The endocrine system has an ongoing important role in ebryological, fetal and postnatal development as well as maintainance of homeostasis and reproductive function.
There are many different factors that can impact on endocrine development or function, only a few are shown on this current page.
Page Links: Introduction | Some Recent Findings | Endocrine Disruptors | Diabetes | Thyroid Disease | Gestational hyperthyroidism | Iodine Deficiency | OMIM | Neural Crest Migration | References | Search PubMed | Glossary | WWW Links
Other Pages: Abnormal Development - Maternal Diabetes | Abnormal Development - Gestational Diabetes | Iodine Deficiency
Schoeters G, Den Hond E, Dhooge W, van Larebeke N, Leijs M. Endocrine disruptors and abnormalities of pubertal development. Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):168-75.
Moral R, Wang R, Russo IH, Lamartiniere CA, Pereira J, Russo J. Effect of prenatal exposure to the endocrine disruptor bisphenol A on mammary gland morphology and gene expression signature. J Endocrinol. 2008 Jan;196(1):101-12.
Exogenous chemicals that interfere with the function of hormones.
There are 3 main mechanisms:
Other suggested chemical disruptors:
Juvenile onset diabetes, is more severe form of illness with increased risk of blindness, heart disease, kidney failure, neurological disease.
This is a T-lymphocyte-dependent autoimmune disease with infiltration and destruction of the islets of Langerhans in the pancreas. (Approx 16 million Americans suffer this disease)
Loosely defined as "adult onset" diabetes but is becoming more common with cases of type 2 diabetes seen in younger people, and increasingly common in children.
Risks of developing diabetes:
Environmental factors - such as food intake and exercise play an important role, either overweight or obese.
Inherited factors - important, genes involved remain poorly defined.
(More? Abnormal Development - Maternal Diabetes | Abnormal Development - Gestational Diabetes)
Links: NCBI Bookshelf - Diabetes
Gestational hyperthyroidism in mothers (autoimmune Graves' disease leading to thyrotoxicosis) occurs in 2/1000 pregnancies potentially leading to abnormalities including: fetal loss, pre-eclampsia, maternal heart failure, premature labour, fetal/newborn thyroid and pituitary dysfunction (fetal hypothalamic-pituitary-thyroid system), neural development, and having a low birthweight baby.
Thyroid Function/Testing pregnancy causes changes in maternal thyroid function (gestational increase in thyroid size, increased thyroid-binding globulin levels, increased serum total T4 and total T3 levels) and also testing for hyperthyroidism is altered in pregnancy.
In normal pregnancies, there is a fluctuation in serum TSH levels (due to hCG) and a decrease in free T4 levels as pregnancy progresses. Human chorionic gonadotropin (hCG), which peaks during first trimester, increases thyroid hormone synthesis and leads to a reciprocal fall in maternal serum TSH levels during this period.
Thionamides (propylthiouracil, methimazole, and carbimazole) inhibit the production of thyroid hormones and have been used in pregnancy for the treatment of hyperthyroidism. Drug preference based upon fetal/neonatal hypothyrodism, crossing the placenta, entering breast milk, and teratogenicity has been controversial. (More? Marx H, Amin P, Lazarus JH. Hyperthyroidism and pregnancy. BMJ. 2008 Mar 22;336(7645):663-7 | BMJ Link)
John Hopkins Medical Institute - Abstract # 274: Wolfberg, Adam J. and David A. Nagey, Thyroid Disease During Pregnancy and Subsequent Congenital Anomalies.
The researchers studied 101 women (64 with hypothyroidism and 50 with the overactive version, hyperthyroidism) who gave birth at The Johns Hopkins Hospital between December 1994 and June 1999. Overall, there were 108 pregnancies with 114 foetuses. Twenty-one babies (18%) had birth defects, including problems in the cardiac, renal and central nervous systems and other disorders such as sunken chest, extra fingers, cleft lip and palate, and ear deformities. Two foetuses died before being delivered.
Congenital Hyperthyroidism (CH) is usually defined as infants with TSH level > 25 mU/mL whole blood.
Links: Therapy Insight: management of Graves' disease during pregnancy | Thyroid disease 'raises birth risk' (BBC report Jan 20, 2002) | Abstract # 274: Wolfberg, Adam J. and David A. Nagey, Thyroid Disease During Pregnancy and Subsequent Congenital Anomalies.
Stage 13/14 Thyroid
Iodine deficiency is the single most common cause of preventable mental retardation and brain damage in the world.
It causes goiters and decreases the production of hormones vital to growth and development. Children with IDD can grow up stunted, apathetic, mentally retarded and incapable of normal movement, speech or hearing. IDD in pregnant women cause miscarriage, stillbirth and mentally retarded children. A teaspoon of iodine is all a person requires in a lifetime, but because iodine cannot be stored for long periods by the body, tiny amounts are needed regularly. In areas of endemic iodine deficiency, where soil and therefore crops and grazing animals do not provide sufficient dietary iodine to the populace, food fortification and supplementation have proven highly successful and sustainable interventions. Iodized salt programs and iodized oil supplements are the most common tools in the fight against IDD.
(More? Iodine Deficiency)
Iodine Deficiency Statistics
(Data: International Council for the Control of Iodine Deficiency Disorders)
Measuring Iodine Deficiency
Three main methods:
Links: Iodine Deficiency | International Council for the Control of Iodine Deficiency Disorders
OMIM Database (Online Mendelian Inheritence in Man Database) search results (1999) OMIM
Search Results with the keyword Adrenal | Pancreas | Parathyroid | Pineal | Pituitary | Thymus | Thyroid
Internet Search OMIM database
Note: This database is an
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from some computers in the
School of Anatomy.
Links: Reviews | Articles | Online Textbooks | Search Textbooks | Search PubMed | Glossary
Reviews
Kelce WR, Monosson E, Gamcsik MP, Laws SC, Gray LE Jr. [See Related Articles] Environmental hormone disruptors: evidence that vinclozolin developmental toxicity is mediated by antiandrogenic metabolites. Toxicol Appl Pharmacol. 1994 Jun;126(2):276-85.
Schoeters G, Den Hond E, Dhooge W, van Larebeke N, Leijs M. Endocrine disruptors and abnormalities of pubertal development. Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):168-75.
Moral R, Wang R, Russo IH, Lamartiniere CA, Pereira J, Russo J. Effect of prenatal exposure to the endocrine disruptor bisphenol A on mammary gland morphology and gene expression signature. J Endocrinol. 2008 Jan;196(1):101-12.
Search PubMed
Search Feb 2008 "Endocrine Disruptors" 1244 reference articles of which 296 were reviews.
Search PubMed: term = Endocrine Disruptors | Iodine Deficiency
Selected Lists of References from PubMed May 1999 search results are available for School of Anatomy computers without internet access.
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Stage 13/14 Embryo | Stage 22 Embryo | Selected Sections Stage 22 Embryo | Abnormal Endocrine Development| Overview Pituitary Development | Overview Thyroid Development | Overview Adrenal Development | Overview of Pancreas Development See also GIT Notes- Pancreas |
