, successful pregnancy was rarely reported during the first half of the 20th century, and miscarriage rates among such women were high.
Even mild thyroid hormone deficiency in a mother may be harmful to the developing fetus. One study found if a mother has Free T4 levels that are less than the 10th percentile at 12 weeks gestation, the baby faces almost 6 times the risk to have impaired psychomotor development
We now know that overt hypothyroidism in a pregnant woman, particularly during the first trimester, is associated with intellectual impairment in the child.
Another study found that women who had elevated TSH levels during the second trimester of pregnancy had significantly reduced IQ in their children at the age of 7 and up.
Source: Casey. B. "Maternal Hypothyroidism: Maternal Fetal Outcomes." Endocrine Society Annual Meeting, May 2005. [S7-2]Iodine and Pregnancy
According to research reported on at the May 2005 Endocrine Society annual meeting, the increased need for thyroid hormone seen in early pregnancy can only be met by increased hormone production by the gland, which depends on there being enough iodine available in the diet.
If there is insufficient iodine, the mother can become increasingly hypothyroid, and the thyroid increases in size (goiter).
The researchers concluded that iodine supplementation should be introduced to women during the early stages of pregnancy, in particular, multivitamins that contain iodine, to ensure that the total dietary intake of iodine is reaching approximately 250 g of iodine per day.
Source: Glinoer, D. "Pregnancy the Thyroid: Importance of the Iodine Nutrition Status." Endocrine Society Annual Meeting, May 2005.[S7-3]
Welcome to the new Endocrinology surgery and Endocrinology
This Web site Target the General Public Seeking Information on Endocrine Disease Hoping you will find the information needed or contact us to ask your question by Sinoe Medical Association Services
This is also a web site for those taking the USMLE part 1 2 3
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From my good close Friend Ed Friedlander .MD http://pathguy.com
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THYROID PATHOLOGY
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� AGENESIS OF THE THYROID
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� PAPILLAR CARCINOMA
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MAH with Elevated Cytokines A variety of manifestations of malignancy including anorexia, cachexia and dehydration may be due to tumor-produced circulating proinflammatory cytokines. Cytokines such as Il-1, IL-6, TNF, and RANKL which are produced in the bone microenvironment have been identified as physiological regulators of bone turnover. PTHrP released from tumors may increase the local production of several of these cytokines however animal studies have reported that tumor activity can increase systemic levels of certain cytokines such as IL-6 and IL-1 which may contribute along with PTHrP to skeletal lysis and hypercalcemia. Some studies of tumor models have implicated a soluble form of RANKL as contributing to MAH (167), and this remains an intriguing possibility. Finally, circulating concentrations of IL-6 have been reported to correlate with tumor burden in a patient with a squamous carcinoma, a protypical malignancy associated with hypercalcemia and elevated PTHrP (168). Overall therefore it seems likely that other modulators of skeletal and calcium metabolism may be secreted by malignancies and, generally in the presence but occasionally in the absence of PTHrP, may contribute to the dysregulation of bone and mineral homeostasis occurring with MAH. |
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Studies of Inherited Diseases of Metabolism This study is currently recruiting
patients.
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This is a close-up view of the neck region of the same cadaver. The thyroglossal duct (5) can be seen inferior to the hyoid bone (6) and anterior to the thyroid cartilage (3). The duct connects the thyroid gland (4) inferiorly with the foramen cecum of the tongue (not shown) superiorly. The internal jugular vein (1) and common carotid artery (2) are seen laterally to the thyroid gland. http://www.upstate.edu/ grossanat/hnpathtgd.shtml |
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Thyroglossal duct cysts are remnants of the embryonic thyroglossal duct that may occur anywhere from the base of the tongue to the thyroid gland. The majority, however, are found at the level of the thyrohyoid membrane, under the deep cervical fascia. They are midline or just off the midline, and move up and down upon swallowing |
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Blood calcium is tested to screen for, diagnose, and monitor a range of
conditions relating to the bones, heart, nerves, kidneys, and teeth. Blood
calcium levels do not directly tell how much calcium is in the bones, but
rather, how much total calcium or ionized calcium is circulating in the blood.
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Calcium balance. On average, in a typical adult approximately 1g of elemental calcium (Ca+2) is ingested per day. Of this, about 200mg/day will be absorbed and 800mg/day excreted. Approximately 1kg of Ca+2 is stored in bone and about 500mg/day is released by resorption or deposited during bone formation. Of the 10g of Ca+2 filtered through the kidney per day only about 200mg appears in the urine, the remainder being reabsorbed.
Production of bone resorbing substances by neoplasms. Tumor cells may release proteases which can facilitate tumor cell progression through unmineralized matrix. Tumors cells can also release PTHrP, cytokines, eicosanoids and growth factors (eg EGF) which can act on osteoblastic stromal cells to increase production of cytokines such as M-CSF and RANKL and to decrease production of OPG. RANKL can bind to its cognate receptor RANK in osteoclastic cells, which are of hepatopoietic origin, and increase production and activation of multinucleated osteoclasts which can resorb mineralized bone
Disordered calcium homeostasis in granulomatous disease. Production of an extra-renal 1a(OH)ase by macrophages in a granuloma can increase conversion of circulating 25(OH)D3 to 1,25(OH)2D3. This secosteroid will increase Ca+2 absorption from the gut and Ca+2 resorption from bone resulting in an increased ECF Ca+2. The increased ECF Ca+2 and 1,25(OH)2D3 will inhibit PTH production by the parathyroid glands. The increased filtered load of Ca+2 through the kidney and suppressed PTH will contribute to hypercalciuria. http://www.endotext.org/parathyroid/parathyroid4/parathyroid4.htm |
