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Rodrigo Fierrobenitez - One of the best experts on this subject based on the ideXlab platform.
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neurological signs in congenital iodine deficiency disorder endemic Cretinism
Developmental Medicine & Child Neurology, 2008Co-Authors: Robert G Delong, John B Stanbury, Rodrigo FierrobenitezAbstract:UMMARY Neurological examinations were made of 67 children and adults with congenital iodine-deficiency disorder (endemic Cretinism) in four rural villages in highland Ecuador. There was a distinct and readily identifiable pattern of neurological deficits. These included, to varying degrees: deaf-mutism or lesser degrees of bilateral hearing-loss or dysarthria; spasticity, particularly involving the proximal lower extremities; mental deficiency of a characteristic type; and rigidity and bradykinesia. Not all of these elements were found in all cases. Less common features were strabismus, kyphoscoliosis and frontal-lobe signs. There were exceptional cases with hypotonia. In contrast, cerebellar function was largely spared, as were functions of emotion and attention, vegetative and autonomic functions, social interaction, and probably memory, except in the most severely involved. RESUME Neurologie des affections congenitales de deficit en iode (crelinisme endemique) Des examens neurologiques ont ete faits chez 67 enfants et adultes presentant une affection congenitale de deficit en iode (Cretinisme endemique) dans quatre villages ruraux des hautes terres d'Equateur. II a ete observe un regroupement particulier et rapidement identifiable des deficits neurologiques. Ceci incluait a des degres divers: une surdimutite ou de moindre degre de perte auditive bilaterale ou dysarthrie; une spasticite atteignant tout specialement la region proximale des membres inferieurs, un deficit mental d'un type caracteristique et une rigidite et bradykinesie. Tous ces elements n'etaient pas presents dans tous les cas. Des signes moins habituels ont ete le strabisme, la cyphoscoliose et les signes frontaux. Des cas exceptionnels d'hypotonie ont ete observes. En revanche, la fonction cerebelleuse etait largement epargnee comme l'etaient les fonctions d'emotion et d'attention, les fonctions du systeme vegetatif et autonome, l'interaction sociale et probablement la memoire, excepte dans les cas les plus graves. ZUSAMMENFASSUNG Die Neurologie der congenitalen Jodmangelkrankheit (endemischer Krelinismus) 67 Kinder und Erwachsene mit der congenitalen Jodmangelkrankheit (endemischer Kretinismus) aus vier landlichen Gemeinden im Hochland von Ecuador wurden neurologisch untersucht. Es wurde ein bestimmtes und leicht erkennbares Muster neurologischer Ausfalle gefunden. Diese bestanden in unterschiedlicher Auspragung in: Taubstummheit oder in abgeschwachter Form in bilateralem Horverlust oder Dysarthrie; Spastik, wobei insbesondere der proximale Bereich der unteren Extremitaten betroffen war; eine charakteristische Art des Schwachsinns; Rigiditat und Bradykinasie. Nicht in jedem Fall wurden all diese Elemente gefunden. Die weniger haufigen Merkmale waren Strabismus, Kyphoskoliose und Frontalhirnzeichen. Es gab Ausnahmefalle mit Hypotonic Dagegen waren die cerebellaren Funktionen, Gefuhl und Aufmerksamkeit, vegetative und autonome Funktionen, soziale Interaktion und wahrscheinlich Gedachtnis normal mit Ausnahme der sehr schwer betroffenen Falle. RESUMEN Neurologia de la enfermedad por deficiencia de iodo (Cretinismo endemico) Se realizaron examenes neurologicos en 67 ninos y adultos con enfermedad por deficiencia congenita de iodo (Cretinismo endemico) en cuatro poblaciones rurales en las tierras altas del Ecuador. Se hallo un patron distintivo y facilmente identifiable de deficits neurologicos, que incluian en diversos grados: sordo-mudez o grados menores de perdida bilateral de la audicion o disartria, espasticidad afectando sobre todo la parte proximal de las extremidades inferiores, deficiencia mental de tipo caracteristico y rigidez y bradicinesia. No todas estas alteraciones se hallaban en todos los casos. Alteraciones menos corrientes fueron: estrabismo, cifoescoliosis y signos de lobulo frontal. Algunos casos excepcionales tenian hipotonia. Contrariamente, excepto en los casos mas graves, las funciones cerebelpsas estaban indemnes, lo mismo que las funciones emotivas y de atencion, las vegetativas y autonomicas, la interaccion social y probablemente la memoria.
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neurological signs in congenital iodine deficiency disorder endemic Cretinism
Developmental Medicine & Child Neurology, 2008Co-Authors: G R Delong, J B Stanbury, Rodrigo FierrobenitezAbstract:Neurological examinations were made of 67 children and adults with congenital iodine-deficiency disorder (endemic Cretinism) in four rural villages in highland Ecuador. There was a distinct and readily identifiable pattern of neurological deficits. These included, to varying degrees: deaf-mutism or lesser degrees of bilateral hearing-loss or dysarthria; spasticity, particularly involving the proximal lower extremities; mental deficiency of a characteristic type; and rigidity and bradykinesia. Not all of these elements were found in all cases. Less common features were strabismus, kyphoscoliosis and frontal-lobe signs. There were exceptional cases with hypotonia. In contrast, cerebellar function was largely spared, as were functions of emotion and attention, vegetative and autonomic functions, social interaction, and probably memory, except in the most severely involved.
Michael B Zimmermann - One of the best experts on this subject based on the ideXlab platform.
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decision analytic modeling studies in prevention and treatment of iodine deficiency and thyroid disorders a systematic overview
Thyroid, 2020Co-Authors: U Rochau, Vjollca Qerimi Rushaj, M Schaffner, Marie Schonhensch, I Stojkov, Beate Jahn, Alicija Hubalewskadydejczyk, Iris Erlund, Betina H Thuesen, Michael B ZimmermannAbstract:Background: Prevention and treatment of iodine deficiency-related diseases remain an important public health challenge. Iodine deficiency can have severe health consequences, such as Cretinism, goi...
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the effects of iodine deficiency in pregnancy and infancy
Paediatric and Perinatal Epidemiology, 2012Co-Authors: Michael B ZimmermannAbstract:Iodine requirements are increased ≥ 50% during pregnancy. Iodine deficiency during pregnancy can cause maternal and fetal hypothyroidism and impair neurological development of the fetus. The consequences depend upon the timing and severity of the hypothyroidism; the most severe manifestation is Cretinism. In moderate-to-severely iodine-deficient areas, controlled studies have demonstrated that iodine supplementation before or during early pregnancy eliminates new cases of Cretinism, increases birthweight, reduces rates of perinatal and infant mortality and generally increases developmental scores in young children by 10-20%. Mild maternal iodine deficiency can cause thyroid dysfunction but whether it impairs cognitive and/or neurologic function in the offspring remains uncertain. Two meta-analyses have estimated that iodine-deficient populations experience a mean reduction in IQ of 12-13.5 points. In nearly all regions affected by iodine deficiency, salt iodisation is the most cost-effective way of delivering iodine and improving maternal and infant health.
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research on iodine deficiency and goiter in the 19th and early 20th centuries
Journal of Nutrition, 2008Co-Authors: Michael B ZimmermannAbstract:In 1811, Courtois noted a violet vapor arising from burning seaweed ash and Gay-Lussac subsequently identified the vapor as iodine, a new element. The Swiss physician Coindet, in 1813, hypothesized the traditional treatment of goiter with seaweed was effective because of its iodine content and successfully treated goitrous patients with iodine. Two decades later, the French chemist Boussingault, working in the Andes Mountains, was the first to advocate prophylaxis with iodine-rich salt to prevent goiter. The French chemist Chatin was the first to publish, in 1851, the hypothesis that iodine deficiency was the cause of goiter. In 1883, Semon suggested myxedema was due to thyroid insufficiency and the link between goiter, myxedema, and iodine was established when, in 1896, Baumann and Roos discovered iodine in the thyroid. In the first 2 decades of the 20th century, pioneering studies by Swiss and American physicians demonstrated the efficacy of iodine prophylaxis in the prevention of goiter and Cretinism. Switzerland's iodized salt program has been operating uninterrupted since 1922. Today, control of the iodine deficiency disorders is an integral part of most national nutrition strategies.
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the impact of iron and selenium deficiencies on iodine and thyroid metabolism biochemistry and relevance to public health
Thyroid, 2002Co-Authors: Michael B Zimmermann, Josef KohrleAbstract:Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous Cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.
Vanderpas Jean-baptiste - One of the best experts on this subject based on the ideXlab platform.
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Historical aspects of iodine deficiency control
'Edizioni Minerva Medica', 2017Co-Authors: Vanderpas Jean-baptiste, Moreno Reyes, Mario RodrigoAbstract:In 1895, iodine was characterized as an essential element of thyroid tissue by Baumann. The efficacy of iodine to prevent goiter was demonstrated by Marine in Northern USA in 1916-1920. Severe endemic goiter and Cretinism had been almost entirely eliminated from continental Western Europe and Northern America before the 1930's; however large populations elsewhere and even some places in Western Europe (Sicily) were still affected up to the 2000's. Public health consequences of iodine deficiency are not limited to endemic goiter and Cretinism. Iodine deficiency disorders include also increased neonatal death rate and decreased intellectual development, although these consequences are not included in the current estimation of the Global Burden Disease related to iodine deficiency. Severe iodine deficiency as a public health problem is now largely under control worldwide, but can still affect isolated places, in hard-To-reach and/or politically neglected populations. We emphasize the importance of maintaining international cooperation efforts, in order to monitor iodine status where iodine deficiency is now adequately controlled, and identify at-risk population where it is not. The goal should be now global eradication of severe iodine deficiency. Commercial distribution of iodized salt remains the most appropriate strategy. A randomized clinical trial in New Guinea clearly showed in the 1970's that correcting severe iodine deficiency early in pregnancy prevents endemic neurological Cretinism. This supports the essential role of thyroid hormones of maternal origin on the normal fetal development, during the first trimester of pregnancy (i.e. when fetal thyroid is still not functional). A randomized clinical trial in Congo (RD) in the 1970's also showed that correcting severe iodine deficiency during pregnancy prevents myxoedematous Cretinism, particularly prevalent in affected Congolese areas.SCOPUS: re.jinfo:eu-repo/semantics/publishe
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Nutritional epidemiology and thyroid hormone metabolism.
'Annual Reviews', 2006Co-Authors: Vanderpas Jean-baptisteAbstract:Severe iodine deficiency was the main cause of endemic goiter and Cretinism. Most of the previously iodine-deficient areas are now supplemented, mainly with iodized salt. The geographical distribution of severe endemic areas has been progressively reduced, and at present, approximately 200 million people living in remote places are still at risk of severe iodine deficiency. International public health programs should be focused first on reaching these populations, and second on auditing and monitoring the operational work of supplementation programs. This second point is essential to prevent iodine-induced hyperthyroidism or interruptions of iodine supplement distribution, which could be catastrophic for the fetus and the young infant. Echography brings a complementary tool to clinical assessment of goiter by palpation. Inductively coupled plasma-mass spectrometry brings at least a definitive gold standard for iodine measurement and thyroid hormone measurement. Thiocyanate overload has been clearly documented as a goitrogen in Central Africa, and when associated with selenium deficiency, it may be included as risk factor for endemic myxedematous Cretinism. Variable exposure to different environmental risk factors is likely the explanation of the variable distribution of two types of endemic Cretinism (neurological and myxedematous), and the clinical overlap of the pathogeny of both syndromes is more important than previously described. It is possible that Kashin-Beck osteoarthropathy is another evanescent endemic disease that will disappear with the correction of iodine deficiency.SCOPUS: re.jinfo:eu-repo/semantics/publishe
G R Delong - One of the best experts on this subject based on the ideXlab platform.
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neurological signs in congenital iodine deficiency disorder endemic Cretinism
Developmental Medicine & Child Neurology, 2008Co-Authors: G R Delong, J B Stanbury, Rodrigo FierrobenitezAbstract:Neurological examinations were made of 67 children and adults with congenital iodine-deficiency disorder (endemic Cretinism) in four rural villages in highland Ecuador. There was a distinct and readily identifiable pattern of neurological deficits. These included, to varying degrees: deaf-mutism or lesser degrees of bilateral hearing-loss or dysarthria; spasticity, particularly involving the proximal lower extremities; mental deficiency of a characteristic type; and rigidity and bradykinesia. Not all of these elements were found in all cases. Less common features were strabismus, kyphoscoliosis and frontal-lobe signs. There were exceptional cases with hypotonia. In contrast, cerebellar function was largely spared, as were functions of emotion and attention, vegetative and autonomic functions, social interaction, and probably memory, except in the most severely involved.
Josef Kohrle - One of the best experts on this subject based on the ideXlab platform.
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the impact of iron and selenium deficiencies on iodine and thyroid metabolism biochemistry and relevance to public health
Thyroid, 2002Co-Authors: Michael B Zimmermann, Josef KohrleAbstract:Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous Cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.