Biomedical subjects
Publications and source records attributed to F Delange.
UNLABELLED: We describe a neonate born of drug dependent parents. This observation documents the variability of expression in the neonatal abstinence syndrome and the interaction with an additional disease. CONCLUSION: The neonatal abstinence syndrome was masked by congenital hypothyroidism until thyroxine treatment had normalised cellular metabolism.
In the beginning of the nineties, 40 years after introduction of iodine prophylaxis in Croatia, on a basis of a frequent reports coming from general practitioners about the presence of a rather high prevalence of goiter among schoolchildren, a nationwide study was initiated with the aim to determine the real prevalence of goiter in the country. A total of 2856 schoolchildren of both sexes, aged 7-15 years, were included into the study. Investigations were designed in a way to cover most of geographical regions in Croatia and subjects were randomly selected. The prevalence of goiter in schoolchildren was assessed by palpation and in part by ultrasonography of the neck. At the same time urinary iodine excretion was measured and iodine content in salt samples was determined. The results have revealed the persistence of mild endemic goiter in inland parts of Croatia with the prevalence of 6-29% in the age group 7-11 years and those of 10-43% among the age group 12-15 years. The overall goiter prevalence in schoolchildren in Croatia fluctuates from 8% to 35%. Such prevalence, most probably due to less than optimum iodine intake, is unlikely to change until iodine content of the salt is increased from its present level of 10 mg of Kl per kg of salt.
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This brief review of the available studies confirms that the administration of iodized oil before or during pregnancy prevents endemic cretinism and brain damage by correcting iodine deficiency and thyroid function in pregnant women, fetuses, neonates, infants and children. The potential benefits derived from using iodized oil immediately before or during pregnancy greatly outweigh the potential risks in areas of moderate and severe prevalence of iodine-deficiency disorders, where iodized salt is not yet available.
The "Thyromobile" project was initiated to update information on iodine supply in school-children aged 6-14 years in Europe. It involved 4 places in France: Lorraine, Rhône-Alpes, Languedoc-Roussillon, Midi-Pyrénées. Schools of the three former places had been investigated in 1986 during the Mornex's study whereas in the latter they had never been investigated in the past. With a mobile unit, all children (n = 1522) had a thyroid echography performed by the same trained investigator, and urinary iodine concentration was determined in 1458 of them. The mean +/- SD of urinary iodine concentration was 13.0 +/- 7.4 micrograms/dl, but 38% of urinary iodine concentrations were below 10 micrograms/dl and 10% were under 5 micrograms/dl. The prevalence of goitre was 4.1% in boys and 3.1% in girls. There was a negative correlation between urinary iodine concentration and thyroid volume (p < 0.001). Therefore, the results of the "Thyromobile" project show that the places, investigated in France, are not in an area of endemic goitre due to iodine deficiency. However, other epidemiological studies must be done to provide further information about iodine supply in all parts of France.
Iodine is a trace element present in the human body in minute amounts (15-20 mg in adults, i.e. 0.0285 x 10(-3)% of body weight). The only confirmed function of iodine is to constitute an essential substrate for the synthesis of thyroid hormones, tetraiodothyronine, thyroxine or T4 and triiodothyronine, T3 (1). In thyroxine, iodine is 60% by weight. Thyroid hormones, in turn, play a decisive role in the metabolism of all cells of the organism (2) and in the process of early growth and development of most organs, especially of the brain (3). Brain development in humans occurs from fetal life up to the third postnatal year (4). Consequently, a deficit in iodine and/or in thyroid hormones occurring during this critical period of life will result not only in the slowing down of the metabolic activities of all the cells of the organism but also in irreversible alterations in the development of the brain. The clinical consequence will be mental retardation (5). When the physiological requirements of iodine are not met in a given population, a series of functional and developmental abnormalities occur (Table 1), including thyroid function abnormalities and, when iodine deficiency is severe, endemic goiter and cretinism, endemic mental retardation, decreased fertility rate, increased perinatal death, and infant mortality. These complications, which constitute an hindrance to the development of the affected population, are grouped under the general heading of Iodine Deficiency Disorders, IDD (6). Broad geographic areas exist in which the population is affected by IDD.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: In view of the fact that, during the first period of life, thyroid hormones are critical for brain development, we investigated whether even transient congenital hypothyroidism could affect the long-term intellectual development of affected infants. DESIGN: A case-control study of intellectual development, auxometric parameters and thyroid function performed in late infancy in children with documented transient congenital hypothyroidism or hyperthyrotrophinaemia at birth. PATIENTS: Nine children born in an endemic goitre area who had short-term transient congenital hypothyroidism or hyperthyrotrophinaemia after birth (TCH) were studied and compared to nine matched children born in the same area at the same time but having normal thyroid function at birth (N). MEASUREMENTS: Global, verbal and performance IQs were evaluated on the Wechsler scale. Height, bone age, total and free thyroid hormones, thyroid volume, thyroglobulin, basal and TRH stimulated TSH were also measured. RESULTS: Height and bone age were similar in the two groups. Thyroid function tests were also similar in the two groups except for basal and TRH stimulated serum TSH and serum Tg which were higher in the TCH than in the control group. Global, verbal and performance IQs were systematically lower in the TCH than in the N group. (78.3 +/- 11.1 vs 90.9 +/- 14.2, P < 0.05; 84.4 +/- 15.4 vs 96.2 +/- 14.8, P NS; 75.0 +/- 8.5 vs 89.2 +/- 12.5, P < 0.01 respectively). CONCLUSION: Infants born and living in an academic goitre area, who had biochemical signs of thyroid hypo-function at birth, had a lower intelligence quotient at the age of 7-8 years than matched controls living in the same environmental conditions but with normal thyroid function at birth. The present findings strongly suggest that abnormalities in thyroid function at birth, even when transient, can adversely affect long-term intellectual development.
One hundred and eighty euthyroid pregnant women were selected at the end of the first trimester of gestation on the basis of biochemical criteria of excessive thyroid stimulation, defined as supranormal serum thyroglobulin (TG > 20 micrograms/L) associated with a low normal free T4 index (< 1.23) and/or an increased T3/T4 ratio (> 25 x 10(-3)). Women were randomized in a double blind protocol into three groups and treated until term with a placebo, 100 micrograms potassium iodide (KI)/day, or 100 micrograms iodide plus 100 micrograms L-T4/day. Parameters of thyroid function, urinary iodine excretion, and thyroid volume were monitored sequentially. Neonatal thyroid parameters, including thyroid volume by echography, were also assessed in the newborns from mothers of the three groups. In women receiving a placebo, the indices of excessive thyroid stimulation worsened as gestation progressed, with low free T4 levels, markedly increased serum TG and T3/T4 ratio. Serum TSH doubled, on the average, and was supranormal in 20% of the cases at term. Urinary iodine excretion levels were low, around 30 micrograms/L at term. The thyroid volume increased, on the average, by 30%, and 16% of the women developed a goiter, confirming the goitrogenic stimulus associated with pregnancy. Moreover, the newborns of these mothers had significantly larger thyroid volumes at birth as well as elevated serum TG levels. In both groups of women receiving an active treatment, the alterations in thyroid function associated with pregnancy were markedly improved. The increase in serum TSH was almost suppressed, serum TG decreased significantly, and changes in thyroid volume were minimized (group receiving KI) or almost suppressed (group receiving KI combined with L-T4). Moreover, in the newborns of the mothers in the two groups receiving an active treatment, serum TG was significantly lower, and thyroid volume at birth was normal. The effects of therapy were clearly more rapid and more marked in the group receiving a combination of T4 and KI than in the women receiving KI alone. The differences could be partly attributed to the slightly higher amount of iodine received by women in the combined treatment. However, the main benefits of the combined treatment were almost certainly attributable to the hormonal effects of the addition of L-T4. Furthermore, the study demonstrated that the administration of T4 did not hamper the beneficial effect of iodine supplementation. In conclusion, the present work emphasizes the potential risk of goitrogenic stimulation in both mother and newborn in the presence of mild iodine deficiency.(ABSTRACT TRUNCATED AT 400 WORDS)
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This paper reviews present knowledge on the etiology, pathophysiology, complications, prevention, and therapy of the disorders induced by iodine deficiency. The recommended dietary allowances of iodine are 100 micrograms/day for adults and adolescents, 60-100 micrograms/day for children aged 1 to 10 years, and 35-40 micrograms/day in infants aged less than 1 year. When the physiological requirements of iodine are not met in a given population, a series of functional and developmental abnormalities occur including thyroid function abnormalities and, when iodine deficiency is severe, endemic goiter and cretinism, endemic mental retardation, decreased fertility rate, increased perinatal death, and infant mortality. These complications, which constitute a hindrance to the development of the affected populations, are grouped under the general heading of iodine deficiency disorders (IDD). At least one billion people are at risk of IDD. Iodine deficiency, therefore, constitutes one of the most common preventable causes of mental deficiency in the world today. Most of the affected populations live in mountainous areas in preindustrialized countries, but 50 to 100 million people are still at risk in Europe. The most important target groups to the effects of iodine deficiency from a public health point of view are pregnant mothers, fetuses, neonates, and young infants because the main complication of IDD, i.e., brain damage resulting in irreversible mental retardation, is the consequence of thyroid failure occurring during pregnancy, fetal, and early postnatal life. The main cause of endemic goiter and cretinism is an insufficient dietary supply of iodine. The additional role of naturally occurring goitrogens has been documented in the case of certain foods (milk, cassava, millet, nuts) and bacterial and chemical water pollutants. The mechanism by which the thyroid gland adapts to an insufficient iodine supply is to increase the trapping of iodide as well as the subsequent steps of the intrathyroidal metabolism of iodine leading to preferential synthesis and secretion of triiodotyronine (T3). They are triggered and maintained by increased secretion of TSH, which is ultimately responsible for the development of goiter. The acceleration of the main steps of iodine kinetics and the degree of hyperstimulation by TSH are much more marked in the pediatric age groups, including neonates, than in adults, and the development of goiter appears as an unfavorable side effect in the process of adaptation to iodine deficiency during growth. The most serious complication of iodine deficiency is endemic cretinism, a syndrome characterized by irreversible mental retardation together with either a predominant neurological syndrome or predominant hypothyroidism, or a combination of both syndromes.(ABSTRACT TRUNCATED AT 400 WORDS)
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A covering letter and a questionnaire covering the diagnosis and treatment of thyrotoxicosis in childhood was circulated between October 1992 and February 1993 amongst 672 European members of the European Thyroid Association (ETA) and members of the European Society for Pediatric Endocrinology (ESPE). Almost 50% replied to the letter and 99 individuals or groups from 22 countries completed the questionnaire. A consensus was reached on the use of total thyroxine (T4) and/or free T4 and thyrotropin as routine diagnostic tools. Two-thirds included total triiodothyronine (T3) and/or free T3 and 32% used a thyrotropin-releasing hormone test. Surprisingly, thyroglobulin autoantibodies were used as a routine test by 78%; 63% included thyrotropin receptor antibodies and 60% microsomal antibodies, whereas only 50% measured thyroperoxidase antibodies. For thyroid imaging, 40% performed a thyroid scintigram and 56% measured the size of the thyroid gland by ultrasound. Antithyroid drugs (ATD) were the basic initial treatment of choice given by 99% of the respondents for children with uncomplicated Graves' disease. Carbimazole, methimazole and thiamazole were the most frequently used drugs, with a median initial dose of 0.8 mg.kg-1.day-1. Two-thirds added beta-blockers and a few used sedatives. The ATD dose was adjusted for each patient by 39%, whereas 56% combined ATD with T4 for long-term treatment; 84% gave treatment for a fixed period (44% for 1-2 years). Surgery was considered the treatment of choice in children with an adenoma (83%), with a nodular (53%) or large goiter (16%) and recurrence after ATD (14%).(ABSTRACT TRUNCATED AT 250 WORDS)
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Using an extraction-concentration technique of circulating calcitonin (exCT) that permits a sensitive and specific assessment of circulating CT monomer levels, we measured exCT levels in 115 healthy children (59 girls and 56 boys), aged 0-16 yr, and 25 patients (15 girls and 10 boys), aged 2 months to 22 yr, with congenital hypothyroidism (CH), a condition characterized by a marked CT deficiency in adults. We found a significant negative correlation between CT levels and age in healthy children (girls, r = -0.83; boys, r = -0.63; P < 0.001). There was a 5-fold decrease in CT levels from the neonatal period to adolescence. The fall in CT levels was particularly marked in early infancy (e.g. for the age category 1 day to 1 yr, 19.0 +/- 1.9 vs. 7.3 +/- 1.2 ng/L for the group 1-5 yr, P < 0.01), but less pronounced thereafter (for the group 5-10 yr, 4.7 +/- 0.8 ng/L; P < 0.001 vs. the group 1 day to 1 yr). The well established sex difference in CT levels in adults was significant only for the age category above 10 yr (2.7 +/- 0.4 ng/L for girls vs. 4.5 +/- 0.7 ng/L for boys, P < 0.05). In patients with CH, the mean exCT level was 2.0 +/- 0.3 ng/L under 3 yr of age (n = 9), whereas all CT values were undetectable after the age of 3 yr, which could contribute to the lower bone mass of adult CH patients. CT values were normal in 3 children with metabolic goiter. In healthy children, our results demonstrate the existence of an age-related decrease in circulating CT levels, which was particularly marked in infancy. The sex difference in CT levels progressively appeared in childhood, but was significant only after 10 yr of age. Such changes in CT levels could be important for neonatal calcium metabolism and contribute to the lower bone mass in females.
Thyroid function was evaluated in cord serum of healthy full-term newborns and compared to that of mothers immediately after parturition. The study was carried out in an area without overt iodine deficiency, but with a marginal iodine supply (less than 100 micrograms/day in 80% of women). The aim of the study was to delineate the interrelationships between the thyroid statuses of mother and child at birth. Maternal thyroid function was characterized at delivery by relative hypothyroxinemia; increased T3/T4 ratios, indicating preferential T3 secretion; slightly increased TSH levels within the normal range in 97% of women; increased serum thyroglobulin (TG) values, which were above normal in 60% of women; and also goiter formation in almost 10% of women. The findings indicated glandular stimulation and confirmed our earlier reports that pregnancy constitutes a stress for the maternal thyroid economy, enhanced by the limited availability of iodine in the diet. By contrast, newborns showed a strikingly distinct pattern: there was no relative hypothyroxinemia and free T4 levels were significantly higher than in the respective mothers (19.4 vs. 14.7 pmol/L; P less than 0.001). In spite of these differences, however, mean neonatal TSH and TG levels were significantly higher than maternal values, respectively 6.0 vs. 1.9 mU/L for TSH (P less than 0.001) and 70 vs. 40 micrograms/L for TG (P less than 0.001). Furthermore, neonatal TG and TSH levels increased in parallel and were highly correlated with maternal data, suggesting a regulatory link between both thyroid economies. The results suggested that the common regulatory link is the limited availability of the iodine supply. In conclusion, the present study demonstrates that even in conditions with a marginally low iodine intake, pregnancy constitutes a stimulus for both the maternal and newborn thyroids. Changes in both groups are associated and the abnormalities in TSH and TG are amplified in the newborns. The TSH and TG alterations at birth in full-term healthy newborns, associated with similar alterations in maternal thyroid function, provide evidence for a common stimulatory factor, relative iodine deficiency. The data emphasize the hypersensitivity of neonatal thyroid function to marginal iodine deficiency and point to the need to increase the iodine supply in groups at risk, such as women during pregnancy, and also newborns in the perinatal period.
The volume of the thyroid gland was determined by ultrasonography in 256 euthyroid subjects aged 0-20 years in Brussels, an area with borderline iodine intake (median urinary iodine: 6.8 micrograms/dl). The volume of each lobe was calculated separately using the formula of an ovoid (Depth x Length x Width x pi/6). The total thyroid volume was obtained by summation of the volume of both lobes. In neonates, mean volume (SD) was 0.84 (0.38) ml and the distribution was asymmetric, skewed towards elevated values (median: 0.76 ml); the volume was best correlated with body surface area (P less than 0.01). Thyroid volume significantly increased (P less than 0.001) until the age of 8 without being influenced by sex and thereafter varied widely: it increased from 2.7 (0.8) ml in prepubertal subjects aged 8-11 years to 11.6 (4.4) ml in late pubertal aged greater than 17 years. This increase was significantly correlated not only with chronological age but also with pubertal stage and seemed to happen early, with the onset of the first clinical signs of puberty. At all ages, the volume of the right lobe was slightly higher than the left lobe but the difference was not significant.