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1/13. Neonatal mydriasis due to effects of atropine used for maternal Tik-20 poisoning.

    A neonate was born to a mother who had consumed an organophosphorus(OPC) compound with suicidal intent. The mother was administered atropine and this caused mydriasis in the neonate without any other pharmacological effects. There was no evidence of placental dysfunction. There are no case reports of OPC consumed in pregnancy and its effect on neonates or of effects of massive doses of atropine in the mother and its effects on the fetus or the newborn.
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2/13. Is ddt exposure during fetal period and breast-feeding associated with neurological impairment?

    The concentration of certain persistent organic pollutants was determined in a family including both parents and one son with neurological impairment suggested to be attention Deficit-Hyperactivity Disorder (ADHD). For comparison control subjects from other ongoing studies were used. They were of the same sex and age group as the respective family member. For polychlorinated biphenyls, hexachlorobenzene, and chlordanes similar results were found in the study groups. The concentration of DDE, the main metabolite of ddt, was increased in the mother, 782 ng/g lipid, compared with mean 403, median 259 (range 51-1354) for the female controls. Also, the son had an increased concentration of 259 ng/g lipid, compared with mean 104, median 72 (range 46-349) for controls. A low concentration was found in the father, 127 ng/g lipid. As a child and as a teenager to the age of 17, the mother was exposed to ddt in her home environment. We discuss the potential of fetal and breast-feeding exposure of the son. Neurodevelopmental impairment has been reported for dioxins and PCBs, but ddt seems to have been less investigated in this respect.
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3/13. 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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4/13. 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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5/13. Congenital renal tubular dysfunction associated with maternal sniffing of organic solvents.

    Two cases of neonatal renal tubular dysfunction and metabolic acidosis due to maternal sniffing of a product containing toluene are reported. Both mothers had been sniffing regularly throughout their pregnancies. The infants were dysmature and had some dysmorphic features. They had hyperchloraemic acidosis and exhibited amino-aciduria. The metabolic changes were however transient. It is suggested that the sniffing of toluene containing solvents during pregnancy may change membrane permeability in both the proximal as well as distal renal tubules and may also enhance liver enzyme activity in the foetus.
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6/13. Congenital anomalies associated with maternal exposure to oxydemeton-methyl.

    Thirty-five workers became ill after they entered a cauliflower field contaminated with residues of three different insecticides, the organophosphates oxydemeton-methyl (Metasystox-R) and mevinphos (Phosdrin), and a carbamate, methomyl (Lannate). One crew member was pregnant with a 4-week-old fetus. At birth, the 3200-g female infant had multiple cardiac defects, bilateral optic nerve colobomas, microphthalmia of the left eye, cerebral and cerebellar atrophy, and facial anomalies. The cardiac defects included ventricular and atrial septal defects, stenosis of the pulmonary artery, and a patent ductus arteriosus. The child died at 14 days of age. There was no family history of birth defects, nor any maternal risk factor present, except that doxylamine (Bendectin) had been prescribed at 9 weeks fetal age. It is unlikely that doxylamine was responsible for the observed anomalies. Of the three chemicals involved, reproductive effects in test organisms have been observed only with oxydemeton-methyl. This case represents the first report of human malformations associated with prenatal exposure to this chemical. Further studies may be warranted to determine if a causal relationship exists.
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7/13. cocaine exposure in a term neonate. Necrotizing enterocolitis as a complication.

    cocaine use has increased dramatically in the past several years, and multiple medical complications associated with its use have been reported in adults, including bowel infarction and colitis. Maternal use of cocaine during pregnancy has been associated with complications in the fetus and newborn infant, including spontaneous abortions, preterm labor, cerebral infarctions, seizures, renal anomalies, and neurobehavioral and neurophysiologic abnormalities. This paper presents a case of necrotizing enterocolitis at birth in a term newborn exposed to cocaine antenatally. Cultures of the bowel grew two types of Clostridia organisms, escherichia coli and group B streptococcus. It is suggested that bowel ischemia was secondary to the vasoconstrictive properties of the maternally abused cocaine and that secondary invasion of the bowel by multiple bacteria ensued. This case presents another possible complication to the newborn of maternal cocaine exposure in utero, namely ischemic infarction of the bowel.
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8/13. Benign glandular inclusions in lymph nodes, endosalpingiosis, and salpingitis isthmica nodosa in a young girl with clear cell adenocarcinoma of the cervix.

    A 12-year-old girl underwent radical surgery for clear cell adenocarcinoma of the endocervix. Bilaterally dilated fallopian tubes with hyperplastic mucosal folds and salpingitis isthmica nodosa were found in association with benign glandular inclusions in a para-aortic lymph node and in the serosa of pelvic organs. Changes in the mullerian-derived epithelium appear to be a common denominator of these unusual lesions in this young girl. A primary growth disturbance of the cells of the mullerian system, which was conditioned during embryonic development and manifested itself later in life in response to appropriate stimuli associated with menarche, is postulated as the underlying abnormality.
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9/13. Developmental language disability as a consequence of prenatal exposure to ethanol.

    Two pre-school-aged patients with a history of prenatal exposure to ethanol had abnormal head size and developmental delay. Both children were strikingly similar in physical appearance, behavior, and cognitive dysfunction. Facial features were typical of fetal alcohol syndrome. head circumference greater than 97th percentile without hydrocephalus and no evidence of prenatal or postnatal growth failure were unusual for ethanol teratogenicity. Each child had a similar pattern of verbal and behavioral dysfunctions characterized by (1) marked hypervigilence, (2) distractability, and (3) cognitive confusion manifested as anxiety and behavioral disorganization. It is suggested that a history of prenatal exposure to ethanol associated with (1) large head circumference, (2) facial features of fetal alcohol syndrome, and (3) early developmental delay, particularly in language acquisition, and impaired modulation of attention and arousal may represent a possible new effect of alcohol teratogenicity.
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10/13. Methylmercury poisoning: long-term clinical, radiological, toxicological, and pathological studies of an affected family.

    For 3 months in 1969 a family in the united states that included a pregnant mother consumed pork containing methylmercury. Children, aged 20, 13, and 8 years and a neonate, developed severe neurological signs. Twenty-two years later, the 2 oldest had cortical blindness or constricted visual fields, diminished hand proprioception, choreoathetosis, and attentional deficits. Magnetic resonance images showed tissue loss in the calcarine and parietal cortices and cerebellar folia. The youngest had quadriplegia, blindness, and severe mental retardation until their deaths. The brain of the 8-year-old who died at age 30 showed cortical atrophy, neuronal loss, and gliosis, most pronounced in the paracentral and parietooccipital regions. The total mercury level in formalin-fixed, left occipital cortex was 1,974 ng/gm as measured by atomic absorption. Regional brain mercury levels correlated with extent of brain damage. A control patient had 38.5 ng of mercury/gm in the occipital cortex. Systemic organs in the patient and a control subject had comparable mercury levels. In mercury-intoxicated rats, we found that only 5 to 10% of total brain mercury was lost by formalin fixation. Brain inorganic mercury in the patient ranged from 82 to 100%. Since inorganic mercury crosses the blood-brain barrier poorly, biotransformation of methyl to inorganic mercury may have occurred after methylmercury crossed the blood-brain barrier, accounting for its persistence in brain and causing part of the brain damage.
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