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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of iodine deficiency disorders and the thyroid status of the population were studied in an endemic goitre area in Algeria. After oral administration of lipiodol (0.5 ml), three treated groups of mother-newborn couples were compared to an untreated group: group A, mothers treated 1-3 months before conception; group B, mothers treated during the first month of pregnancy; group C, mothers treated during the third month of pregnancy. Untreated mothers were used as a control (group D). After lipiodol treatment, all newborn babies and mothers were clinically euthyroid. All tested newborn babies were full term and no goitre was observed in the four groups. In the mothers, goitre prevalence and thyrotrophin levels decreased significantly, whereas maternal milk and urinary iodine and serum-free thyroxine levels were significantly higher after treatment. The rate of prematurity, stillbirths and abortions in the treated groups was reduced when compared to the untreated group, whereas placental and birth weights were significantly higher. In group D two cases of neonatal hypothyroidism were detected. Their re-evaluation confirmed that hypothyroidism was transient. Groups A, B and C were statistically different from group D with regard to neonatal thyrotrophin and thyroxine. Positive correlations were found between neonatal thyroxine and birth weights and placental weights on the one hand, and maternal urinary iodine and free thyroxine on the other. Consequently, these data indicate that oral administration of lipiodol before or during the first trimester of pregnancy normalizes thyroid function in newborn babies and mothers, increases placental and birth weight and reduces the frequency of iodine deficiency disorders.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of iodine deficiency disorders by oral administration of lipiodol during pregnancy. 820 51

The prevalence of hyperthyroidism in pregnancy is about 0.2%. The most common cause is Graves' disease. Maternal, fetal, and neonatal morbidity and mortality may be reduced to a minimum with careful attention to the clinical symptoms and interpretation of thyroid tests. Ideally, hyperthyroid women should be rendered euthyroid before considering conception. The incidence of maternal and neonatal morbidity is significantly higher in those patients whose hyperthyroidism is not medically controlled. Even the incidence of thyroid storm is high in women who are under poor medical supervision in the presence of a medical or obstetric complication. Maternal morbidity includes a higher incidence of toxemia, premature delivery, placenta abruptio, congestive heart failure, and thyroid crisis. In some series, anemia and infections were also reported. Neonatal morbidity includes SGA neonates, intrauterine growth retardation, LBW infants, and prematurity. Fetal goiter and transient neonatal hypothyroidism is occasionally reported in infants of mothers who have been overtreated with ATD. Propylthiouracil and MMI are equally effective in controlling the disease. In most patients, symptoms improved and thyroid tests returned to normal in 3-8 weeks after initiation of therapy. Resistance to ATD is extremely rare, most cases are caused by patient poor compliance. Surgery for the treatment of hyperthyroidism is reserved for the unusual patient who is allergic to both ATD; to those who have large goiters; to those who require large doses of ATD; or to those patients who poorly comply. Fetal and neonatal hyperthyroidism can be predicted in the majority of cases by the previous maternal medical and obstetric history and by the proper interpretation of thyroid tests. Finally, hyperthyroidism may recur in the postpartum period.
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PMID:Hyperthyroidism in pregnancy. 910 49

Congenital hyperthyroidism is a very rare disease. But, for each affected child it has to be considered as a serious condition because of the negative impact of hyperthyroidism on fetal and postnatal development. If the manifestation occurs during fetal life tachycardia, cardiac arrhythmia, growth retardation and, most significant, prematurity are the consequences. Postnatal signs of hyperthyroidism are irritability, tachycardia, hypertension, poor weight gain and thyroid enlargement. Even cardiac failure may occur if hyperthyroidism is severe and treatment not adequate which explains the high early mortality rate of 16%. The main complication of persistent hyperthyroidism in the neonatal period and during infancy is craniosynostosis. Severe developmental delay or even mental retardation can be the consequence of inadequate high T4-levels during fetal and neonatal life. Congenital hyperthyroidism was first recognized in infants born to mothers with Graves' disease. The description of transplacental passage of the maternal thyroid stimulating antibodies elucidated the molecular mechanism in this major group of patients with "autoimmune congenital hyperthyroidism". In contrast to this transient, self-limited character of "autoimmune congenital hyperthyroidism", due to the clearance of maternal antibodies from the infant's circulation, some cases of persistent congenital hyperthyroidism without signs of thyroid autoimmunity have been recognized. Activating mutations in the thyroid-stimulating hormone receptor were described recently as the underlying molecular pathogenesis in this group of "non-immune congenital hyperthyroidism". Therefore the possibility of a molecular differential diagnosis of both groups of congenital hyperthyroidism now exists and opens the opportunity of optimal treatment for each patient.
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PMID:Congenital hyperthyroidism. 943 7

Neonatal hyperthyroidism has mostly been described in the context of maternal Graves' disease. It has been estimated that about 0.2% of pregnant women have Graves' disease; however only 1% of the children born to these women are described as having hyperthyroidism. In most of the cases, the disease is due to maternal antibodies transferred from the mother into the fetal compartment, which stimulate the fetal thyroid by binding to the thyrotropin (TSH) receptor. In this form of neonatal hyperthyroidism, thyrotoxicosis disappears with the clearance of the maternal antibodies and usually signs disappear during the first 4 months of life. Rare forms of persistent, nonimmune neonatal hyperthyroidism are explained by molecular abnormalities of the TSH receptor. Prematurity is frequent, as well as hypotrophia. Tachycardia, goiter, hyperexcitability, poor weight gain, hepatomegaly and/or splenomegaly, stare and/or eyelid retraction are among the most frequent neonatal thyrotoxicosis clinical signs. Diagnosis is based on the determination of the blood level of thyroxine (T4), triiodothyronine (T3), and TSH. Even if these levels are normal in the cord blood, tests should be repeated 3 to 10 days later to detect possible delayed appearance of the disorder. These parameters should be interpreted according to the age of the neonate. To confirm the immune nature of this hyperthyroidism, thyroid-stimulating immunoglobulins (TSI) should be determined. The TSI determination is crucial in identifying nonimmune causes of neonatal hyperthyroidism: in this neonatal hyperthyroidism, TSI are not detected, either by radioreceptor assay and/or by functional assay, and molecular studies are needed to identify the mutation. Mutation of the TSH receptor leading to its constitutive activation and to neonatal hyperthyroidism have been described. Germline mutations are found in hereditary hyperthyroidism; de novo germline mutations can cause sporadic congenital hyperthyroidism.
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PMID:Hyperthyroidism in early infancy: pathogenesis, clinical features and diagnosis with a focus on neonatal hyperthyroidism. 992 Mar 74

A 29-yr-old woman with pituitary resistance to thyroid hormones (PRTH) was found to harbor a novel point mutation (T337A) on exon 9 of the thyroid hormone receptor beta (TRbeta) gene. She presented with symptoms and signs of hyperthyroidism and was successfully treated with 3,5,3'-triiodothyroacetic acid (TRIAC) until the onset of pregnancy. This therapy was then discontinued in order to prevent TRIAC, a compound that crosses the placental barrier, from exerting adverse effects on normal fetal development. However, as the patient showed a recurrence of thyrotoxic features after TRIAC withdrawal, we sought to verify, by means of genetic analysis and hormone measurements, whether the fetus was also affected by RTH, in order to rapidly reinstitute TRIAC therapy, which could potentially be beneficial to both the mother and fetus. At 17 weeks gestation, fetal DNA was extracted from chorionic villi and was used as a template for PCR and restriction analysis together with direct sequencing of the TRbeta gene. The results indicated that the fetus was also heterozygous for the T337A mutation. Accordingly, TRIAC treatment at a dose of 2.1 mg/day was restarted at 20 weeks gestation. The mother rapidly became euthyroid, and the fetus grew normally up to 24 weeks gestation. At 29 weeks gestation mild growth retardation and fetal goiter were observed, prompting cordocentesis. Circulating fetal TSH was very high (287 mU/L) with a markedly reduced TSH bioactivity (B/I: 1.1 +/- 0.4 vs 12.7 +/- 1.2), while fetal FT4 concentrations were normal (8.7 pmol/L; normal values in age-matched fetuses: 5-22 pmol/L). Fetal FT3 levels were raised (7.1 pmol/L; normal values in age-matched fetuses: <4 pmol/L), as a consequence of 100% cross-reactivity of TRIAC in the FT3 assay method. To reduce the extremely high circulating TSH levels and fetal goiter, the dose of TRIAC was increased to 3.5 mg/day. To monitor the possible intrauterine hypothyroidism, another cordocentesis was performed at 33 weeks gestation, showing that TSH levels were reduced by 50% (from 287 to 144 mU/L). Furthermore, a simultaneous ultrasound examination revealed a clear reduction in fetal goiter. After this latter cordocentesis, acute complications occured, prompting delivery by cesarean section. The female neonate was critically ill, with multiple-organ failure and respiratory distress syndrome. In addition, a small goiter and biochemical features ofhypothyroidism were noted transiently and probably related to the prematurity of the infant. At present, the baby is clinically euthyroid, without goiter, and only exhibits biochemical features of RTH. In summary, although further fetal studies in cases of RTH are necessary to determine whether elevated TSH levels with a markedly reduced bioactivity are a common finding, our data suggest transient biochemical hypothyroidism in RTH during fetal development. Furthermore, we advocate prenatal diagnosis of RTH and adequate treatment of the disease in case of maternal hyperthyroidism, to avoid fetal thyrotrope hyperplasia, reduce fetal goiter, and maintain maternal euthyroidism during pregnancy.
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PMID:Prenatal diagnosis of thyroid hormone resistance. 1002 91

Premature newborns are particularly vulnerable to iatrogenic hypothyroidism due to iodine exposure, usually through skin absorption of iodine-containing disinfectants or intravenous administration of iodinated contrast agents. We report here a case of severe iatrogenic hypothyroidism with goiter and cholestasis, discovered six weeks after a contrast enema using sodium ioxitalamate, an iodinated contrast agent. Prematurity, intrauterine growth retardation, and enteral feeding intolerance could explain why this complication occurred after contrast enema. Our observations suggest that indications of contrast enema in neonates need to be carefully considered, and when necessary, thyroid function should be monitored, especially in very premature infants.
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PMID:Severe hypothyroidism after contrast enema in premature infants. 1861 40

The objective of the present study was to elicit opinion from two groups of veterinarians [subject matter experts and non-subject matter experts] about the causes of bovine perinatal mortality and the criteria used to assign such causes. The subject matter experts were selected on the basis of their scientific publications or experience of working in a veterinary diagnostic or research laboratory in the area of bovine perinatal mortality. The non-subject matter experts were self-selected as cattle veterinarians without particular expertise in bovine perinatology. A total of 74 veterinarians (46 subject matter experts and 28 non-subject matter experts) from 23 countries responded. The study was conducted using Delphi methodology over seven rounds. Respondents were asked to agree the causes of bovine perinatal mortality and for each cause to agree the supporting diagnostic criteria. There was a close agreement between groups on 16 causes of death apart from intra-uterine growth retardation (IUGR) and micronutrient imbalances which were accepted by fewer subject matter experts. There was inter-group consensus on the criteria to diagnose accidents, congenital defects, dystocia, hyperthermia, infections, premature placental separation, prematurity and prolonged calving. There was inter-group consensus on the criteria to diagnose anoxia, apart from gingival cyanosis; on haemorrhage, apart from haemorrhagic anaemia; on IUGR, apart from organ weights; and on iodine imbalance, apart from goitre and thyroid iodine content. The results from this study highlighted the current lack of standardization of the criteria used to define the cause of death for bovine perinatal mortality and the need for such standardization.
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PMID:An international delphi study of the causes of death and the criteria used to assign cause of death in bovine perinatal mortality. 2328 77