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1/10. Multimodal cancer chemotherapy during the first and second trimester of pregnancy: a case report.

    This paper reports treatment with combined chemotherapy during pregnancy. A 39-year-old woman with breast cancer was given adjuvant chemotherapy including cyclophosphamide, methotrexate and 6-fluorouracil from the 6th to the 24th week of gestation. The possibility of teratogenic effects on the fetus was explained to the patient however she refused to terminate the pregnancy. A 30-week male infant with only a minor malformation was delivered. The authors reviewed the literature regarding chemotherapeutic agents given during the first trimester of pregnancy. Most cytotoxic drugs have teratogenic effects on experimental animal subjects. However, actual data on human fetuses are sparse because of the variety of therapeutic regimens and the rarity of administering chemotherapy during pregnancy. The long-term effects of exposure to cytotoxic drugs in utero, needs further research.
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2/10. Humeroradial synostosis, ulnar aplasia and oligodactyly, with contralateral amelia, in a child with prenatal cocaine exposure.

    Humeral "bifurcation" due to humeroradial synostosis, and amelia are both very rare limb anomalies. We report on a Canadian. Aboriginal boy with both these limb deficiencies. The family history was unremarkable, but he was exposed prenatally to cocaine at the time of limb development. Humeroradial synostosis with ulnar aplasia has been reported by several authors. The majority of cases are unilateral. When both upper limbs arms are involved, cases with oligodactyly often have asymmetrical limb deficiencies and have all been sporadic to date. Some appear to represent cases of the femur-fibula-ulna or FFU complex. Affected individuals with normal hands usually have symmetrical defects and show an autosomal recessive pattern of inheritance. Limb deficiencies have been reported in several infants exposed prenatally to cocaine and have been inducible in animal models. Most are terminal transverse defects or deficiencies of middle digits. When more than one limb is involved, the defects are usually asymmetric. Our case appears to be one of the most severely affected children reported to date.
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3/10. Cardiovascular anomalies associated with prenatal exposure to theophylline.

    theophylline has been shown to be a potent cardiovascular teratogen in animals, but there has been no evidence linking theophylline with congenital anomalies in infants. The cardiovascular anomalies in our three patients were aortic anomalies, double-outlet right ventricle, transposition of the great arteries, total anomalous pulmonary venous connection, and hypoplasia of the left ventricle. Some of these rare defects were also induced frequently in animal experiments with theophylline, which suggests that this drug can be a cardiovascular teratogen in a susceptible human fetus.
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4/10. oligohydramnios sequence and renal tubular malformation associated with maternal enalapril use.

    We present the case of a child who died of pulmonary hypoplasia as a result of the oligohydramnios sequence. The mother was taking enalapril, as well as propranolol and hydrochlorothiazide, for treatment of hypertension associated with systemic lupus erythematosus. autopsy examination revealed severe renal tubular malformation. Correlation of animal data with previous case reports of neonatal anuria in association with maternal angiotensin converting enzyme inhibitors suggests that these agents may have a deleterious effect on fetal renal development and general well-being.
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5/10. The persistent threat of lead: medical and sociological issues.

    Lead exposure is an ancient malady. Its history serves as a useful paradigm through which to understand many other pollutants that our technological society has inserted into the human environment and may guide preventive steps for other agents. lead poisoning was first recognized in workers exposed to high doses. The discovery of childhood toxicity occurred a century ago in australia, when children with striking symptoms of paralysis, ophthalmoplegia, or meningitis were found to be highly lead exposed. Encephalopathy generally occurs at blood lead levels of 80 micrograms/dL or more, but unequivocal brain damage has been demonstrated at doses well below this level. At lower doses, the neurocognitive effects of lead are expressed as diminished psychometric intelligence, attention deficits, conduct problems, alterations in the electroencephalogram, school failure, and increased referral rates for special needs. Careful epidemiologic studies, which have controlled for the important confounders, have set the effect level at 10-15 micrograms/dL. Elegant animal studies in which confounding is not an issue have confirmed these findings. Although blood lead levels in the population have dropped over time for a number of reasons, there are some 3-4 million American children with blood lead levels of more than 15 micrograms/dL. Biochemical and functional changes have been demonstrated in the heme biosynthetic pathway and in the renal, cardiovascular, endocrine, immune, and nervous systems. The threshold for effect depends on the sensitivity of the methods used. A no-effect level has not been found. Further, this is not a disease of the poor alone. But the poor are exposed to much more lead than are the more economically favored. Deficiencies in body calcium, zinc, iron, and protein stores are associated with increased uptake. Optimizing nutrition enhances the resistance to lead. All children should be screened for lead at regular intervals, especially those with anemia, growth failure, and developmental or behavioral problems. Treatment protocols are well worked out, but chelation is only part of the therapy. Controlling the environment, strengthening the family's supports, enhancing nutrition, and offering remedial education are essential to a successful therapeutic outcome. Lead control has involved a continuing struggle between vested economic interests and regulatory agencies. In one area, the control of airbone lead, science, and public health have prevailed. In the past decade, the amount of alkyl lead consumed in gasoline additives has been reduced by 99%. Body lead burdens have dropped in close correspondence.(ABSTRACT TRUNCATED AT 400 WORDS)
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6/10. Teratogenicity and carcinogenicity in a twin exposed in utero to cyclophosphamide.

    A 29-year-old pregnant woman diagnosed with acute lymphocytic leukemia maintained remission with daily cyclophosphamide and intermittent prednisone treatment. She delivered a male twin with multiple congenital abnormalities who was diagnosed with papillary thyroid cancer at 11 years of age and stage III neuroblastoma at 14 years of age. The female twin was unaffected and has exhibited normal development to date. First trimester exposure to cyclophosphamide has been associated with major malformations. Metabolites of cyclophosphamide have been demonstrated to be teratogens and carcinogens in animals. Differences in placental or fetal hepatic cytochrome P-450 may account for the variability in response between the twins. In addition, disparity between the twins may be the result of differences in metabolite inactivating enzymes present either in fetal liver or placenta. The risk of second malignancies caused by alkylating agents such as cyclophosphamide has been well documented in adults and children but to the best of our knowledge this is the first description of transplacental second cancer.
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7/10. holoprosencephaly and trisomy 13 in a fetus with maternal early gestational amphetamine abuse--a case report.

    We report a congenital anomalous fetus with holoprosencephaly, prenatally diagnosed by sonography and MR scan at the twenty-sixth week during the gestational period. Chromosome analysis by amniocentesis revealed trisomy 13 (47,XY, 13). The diagnosis was confirmed by autopsy. After induction, external examination showed a proboscis-like nose on the normal nose position. The right foot showed polydactylia with wide separation of the fifth and sixth toes. We found that the mother was an abuser of amphetamine at an early gestational age. The teratogenic effect of D-amphetamine on animals has been noted, but no previous clinical case of a congenital anomalous fetus and maternal abuse of amphetamine has been reported. This case report is the first to reveal holoprosencephaly and trisomy 13, with maternal early gestational abuse of amphetamine.
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8/10. Development of the eye after gestational exposure to cocaine. Vascular disruption in the retina of rats and humans.

    Clinical and basic research in the area of drugs of abuse are of utmost importance since they provide the necessary background for health programs in one of the main problems of contemporary society. The available data in this field demonstrate that acute, subacute and/or chronic abuse of illicit drugs, e.g., cocaine, alters the neurochemistry and functioning of the neural circuitries. Although recent works demonstrated that the visual system is lesioned after exposure to cocaine during the active periods of development, no studies have provided detailed information on the effects of these substances on the development of this sensory system. The present paper will report: 1) the vulnerability of the developing visual system to gestational exposure to cocaine; 2) the effects of cocaine in the visual system during the more active periods of development in humans and, as far as possible, the establishment of homologies with animal models where exposure is made in corresponding periods of human gestation, and 3) the characterization of the vascular disruption caused by ischemic/hypoxic mechanisms. The clinical study focused the ophthalmologic evaluation of newborns exposed in utero to illicit drugs. Newborns exposed to cocaine in utero showed marked vascular disruption in the retina: superficial and deep hemorrhages that, although morphologically similar to neonatal retinal hemorrhages, presented a longer reabsorption time when compared with the neonatal hemorrhagic lesions due to birth trauma in the general population. Prolonged eyelid edema was also a prominent finding. The animal study was conducted in Wistar rats exposed prenatally (gestational days 8 to 22) and postnatally (postnatal days 1-6, 1-13 and 1-29) to 60 mg/kg body weight/day and 15 mg/kg body weight/day, respectively, to cocaine hydrochloride administered subcutaneously; control groups included pair-feeding during the same experimental periods. Similar alterations to those observed in the newborns where exposure to cocaine was affirmative, were found: intraretinal hemorrhages allied to signs of chronic ischemia both in the outer retina-photoreceptor rosettes and in the inner retina-epiretinal glial membranes. Taking into consideration that the visual system is one of the more important sensory systems, the identification and characterization of these alterations, the similarity between animal and human findings, and their relation with cocaine per se, can provide a sound data base for illicit drug prevention programs.
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9/10. Severe cervical dysplasia and nasal cartilage calcification following prenatal warfarin exposure.

    We present an infant who was exposed to warfarin throughout pregnancy and has warfarin embryopathy. When the child was examined radiologically at 20 months areas of calcification were visible in the septal and alar cartilages of the small external part of the nose. The location of this ectopic calcification is consistent with that seen in an animal model of the warfarin embryopathy. It supports the hypothesis that warfarin interferes with the prenatal growth of the cartilaginous nasal septum by inhibiting the normal formation of a vitamin k-dependent protein that prevents calcification of cartilage. The child also had severe abnormalities of the cervical vertebrae and secondary damage to the spinal cord. Cervical vertebral anomalies are a relatively common finding in the warfarin embryopathy and in the related Binder syndrome.
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10/10. The Cantrell-sequence: a result of maternal exposure to aminopropionitriles?

    The characteristic features of the Cantrell-sequence--anterior thoraco-abdominal wall defect with ectopia cordis and diaphragm, sternum, pericardium, and heart defects--have been observed in animals following maternal administration of beta-aminopropionitrile, a toxic amino-acid derivative. We report on an unusual case of the Cantrell-sequence in a premature infant with associated dysmelia, aplasia of the right kidney, cerebellar hypoplasia and circumscribed aplasia of the cutis, which has not been reported previously. Maternal history suggested an occupational exposure to aminopropionitriles prior to pregnancy. Prenatal ultrasound, differential diagnosis, perinatal management, and the teratogenic role of aminopropionitriles in this rare genetic disorder are discussed.
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