M
Anton Sebastian in A Dictionary of the History of Medicine, 2018
Myxedema [Greek: myxa, slime + oidema, swelling] Five cases of cretinism in adults were described by Thomas B. Curling (1811–1888) of the London Hospital and Sir William Withey Gull (1816–1890) of Guys Hospital in 1873. The disease was previously described by J.B. Bramwell in 1869. The term was coined by William Miller Ord (1834–1902) of St Thomas’ Hospital in 1877. The term ‘cachexia strumpriva’ was used in 1883 by Swiss surgeon, Theodor Kocher (1841–1917), to denote myxedema after total removal of the thyroid gland. In the same year, Sir Felix Semon (1848–1921) recognized loss of thyroid function as a common cause of cachexia strumpriva, cretinism, and myxedema. It was treated successfully with injections of glycerin extract of thyroid gland of sheep by George R. Murray (1865–1939) of Newcastle-upon-Tyne in 1891. See cretinism, thyroid gland.
SBA Answers and Explanations
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury in SBAs for the MRCS Part A, 2018
The thyroid gland primarily produces T4 which is converted to T3 (the more active form) in the periphery. Thyroxine is released when TSH, produced from the anterior pituitary, binds to cell surface receptors on the thyroid gland. TRH is a hypothalamic hormone which causes TSH secretion. TSH release is under inhibitory control by dopamine. Thyroxine increases basal metabolic rate. Protein, carbohydrate, and fat metabolism is increased. Thyroxine, although not a steroid, does not act on cell surface receptors, but acts on intracellular receptors bound to promoters of genes. It directly affects gene transcription in this way. Thyroxine plays an extremely important role in the myelination of axons during brain development. Neonatal deficiency leads to reduced axonal conduction velocities at the critical time in development when the brain is growing and maturing, resulting in developmental delay and mental retardation. This is known as cretinism or congenital hypothyroidism. Thyroid replacement therapy must be initiated soon after birth if mental retardation is to be prevented. Affected infants should be identified on neonatal biochemical screening (Guthrie test).
Effectiveness of Nutrition-Specific Interventions in Pregnancy and Early Childhood
Crystal D. Karakochuk, Kyly C. Whitfield, Tim J. Green, Klaus Kraemer in The Biology of the First 1,000 Days, 2017
Salt iodization is the most common form of food fortification globally. Iodine deficiency can cause hypothyroidism and, when it occurs among pregnant women, can harm fetal neurological development. The prevention of cretinism is the primary outcome of increased iodine supply, but there is also mixed evidence that it reduces neonatal mortality. Similar to the 2013 Lancet series, a 2014 review on population-wide salt iodization deemed the evidence insufficient to draw any conclusions about mortality effects [13], but a 2012 review of iodized oil supplementation for pregnant women that included two randomized controlled trials with over 37,000 participants showed a significant but varied impact on infant mortality (25% to 60% reduction, depending on the severity of iodine deficiency and baseline infant mortality levels) [14].
Availability of adequately iodised salt at household level and its associated factors in Robe town, Bale Zone, South East Ethiopia: community-based cross-sectional study
Published in South African Journal of Clinical Nutrition, 2020
Nagasa Dida, Abiyot Legese, Abdurhim Aman, Bilkisa Muhamed, Teshome Damise, Tizita Birhanu, Sintayehu Hailu, Jiregna Darega, Bedasa Woldamichael, Eshetu Gadisa
Iodine deficiency is the world’s major cause of preventable mental retardation.4,6 Around 2 billion people in 130 countries worldwide have insufficient intakes of iodine. Europe (57%), the Eastern Mediterranean (54%), Africa (43%), Southeast Asia (40%), the Western Pacific (24%), and the Americas (10%) are the countries most affected.4,7 Nearly 38 million newborns in developing countries every year remain unprotected from the lifelong effect of brain damage due to iodine deficiency disorders (IDD).8 In Africa about 260 million people have inadequate iodine intake resulting in iodine deficiency states, which may be related to a 10–15% lowering of average intellectual capacity.9 Severity of iodine deficiency can range from mild intellectual blunting to frank cretinism. Impairment of the developing brain results in individuals being poorly equipped to achieve their intellectual potential, work effectively and have healthy birth outcomes. The consequences of iodine deficiency disorders affect all stages of life from foetus to adulthood as well as old age.4,8,10
Toward a science-based testing strategy to identify maternal thyroid hormone imbalance and neurodevelopmental effects in the progeny – part I: which parameters from human studies are most relevant for toxicological assessments?
Published in Critical Reviews in Toxicology, 2020
Ursula G. Sauer, Alex Asiimwe, Philip A. Botham, Alex Charlton, Nina Hallmark, Sylvia Jacobi, Sue Marty, Stephanie Melching-Kollmuss, Joana A. Palha, Volker Strauss, Bennard van Ravenzwaay, Gerard Swaen
The present first review addressing the human evidence on how lower maternal thyroid hormone levels affect child neurodevelopment was aligned with the topics of Appendix A of the EFSA and ECHA (2018) Guidance. With respect to maternal serum parameters, hypothyroidism (low fT4 with concordant high TSH) and hypothyroxinaemia (isolated low fT4) were addressed. Importantly, focus is not on severe states of congenital hypothyroidism caused by e.g. pronounced maternal iodine deficiency leading to cretinism (Boyages and Halpern 1993), but rather on more subtle effects on maternal thyroid function.
Selenium and thyroid cancer: a systematic review
Published in Nutrition and Cancer, 2020
Mônica de Oliveira Maia, Bruna Aparecida Melo Batista, Morgana Pinheiro Sousa, Luana Matos de Souza, Carla Soraya Costa Maia
In this sense, Se deficiency has been associated with a number of diseases, highlights its association with increased risk of cancer, including thyroid cancer, infections and immunodepression states, male infertility, Alzheimer's and Parkinson's disease, diabetes and mood disorders, further to both already characterized, Keshan's disease and endemic myxedema cretinism (31,32). The role of Se deficiency in the pathogenesis of these diseases may be related to the oxidative stress increased by lack of mineral to the protection system (33).
Related Knowledge Centers
- Congenital Hypothyroidism
- Infertility
- Iodine
- Ovulation
- Puberty
- Thyroid Hormones
- Levothyroxine
- Hypothyroidism
- Goitre
- Bone Age