Effect of perinatal asphyxia on thyroid-stimulating hormone and thyroid hormone levels

AIM: To compare serum concentrations of thyroid hormones--T4, T3, free T4 (FT4) and reverse T3 (rT3)--and thyroid-stimulating hormone (TSH) found in the umbilical cord blood of term newborns with and without asphyxia and those found in their arterial blood collected between 18 and 24 h after birth. A further aim of the study was to assess the association between severity of hypoxic-ischemic encephalopathy and altered thyroid hormone and TSH levels, and between mortality and FT4 levels in the arterial blood of newborns between 18 and 24 h of life. METHODS: A case-control study was carried out. The case group comprised 17 term newborns (Apgar score < or = 3 and < or = 5 at the first and fifth minutes; umbilical cord blood pH < or = 7.15) who required bag and mask ventilation for at least one minute immediately after birth. The control group consisted of 17 normal, term newborns (Apgar score > or = 8 and > or = 9 at the first and fifth minutes; umbilical cord blood pH > or = 7.2). Cord blood and arterial blood samples were collected immediately after birth and 18 to 24 h after birth, respectively, and were used in the blood gas analysis and to determine serum concentrations of T4, T3, FT4, rT3 and TSH by radioimmunoassay. All newborns were followed-up until hospital discharge or death. RESULTS: Gestational age, birthweight, sex, size for gestational age, mode of delivery and skin color (white and non-white) were similar for both groups. No differences were found in mean levels of cord blood TSH, T4, T3 and FT4 between the groups. In the samples collected 18 to 24 h after birth, mean levels of TSH, T4, T3 and FT4 were significantly lower in the asphyxiated group than in the control group. Mean concentrations of arterial TSH, T4 and T3 between 18 and 24 h of life were lower than concentrations found in the cord blood analysis in asphyxiated newborns, but not in controls. In addition, asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy presented significantly lower mean levels of TSH, T4, T3 and FT4 than those of controls. None of the asphyxiated newborns with FT4 > or = 2.0 ng/dl died; 6 out of the 11 asphyxiated newborns with FT4 < 2.0 ng/dl died. CONCLUSIONS: Serum concentrations of TSH, T4, T3 and FT4 are lower in asphyxiated newborns than in normal newborns between 18 and 24 h of life; this suggests central hypothyroidism secondary to asphyxia. Asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy present a greater involvement of the thyroid function and consequently a greater risk of death.     

Interleukin-6 and tumor necrosis factor-alpha levels in plasma and cerebrospinal fluid of term newborn infants with hypoxic-ischemic encephalopathy

OBJECTIVES: To determine plasma and cerebrospinal fluid (CSF) levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in hypoxic-ischemic encephalopathy (HIE). STUDY DESIGN: A controlled, prospective study of 20 control neonates, 19 term newborn infants presenting with sepsis and no meningitis, and 19 asphyxiated term newborn infants. Blood and CSF samples were collected within 48 hours of birth for IL-6 and TNF-alpha determinations. RESULTS: Median plasma IL-6 was similar in sepsis and asphyxia but significantly higher than in control neonates. Median plasma TNF-alpha was similar in asphyxia and control neonates but significantly lower than in sepsis. In asphyxiated newborn infants, median CSF IL-6 and TNF-alpha were significantly higher than in sepsis and control neonates. Median CSF IL-6 was significantly higher in sepsis than in control neonates. Median CSF TNF-alpha was similar in newborn infants with sepsis and control neonates. IL-6 and TNF-alpha CSF/plasma ratios were similar in newborn infants with sepsis and control neonates but lower than in asphyxiated newborn infants. CONCLUSIONS: Term newborn infants with HIE have elevated CSF IL-6 and TNF-alpha levels. Plasma IL-6 is increased in asphyxia and sepsis. Plasma TNF-alpha is increased only in sepsis. High IL-6 and TNF-alpha CSF/plasma ratios in asphyxia suggest that these cytokines are produced in the brain of term newborn infants with HIE.     

新生儿窒息复苏首选纯氧还是空气的Meta分析

目的收集现有比较采用空气或者纯氧复苏窒息新生儿效果的临床文献,对其进行系统评价,试图寻找比较合理的新生儿复苏气源。方法检索在美国医学索引（MEDLINE）,荷兰医学文摘（EMBASE）,中国生物医学文摘（CBMA）及Cochrane图书馆（CL）上收录的自1966年1月至2005年6月,有关窒息新生儿复苏气源比较的文献,对符合纳入要求的文献进行系统评价,比较空气或者纯氧作为复苏气源在窒息新生儿病死率,缺氧缺血性脑病发生率,以及复苏失败率等方面内容。结果6篇文献符合纳入标准,共包括1940个窒息新生儿,其中采用空气复苏窒息新生儿988个,采用纯氧复苏窒息新生儿952个。对上述内容进行系统评价,得出采用空气复苏窒息新生儿病死率8．7％,与采用纯氧复苏窒息新生儿病死率13．4％比较,两者差异有显著统计学意义（P〈0．001）。OR为0．64,其95％可信区间（95％confidence interval,95％CI）为0．44-0．94。我们对其中5篇文献的窒息足月儿和窒息早产儿病死率进行分层系统评价,得出空气复苏窒息足月新生儿病死率5．9％,与纯氧复苏9．8％比较,两者差异有显著统计学意义（P〈0．001）,两者OR为0．59,其95％CI为0．40-0．87,在对窒息早产新生儿病死率的分析中也得到相似结果。空气或者纯氧复苏后窒息新生儿的其他情况如2-3度缺氧缺血性脑病（hypoxia ischemia encephalopathy,HIE）的发生率,复苏失败率等,两组比较差异无统计学意义（P〉0．05）。结论进行窒息新生儿复苏,空气和纯氧比,空气能降低窒息新生儿病死率,且不增加新生儿2-3度的HIE发生率和复苏失败率。但研究纳入文献的数量有限,对此结论的运用和推广仍应谨慎。     

Initial treatment dose of L-thyroxine in congenital hypothyroidism

OBJECTIVES: To determine the optimal initial treatment dose of L-thyroxine in congenital hypothyroidism (CH) by evaluating the time course of rise of thyroxine (T(4)) and free T(4) concentrations into an established "target range" and normalization of thyroid-stimulating hormone (TSH) and to reevaluate the "target range" for T(4) and free T(4) concentrations during the first 2 weeks of CH treatment. STUDY DESIGN: Infants of birth weight 3 to 4 kg with CH (n = 47) detected by newborn screening were randomly assigned into three L-thyroxine treatment dose arms: 37.5 microg/day (group 1); 62.5 microg/day for 3 days, then 37.5 microg/day (group 2); and 50 microg/day (group 3). Serum T(4), free T(4), triiodothyronine (T(3)), free T(3), and TSH were measured before treatment and at 3 days and 1, 2, 4, 8, and 12 weeks after treatment. RESULTS: T(4) and free T(4) concentrations increased into the target range (10 to 16 microg/dL) by 3 days of therapy in infants in groups 2 and 3 and by 1 week in group 1; 50 microg/day (average 14.5 microg/kg/day) provided the most rapid normalization of TSH by 2 weeks. With the use of linear regression analysis of T(4) versus TSH or free T(4) versus TSH plots, the intercept at the lower range of normal for TSH (1.7 mU/L) showed T(4) = 19.5 microg/dL and free T(4) = 5.23 ng/dL. CONCLUSIONS: Initial dosing of 50 microg/day (12-17 microg/kg per day) raised serum T(4) and free T(4) concentrations to target range by 3 days and normalized TSH by 2 weeks of therapy. We recommend consideration of a somewhat higher "target range" of 10 to 18 microg/dL for T(4) and 2 to 5.0 ng/dL for free T(4) during the first 2 weeks of L-thyroxine treatment. After 2 weeks of treatment, the target range drops to 10 to 16 microg/dL for T(4) and 1.6 to 2.2 for free T(4).     

Early cranial ultrasound changes as predictors of outcome during first year of life in term infants with perinatal asphyxia

OBJECTIVES: To identify the types of early cranial ultrasound changes that were significant predictors of adverse outcome during the first year of life in asphyxiated term infants. METHODOLOGY: This was a prospective cohort study. Shortly after birth, cranial ultrasonography was carried out via the anterior fontanelles of 70 normal control infants and 104 asphyxiated infants with a history of fetal distress and Apgar scores of less than 6 at 1 and 5 min of life, or requiring endotracheal intubation and manual intermittent positive pressure ventilation for at least 5 min after birth. Neurodevelopmental assessment was carried out on the survivors at 1 year of age. RESULTS: Abnormal cranial ultrasound changes were detected in a significantly higher proportion (79.8%, or n = 83) of asphyxiated infants than controls (39.5%, or n = 30) (P < 0.0001). However, logistic regression analysis showed that only three factors were significantly associated with adverse outcome at 1 year of life among the asphyxiated infants. These were: (i) decreasing birthweight (for every additional gram of increase in birthweight, adjusted odds ratio (OR) = 0.999, 95% confidence interval (CI) 0.998, 1.000; P = 0.047); (ii) a history of receiving ventilatory support during the neonatal period (adjusted OR = 8.3; 95%CI 2.4, 28.9; P = 0.0009); and (iii) hypoxic-ischaemic encephalopathy stage 2 or 3 (adjusted OR = 5.8; 95%CI 1.8, 18.6; P = 0.003). None of the early cranial ultrasound changes was a significant predictor. CONCLUSIONS: Early cranial ultrasound findings, although common in asphyxiated infants, were not significant predictors of adverse outcome during the first year of life in asphyxiated term infants.     

Significance of transient postnatal hypothyroxinemia in premature infants with and without respiratory distress syndrome

The significance of relatively low thyroxine (T4) levels in preterm infants with and without respiratory distress syndrome (RDS) was assessed by evaluating the free T4 level, the thyrotropin (TSH) response to thyrotropin releasing hormone (TRH), and intellectual development in infants less than or equal to 35 weeks with cord blood T4 concentrations less than 6.5 microgram/100 ml. Fifty-four (19 well, 28 with RDS, and seven without RDS and sick) of 215 premature infants (25%) and 27 of 8,831 term infants (0.3%) had cord T4 levels less than 6.5 microgram/100 ml. Serum T4 levels were measured in 39 surviving preterm infants (20 RDS and 19 well) during the first 5 days of life and at 2, 4, 24, and 52 weeks postnatally. Serum total T4 level during the first week was 4.5 +/- 0.3 microgram/100 ml (mean +/- SEM). Free T4 levels ranged from 1.1 to 2.2 ng/100 ml (normal adult range 0.8 to 2.3 ng/100 ml). Administration of TRH resulted in a clear increase in both TSH and T4 levels in all infants. T4 levels increased significantly (r = .70, P less than .01) with increasing postnatal age, reaching stable levels by 6 to 7 weeks. Developmental quotients obtained in the infants with low T4 levels were no different from those found in a matched control population at 12 months of age. The low T4, free T4, and TSH concentrations and normal TSH responses to TRH found in these infants are characteristic of hypothalamic (tertiary) hypothyroidism, but differ from classic tertiary hypothyroidism in that the disorder was transient. The normal intellectual development at 12 months of age and the spontaneous increase in T4 levels that occurs over the first six weeks of life suggest that the low T4 levels in these infants reflect a benign relative delay in maturation of hypothalamic-pituitary-thyroid control.     

Comparison of serum cardiac troponin T and creatine kinase MB isoenzyme mass concentrations in asphyxiated term infants during the first 48 h of life

OBJECTIVE: This prospective study aimed to compare serum creatine kinase MB isoenzyme (CK-MB) mass concentrations and cardiac troponin T (cTnT) concentrations during the first 48 h of life in asphyxiated term infants. METHODS: Serum cTnT and CK-MB mass concentrations of 50 term infants with clinical features of perinatal asphyxia were measured at birth and at 12, 24 and 48 h of age by chemiluminescence immunoassay. These infants were followed up until discharge or death. Cord blood CK-MB and cTnT concentrations of 50 healthy term infants were also assayed. RESULTS: At birth, asphyxiated infants had significantly higher concentrations of cTnT and CK-MB than controls (P < 0.0001). Serum cTnT of asphyxiated infants with low ejection fraction <60% was significantly higher at 12 and 24 h than those with normal ejection fraction (P < 0.05). Asphyxiated infants with congestive cardiac failure had significantly higher serum cTnT concentration during the first 48 h of life than those without congestive cardiac failure (P or= 0.1). CONCLUSION: Unlike CK-MB, serum cTnT concentrations are significantly higher in asphyxiated infants who die or develop cardiac dysfunction.     

Plasma thyroid hormones and prolactin in premature infants and their mothers after prenatal treatment with thyrotropin-releasing hormone.

We assayed TSH, triiodothyronine, free thyroxine, and prolactin (PRL) in plasma of women and infants participating in a trial of prenatal thyrotropin-releasing hormone (TRH) treatment for prevention of newborn lung disease. Women in labor at 26-34 wk of gestation received 400 micrograms of TRH i.v. every 8 h (one to four doses) plus 12 mg betamethasone (one or two doses); controls received saline plus betamethasone. Mean cord concentrations in control infants were TSH 9.7 mU/L, triiodothyronine 0.6 nmol/L (40.2 ng/dL), free thyroxine 14.4 pmol/L (1.13 ng/dL), and PRL 67.6 micrograms/L. TRH increased maternal plasma TSH by 100% at 2-4 h after treatment and decreased levels by 28-34% at 5-36 h. In cord blood of treated infants delivered at 2-6 h, TSH, triiodothyronine, and PRL were all increased about 2-fold versus control, and free thyroxine was increased 19%; the response was similar after one, two, three, or four doses of TRH. In treated infants delivered at 13-36 h, cord TSH and triiodothyronine levels were decreased 62 and 54%, respectively, and all thyroid hormones were lower after birth at 2 h of age versus control. We conclude that prenatal TRH administration increases thyroid hormones and PRL in preterm fetuses to levels similar to those normally occurring at term. Pituitary-thyroid function is transiently suppressed after treatment to a greater extent in fetus than mother, and infants born during the early phase of suppression do not have the normal postnatal surge in thyroid hormones.     

Thyroid function and dysfunction in premature infants

During the past four decades major advances in the management of premature infants have led to progressive reduction in mortality. During this period mortality in very low birth weight infants (VLBW, <1500 grams and <30 weeks gestation age) has decreased, and more than 50% of infants less than 24 weeks gestation age now survive, increasing the population of VLBW infants in intensive care nursery environments. Thyroid function in these infants is characterized by decreased TSH and T4 responses to parturition, low serum total T4 and TSH levels and variable free T4 concentrations during the first 2-4 postnatal weeks of life. These features reflect a state of transient hypothalamic-pituitary or central hypothyroidism. There is a high prevalence of morbidity in these infants, as well, often associated with further reductions in serum total T4, T3, TBG and TSH concentrations and variable levels of free T4 and reverse T3, resembling the non-thyroidal illness (NTI) syndrome in adults. The etiologic roles of thyroid system immaturity and NTI in the transient hypothyroxinemia of prematurity (THOP) and the impact of THOP on the subsequent neurological deficits in VLBW infants remains unclear. Several thyroxine supplementation trials have been conducted with inconclusive results. Further studies are planned or in progress.     

Troponin-T levels in perinatally asphyxiated infants during the first 15 days of life

Aim: To measure serial cardiac troponin‐T, creatine kinase, creatine kinase‐MB, aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase levels in asphyxiated newborn infants during the first 15 d of life. Methods: Troponin‐T, creatine kinase, creatine kinase‐MB, aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase (LDH) concentrations were measured prospectively in blood samples obtained from 45 asphyxiated and 15 healthy term neonates within the first 2–4 h, third, seventh and 15th days. Results: Infants with severe asphyxia had significantly higher cardiac troponin‐T levels than grade I and II asphyxiated and healthy neonates within the first 2–4 h of life (0.34 ± 0.21 ag/ml vs 0.07 ± 0.03 ag/ml, 0.12 ± 0.07 ag/ml, 0.04 ± 0.02 ag/ml, respectively). Troponin‐T levels remained high on days 3 and 7 in severely asphyxiated neonates. The creatinine kinase‐MB levels were significantly higher in grade II and III asphyxiated neonates than grade I asphyxiated and healthy neonates within the first 2–4 h. No difference was found in creatinine kinase‐MB on day 3. There was cardiac involvement in 12 (80%) newborns of group III on B mode echocardiographic images on day 1. However, no echocardigraphic pathology was found in the seventh‐ and 15th‐day echocardiographic analysis in any groups. Conclusion: Our results suggest that asphyxia‐related cardiac changes were significant but reversible in severely asphyxiated neonates, and troponin T is a good determinant of the degree of injury to the heart within the first week of life. Cardiac troponin T also has a wider diagnostic frame than other diagnostic markers of myocardial damage.     

窒息新生儿血清总胆汁酸、前白蛋白变化及其临床意义探讨

目的探讨窒息时新生儿血清总胆汁酸(TBA)、前白蛋白(PAB)变化及其临床意义。方法检测各30例轻度、重度窒息新生儿及20例缺氧缺血性脑病(HIE)新生儿的(TBA)、(PAB)、丙氨酸转氨酶(ALT)、白蛋白(ALB)水平,并设30例正常新生儿为对照。结果轻度、重度窒息儿和HIE新生儿血清TBA、PAB水平与正常儿比较差异均有非常显著性(P<0.001)窒息时血清TBA、PAB水平与Apgar评分均呈线性相关(r=0.571,-0.689,P<0.001),随病情好转血清TBA和PAB水平逐渐恢复正常。结论血清TBA和PAB是反映窒息儿肝功能损害灵敏的生化指标,动态测定血清TBA和PAB水平变化能很好地、灵敏地反映窒息儿肝脏损害情况及病情转归。     

Thyroid function in healthy premature infants.

Thyroid function was studied in healthy premature and term infants between 12 hours and 3 months of age. T4 and FT4I followed parallel courses in both groups; during the first 45 days, however, the values were significantly lower in premature infants under 34 weeks' EGA than in term infants (P less than 0.001). The post-delivery peak in TSH concentration (mean +/- SD) was 71.8 +/- 19.2 microunits/ml in the premature infants. In five premature infants, injection of TRH elicited a TSH increment of 29.4 +/- 20.7 microunits/ml at 30 minutes. T3 concentration was not significantly different in premature and term infants.     

窒息新生儿凝血功能状态的研究

目的探讨窒息足月、早产新生儿凝血功能的变化。方法检测10例正常儿、44例窒息足月儿、32例窒息早产儿凝血指标。结果与对照组比较,窒息足月儿PT、APTT、FIB、PLT无显著差异,D-D明显升高,且与窒息程度正相关。窒息早产儿与窒息足月儿比较PT、APTT延长,FIB、PLT降低,D-D无明显差异。结论窒息足月儿大都存有高凝为特征的前DIC或DIC早期;窒息早产儿更易发生DIC,且有向低凝期发展的趋势。     

Transient elevation of aldosterone levels in perinatal asphyxia

Abstract We measured plasma aldosterone levels in cord blood and peripheral blood collected 18–24 h after birth in 19 asphyxiated and 19 normal term newborn infants. The asphyxiated newborn infants had significantly higher aldosterone levels in cord blood than the normal newborn infants. At 18–24 h after birth there was no difference between the groups with respect to aldosterone levels. There was a positive significant correlation between aldosterone levels and PCO₂ in cord blood by multiple linear regression analysis. There is a transient elevation of aldosterone levels in perinatal asphyxia.     

Comparison of T4, T3, rT3 and TSH concentrations in cord blood and serum of infants up to 3 months of age

T4, T3, TSH and rT3 concentrations were measured by radioimmunoassay in cord and postnatal (8--94 days of age) serum samples from randomly selected normal newborn infants (Group I). T4 and TSH levels also were determined in cord and postnatal sera from an additional group of apparently healthy infants 8--260 days of age, whose cord serum T4 levels were in the upper or lower 10% of the normal range of values (Group II). Postnatal T4, T3 and TSH concentrations were stable over this age range; there were no significant differences between male and female infant samples. However, there was a significant decrease in serum rT3 concentrations from 8 to 50 days of age. For the Group I infants, there were significant positive correlations between cord serum T4 and postnatal serum T4 levels, cord serum TSH and postnatal serum TSH levels, and cord serum rT3 and postnatal serum rT3 concentrations. For Group II infants, a significant positive correlation was found for cord T4--postnatal T4 serum concentrations.     

The use of L-T4 as liquid solution improves the practicability and individualized dosage in newborns and infants with congenital hypothyroidism

Dosage recommendations for the initial therapy of congenital hypothyroidism (CH) in newborns vary between 8 microg/kg/d and 10-15 microg/kg/d. AIM: To evaluate the practicability of LT4 in liquid form and to define the initial dosage for optimal treatment. METHODS: Liquid LT4 solution was administered to 28 consecutive newborns with primary CH. We measured TSH, T3, T4, free T3 and free T4 before therapy and during follow-up up to 2 years. After 2 years a standardized developmental test (Griffith) was performed. RESULTS: The median dosage at start of therapy was 12.3 microg LT4/kg/d and decreased to about 5 microg LT4/kg/d after 9 months. The median time of normalization of TSH (< or =6 mU/l) was 2 weeks. In 21 patients, who received a median starting dosage of 12.7 microg LT4/kg (range 9.8-17.1 microg/kg), TSH levels normalized within a median of 1 week. Seven patients receiving only 10.1 microg LT4/kg normalized their TSH only after a median of 2 months. CONCLUSIONS: Newborns with CH should normalize their TSH within 1-2 weeks. The initial dose necessary to normalize TSH is not lower when a liquid solution is used. The higher dose used in tablets is not due to inefficient absorption, but rather reflects the increased demand for thyroid hormone in the first weeks of life.     

Congenital hypothyroidism with delayed rise in serum TSH missed on newborn screening

We report on a female patient with congenital hypothyroidism (CH) missed on a newborn screening test. She is now 10 years old with retarded development. The patient was born premature at 34 weeks of gestation with birth-weight of 1515 g, and was judged to be normal in the screening programme of Niigata Prefecture. However, she gradually suffered from poor weight gain and retarded development with stridor at breathing. Serum thyroid stimulating hormone (TSH) levels were rechecked and showed high values with normal T3 and T4 levels. She was referred to our hospital at the age of 13 months. She was diagnosed as having CH (ectopic thyroid) with a delayed rise in blood TSH concentration, probably due to the prematurity of the hypothalamic-pituitary-thyroid axis. l -thyroxine therapy brought a decline in TSH levels with partial improvement of her symptoms. Regardless of the result of newborn screening, infants with elevated serum TSH levels should be carefully examined for possible CH, even when T3, T4 and free T4 values are in the normal range.     

Periodontal disease in pregnancy and low birth weight

OBJECTIVE: Recently, it has been suggested that periodontal disease during pregnancy could have a causal relationship with low weight at birth. Our objective was to evaluate the influence of periodontal disease during pregnancy on the birth weight of newborn infants. METHODS: Mothers who gave birth to low-birth-weight infants were randomly selected (Group 1 - G1; n=13). Immediately after inclusion of each mother in group 1, the mother of the next term newborn with birth weight of > 2,500 g (Group 2 - G2; n=13) was included as control. Mothers were examined by a periodontist who was not informed of the group the child belonged to. A probe was used to measure attachment loss of the alveolar bone. The extension index (EI) and severity index (SI) of the periodontal disease were determined. RESULTS: Both groups of mothers were similar in terms of maternal age, parity, color of skin, height, nutrition, smoking, drinking, socioeconomic status, prenatal examinations, premature rupture of membranes, chorioamnionitis, bacteriuria, placenta previa, abruptio placentae, previous hypertensive disease, preeclampsia, and heart disease. The characteristics of the newborns were: birth weight - G1 = 1,804 -/+ 675 g x G2 = 3,030 -/+ 516 g; gestational age - G1 = 33 -/+ 5 weeks x G2 = 39 -/+ 2 weeks; length of stay in the neonatal intensive care unit (NICU) - G1 = 128 days x G2 = 0 days. Average EI: G1 = 89.788 -/+ 18.355 x G2 = 72.420 -/+ 20.717; p=0.033. Average SI: G1 = 1.377 -/+ 0.626 x G2 = 0.754 -/+ 0.413 (OR=18.3; CI95%: 2.5-133.3; p = 0.006). After adjustment for risk factors for low birth weight, such as smoking, maternal height, bacteriuria, and previous hypertension, the odds ratio for SI dropped to 7.2 (CI95% = 0.4-125.4; P = 0.176). CONCLUSION: The multivariate analysis indicated a marked association between periodontal disease measured by SI score and low birth weight. Our data suggested that periodontal disease during pregnancy may be a risk factor for low weight at birth.     

Efficacy of congenital hypothyroidism neonatal screening in preterms less than 32 weeks of gestational age: more evidence

OBJECTIVE: To evaluate the double screening performed for congenital hypothyroidism (CH) to preterm infants <32 weeks of gestational age (GA) between 1994 and 2003. INFANTS AND METHODS: TSH was assessed by IFMA. Infants were classified as: term (T) (>37 weeks GA); preterm (PT) (33-37 weeks GA); and very preterm (VPT) (< or =32 weeks GA). RESULTS: In 585,221 screened infants, CH was confirmed in 228 T, 23 PT and seven VPT. An increasing incidence of CH was found with decreasing GA, affecting 1:1,603 PT and 1:585 VPT. PT infants had 1.5 times more risk than full-term infants of suffering CH, and VPT 4 times more. Only 4/7 affected VPT had an adequate double screening as requested. Three had elevated TSH values in the first sample and in one a normal TSH (10.3 mIU/l) at 3 days rose to 240 mIU/l after day 15. In the remaining three VPT, TSH in the unique filter paper sample (21 to 34 days) was markedly elevated. CONCLUSIONS: Our findings reinforce the need for awareness in neonatal settings for adequate screening of VPT infants. Screening in the first week of life was effective in detection of most but not all affected VPT. Larger studies are needed in order to establish accurate screening recommendations for VPT newborns. Until this step is reached, repeated screening is advised in these infants.     

Influence of body temperature on thyrotropic hormone release and lipolysis in the newborn infant

The present study investigated possible interactions between body temperature, lipolysis and thyrotropin (TSH), the only hormone with a documented lipolytic effect in vitro in newborn infants. Healthy infants were either nursed in the usual way ( n = 18) or protected from a decrease in body temperature ( n = 17) during the first postnatal hour. The infants'axillary temperatures were measured immediately after birth and after 10 and 60 min. Blood samples were collected from the umbilical vein and from the infants 10 and 60 min after birth for analysis of TSH, glycerol, free fatty acids, 3-OH-butyric acid and glucose. We found that the mean (±SD) infant axillary temperature was 37.6 ± 0.4^oC immediately after birth. In the routinely nursed infants, body temperature decreased to 37.0 ± 0.5^oC at 10 min ( p = 0.01) and to 36.6 ± 0.4^oC at 60 min ( p = 0.01); the cold-protected infants maintained their fetal temperature at 60 min of age. There was a four-fold increase in plasma TSH levels at 10 min, independent of the infant's body temperature, and the hormone level remained invariably high at 60 min. Plasma glycerol levels increased progressively at 10 min ( p = 0.01) and 60 min ( p = 0.01) in both infant groups, but were higher ( p = 0.02) in the routinely nursed infants at 60 min. No significant relationship was found between TSH and glycerol levels. Infant body temperature did not affect the levels of free fatty acids, 3-OH-butyric acid or glucose. We conclude that the change in environmental temperature as a result of extrauterine adaptation causes thermal stimulation of the infant's body surface which leads to activation of the hypothalamic-pituitary TSH axis, resulting in maximal TSH release, and thus to induction of the lipolytic process. A decrease in body temperature may be an additive stimulus for further enhancement of lipolysis.