| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on July 16, 2003
Accepted on September 11, 2003
1 Institute of Interdisciplinary Research (IRIBHN), Laboratory of Clinical Biology and, Laboratory of Epidemiology, Free University of Brussels (ULB); Laboratory of Histology, Catholic University of Louvain (UCL), Brussels, Belgium; Instituto de Investigationes Biomedicas Arturo Duperier, Madrid, Spain.
* To whom correspondence should be addressed. E-mail: many{at}isto.ucl.ac.be.
Thyroid destruction leading to endemic myxoedematous cretinism is highly prevalent in Central Africa, where iodine (I) and selenium (SE) deficiencies as well as thiocyanate (SCN) overload are combined. All three factors have been studied experimentally in the etiology of the disease, but never all combined. In a model using rats, we have previously shown that combining iodine and selenium deficiencies increases the sensitivity of the thyroid to necrosis, after iodide overload, an event unlikely to occur in the African situation. To develop a model that would more closely fit with the epidemiological findings, we have determined whether, or not, a SCN overload would also result in thyroid necrosis as the iodine overload does. Combination of the three factors increased 3.5 times the amount of necrotic cells, from 5.5 ± 0.3% in the I- SE+ thyroids to 18.9 ± 1.6% in the I-SE- SCN overloaded ones. Methimazole administration prevented the SCN induced necrosis. SE- thyroids evolved to fibrosis while SE+ thyroids did not. TGF-
was prominent in macrophages present in SE- glands.
Thyroid destruction in Central Africa might therefore originate from the interaction of three factors: iodine and selenium deficiencies by increasing H202 accumulation, selenium deficiency by decreasing cell defense and promoting fibrosis, and SCN overload by triggering follicular cell necrosis.
This article has been cited by other articles:
 |
|
 |
|
  S. Poncin, A.-C. Gerard, M. Boucquey, M. Senou, P. B. Calderon, B. Knoops, B. Lengele, M.-C. Many, and I. M. Colin Oxidative Stress in the Thyroid Gland: From Harmlessness to Hazard Depending on the Iodine Content Endocrinology, January 1, 2008; 149(1): 424 - 433. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Song, N. Driessens, M. Costa, X. De Deken, V. Detours, B. Corvilain, C. Maenhaut, F. Miot, J. Van Sande, M.-C. Many, et al. Roles of Hydrogen Peroxide in Thyroid Physiology and Disease J. Clin. Endocrinol. Metab., October 1, 2007; 92(10): 3764 - 3773. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. E. Pedraza, M.-J. Obregon, H. F. Escobar-Morreale, F. Escobar del Rey, and G. M. de Escobar Mechanisms of Adaptation to Iodine Deficiency in Rats: Thyroid Status Is Tissue Specific. Its Relevance for Man Endocrinology, May 1, 2006; 147(5): 2098 - 2108. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Schomburg, C. Riese, M. Michaelis, E. Griebert, M. O. Klein, R. Sapin, U. Schweizer, and J. Kohrle Synthesis and Metabolism of Thyroid Hormones Is Preferentially Maintained in Selenium-Deficient Transgenic Mice Endocrinology, March 1, 2006; 147(3): 1306 - 1313. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Kohrle, F. Jakob, B. Contempre, and J. E. Dumont Selenium, the Thyroid, and the Endocrine System Endocr. Rev., December 1, 2005; 26(7): 944 - 984. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
