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11/95. Early dialysis in a neonate with intrauterine lisinopril exposure.

    In general, angiotensin converting enzyme (ACE) inhibitors should be discontinued in pregnancy, as they can induce an ACE fetopathy. For the treatment of the latter, early peritoneal dialysis is recommended for in utero exposure to captopril and enalapril, although the outcome is poor. Early peritoneal dialysis has not previously been reported for lisinopril induced multiorgan failure. A case is reported in which treatment was given on postnatal day 3. The patient recovered from oligoanuria to almost normal renal function, and heart, brain, and musculoskeletal injury was reversible. This is despite relatively poor clearance of the drug through peritoneal dialysis. Analysis of the pharmacokinetic data suggests that haemodialysis or haemofiltration would be more efficacious for removal of the drug, and these treatments should be performed if available.
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12/95. Fatal double aortic arch anomaly and maternal cocaine abuse.

    We report a case of 2 months old female (born to a cocaine abuser mother) having respiratory dysfunction attributed to pneumonia. autopsy, following a sudden, unexpected death, revealed a double aortic arch which was compressing the trachea and the esophagus. health care professionals should conduct a detailed cardiac assessment on all cocaine-exposed infants at the time of birth and during infancy. Double aortic arch should be considered as a possible complication of intrauterine cocaine exposure and may present as sudden death.
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13/95. carbimazole-related gastroschisis.

    OBJECTIVE: To report a case of gastroschisis in a newborn secondary to carbimazole exposure in utero. CASE SUMMARY: A 25-year-old white woman was treated for graves disease with carbimazole throughout pregnancy. A boy was born prematurely by vaginal delivery, with a gastroschisis without associated malformative syndrome. death occurred in the 25th hour of life after surgical repair. DISCUSSION: carbimazole is completely metabolized to methimazole after absorption. carbimazole or methimazole intake during pregnancy has been associated with an increased incidence of scalp aplasia. abdominal wall defects secondary to carbimazole or methimazole exposure in utero seem to be a rare occurrence. However, other cases of abdominal wall defects have been reported in 4 newborns, 2 of them associated with scalp aplasia. An objective causality assessment revealed that the relationship between the gastroschisis and the exposure to carbimazole in utero was possible. CONCLUSIONS: It is important to emphasize the possible risk of abdominal wall defects in newborns to pregnant women taking carbimazole or methimazole.
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14/95. Assessment of visual functions following prenatal exposure to organic solvents.

    Prenatal exposure to organic solvents has been previously associated with increased risk of color vision deficits and reduced visual acuity in young children. These findings prompted us to evaluate visual functioning in solvent-exposed infants using more sensitive non-invasive visual evoked potential (VEP) techniques. VEP techniques are described in the context of an ongoing prospective longitudinal cohort study of infants exposed to organic solvents in utero. VEPs are recorded via three active electrodes fitted over the occipital cortex while infants view changing visual stimuli. The sweep VEP is used to assess contrast detection and visual acuity by presenting sinusoidal gratings that "sweep" across a range of contrasts and spatial frequencies. Transient VEPs are used to assess responses to equiluminant chromatic- and luminance-modulated sinusoidal gratings presented in pattern onset-offset format. A single case study is presented showing abnormal chromatic responses and reduced contrast sensitivity in a 2.5-year-old boy following prenatal exposure to perchloroethylene (PCE). These VEP techniques therefore appear promising for the clinical assessment of visual toxicity in pediatric populations.
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15/95. Ovarian carcinoma in an adolescent with transgenerational exposure to diethylstilbestrol.

    Small cell carcinoma of the ovary is rare in adolescence. The etiology of such tumors is unknown. Several reports suggest that transgenerational exposure to diethylstilbestrol (DES) may have deleterious effects on the genitourinary tract. The authors describe a 15-year-old girl with small cell carcinoma of the ovary whose maternal grandmother had been taking DES while she was pregnant with the patient's mother. This case, while anecdotal, suggests that a transgenerational history of DES exposure should be noted, and that granddaughters with persistent abdominal pain even during childhood may need evaluation for genital tract abnormalities.
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16/95. Hypothalamic-pituitary-adrenal axis function in premature neonates after extensive prenatal treatment with betamethasone: a case history.

    Tests of hypothalamic-pituitary-adrenal axis function were performed on a set of 32-weeks' gestation triplets whose mother received 16 injections of betamethasone over 8 weeks prior to delivery to induce fetal lung maturation. The purpose of these studies was to determine if clinically significant suppression of fetal adrenocortical function occurred as a result of this repeated and prolonged prenatal exposure to glucocorticoids. serum cortisol levels were measured on cord blood from each patient. Morning serum cortisol and 11-deoxycortisol levels were measured before and after an oral dose of metyrapone given at midnight on day 5. All three infants were clinically well at birth and had no evidence of hyaline membrane disease. Cord blood cortisol levels were low in each infant (1.97 /- 0.25 micrograms/dl). By day 5, morning cortisol levels had become normal for each infant (10.77 /- 2.42 micrograms/dl). Following the metyrapone dose, the 11-deoxycortisol levels rose 10- to 20-fold for each infant, indicating normal function of the hypothalamic-pituitary-adrenal axis by day 6. Adrenocortical suppression following multiple courses of prenatal betamethasone appears to be similar in degree and duration to that reported following brief antenatal therapy with this medication. Further studies are needed to confirm these anecdotal observations.
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17/95. Multiple congenital malformations including generalized hypertrichosis with gum hypertrophy in a child exposed to valproic acid in utero.

    Fetal valproate syndrome results from in utero exposure to valproic acid. It is characterized by a distinctive facial appearence, a cluster of minor and major anomalies, and central nervous system dysfunction. We report on a child exposed prenatally to valproic acid with unusual anomalies. This patient was the first child of young parents. Mother had several generalized seizures one year before this pregnancy, and since than she took valproic acid. pregnancy was otherwise uneventful. At birth physical examination showed generalized hypertrichosis sparing palms and soles, coarse face, gum hypertrophy, hypotonia, club feet and club hands, two annular constrictions of the right lower leg, and abnormal dermatoglyphics. Skeletal x-rays were normal. Gum hypertrophy and hypertrichosis may be part of a broader pattern of altered morphogenesis in fetus exposed to valproic acid or this patient had two conditions, fetal valproate syndrome and hypertrichosis with gum fibromatosis.
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18/95. In utero exposure to nonsteroidal anti-inflammatory drugs: neonatal renal failure.

    We report a case of neonatal transient renal failure after maternal ingestion of diclofenac, paracetamol, and nimesulide during pregnancy. The baby girl was delivered at the 33 weeks gestation for complete absence of amniotic fluid. Acute renal failure was present. urine output started 12 h after birth, increasing to polyuria on day 6, and then decreasing gradually to normal values. serum creatinine normalized on day 6. Several cases of severe and sometimes irreversible renal problems have been described in neonates exposed to indomethacin, a non-selective cyclooxgenase (COX) inhibitor, during their fetal life. More recently, the use of nimesulide, a selective COX-2 inhibitor, as a tocolytic agent has been advocated. Although it is difficult to ascribe the observed side effects to one specific drug in our patient, using the Naranjo ADR probability scale, renal failure was probably related to nimesulide exposure. Paracetamol is considered safe at therapeutic doses, and there are no reports of prenatal diclofenac toxicity. However, recently there have been some reports of neonatal renal failure associated with maternal nimesulide consumption and probably modulated by genetic factors. Hence, cautious use of nimesulide during pregnancy must be advocated.
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19/95. Limb reduction defects in the first generation and deafness in the second generation of intrauterine exposed fetuses to diethylstilbestrol.

    Maternal treatment with diethylstilbestrol (DES) during pregnancy can produce vaginal adenocarcinoma and other abnormalities of the vagina in her daughters when they reach adolescence or adulthood, miscarriages and absence of full term infants. Concerning malformations in newborns whose mothers were treated with DES, clitoromegaly and malformations of the uterus were reported in females and genital lesions in males. However, the frequencies of major congenital anomalies were not greater than expected. We report three cases of limb reduction defects (LRD) in the first generation of children whose mothers were treated with DES during pregnancy, and two children (one male, one female) with deafness in the second generation after intrauterine exposure to DES. The LRD were not associated with other congenital anomalies. The malformed children with LRD were born between 1965 and 1973. The deafness was also isolated. The two mothers who have no hearing problems and who are healthy were exposed in utero to DES in 1963 and 1965, respectively. Their children were born in 1989 and 1994, respectively. In conclusion, the association of LRD and hearing loss with intrauterine exposure to DES could be coincidental. However, some hypothesis may explain these associations. Congenital hearing loss in the second generation may suggest a transgenerational effect.
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20/95. Binder's syndrome due to prenatal vitamin k deficiency: a theory of pathogenesis.

    There is evidence that vitamin K-deficiency during human pregnancy can be caused by the therapeutic use of warfarin or phenytoin. The pregnancy histories of three cases of Binder's syndrome are reported. One was associated with warfarin exposure, one with phenytoin exposure and one with alcohol abuse. It is proposed that Binder's syndrome can be caused by prenatal exposure to agents that cause vitamin K-deficiency. Sprague-Dawley rats were treated from postnatal day 1 to 12 weeks with daily doses of warfarin (100 mg/kg) and concurrent vitamin K1 (10 mg/kg). This regimen creates a net extra-hepatic vitamin K-deficiency. The treated rats developed with a distinct facial appearance characterized by a markedly reduced snout. Histological examination showed that the normally non-calcified septal cartilage was extensively calcified. It is proposed that normal growth of the septal cartilage is necessary for the development of the profile of the nose and midface and that normal growth will only take place while the septal cartilage is uncalcified.
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