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Perinatal mortality

Mavalankar, D. V., Trivedi, C. R., Gray, R. H. (1991). Levels and Risk Factors for Perinatal Mortality inAhmedabad, India. WHO, Bulletin. [Pg.431]

Structural and numerical chromosomal aberrations in somatic cells may be involved in the etiology of neoplasia and in germ cells can lead to perinatal mortality, dominant lethality or congenital malformations in the offspring (Chandley, 1981), and some tumors (Anderson, 1990). [Pg.189]

Turner, M.R. (1973). Perinatal mortality, growth, and survival to weaning in offspring of rats reared on diets moderately deficient in protein. Br. J. Nutr. 29 139-147. [Pg.295]

Such patients have a high incidence of perinatal mortality and rarely survive beyond 1 year. [Pg.113]

Done, D.J., Johnstone, E.C., Frith, C.D., Golding, J., Shepherd, P.M., and Crow, TJ. (1991) Complications of pregnancy and delivery in relation to psychosis in adult life data from the British perinatal mortality survey sample. BMJ 302 1576-1580. [Pg.192]

Slone, D., Siskind, V, Heinonen, O.P., Monson, R.R., Kaufman, D.W, and Shapiro, S. (1977) Antenatal exposure to the phenothiazines in relation to congenital malformations, perinatal mortality rate, birth weight, and intelligence quotient score. Am J Obstet Gynecol 128 486 88. [Pg.652]

Finally, when given in large doses, lithium may increase the risk of fetal macrosomia, premature delivery, and perinatal mortality (based on unpublished data on 241 infants). [Pg.214]

Prolonged contact between toluene and human skin may cause nonallergic contact dermatitis. Human exposure to toluene also causes nervous system symptoms and signs and excessive exposure may cause adverse effects on the kidney and liver. Adverse effects on the nervous system have been observed in experimental animals. In studies of spontaneous abortion, perinatal mortality and congenital malformations in humans, the numbers of cases were small and the mothers had also been exposed to other substances. Embryotoxicity that generally occurs concurrently with maternal toxicity has been seen in some studies in mice and rats but not rabbits (lARC, 1989a). [Pg.844]

In an audit in Auckland there was no increase in perinatal mortality or pre-eclampsia (115). The MIG prospective randomized comparison of metformin and insulin aims to recruit 750 women 70 have been recruited so far without serious adverse events in the metformin arm. [Pg.375]

Sulfonylureas (n = 68) and metformin (n = 50) have been compared retrospectively with insulin (n = 42) in pregnancy (131). There were no severe attacks of hypoglycemia, no jaundice, and no differences in neonatal morbidity. However, in those who took metformin, preeclampsia and perinatal deaths were more common. Since metformin was given to obese women, and since obesity contributes to pre-eclampsia and perinatal mortality, this may have been an effect of obesity. [Pg.448]

Most of the developmental toxicity evaluations of DEHP are traditionally designed studies in which physical development was evaluated just prior to birth in pups of rodents that were orally exposed during gestation only. These studies clearly show that gestational exposure to DEHP was embryotoxic and teratogenic in rats and mice. A range of effects were observed including intrauterine deaths, skeletal and cardiovascular malformations, neural tube closure defects, increased perinatal mortality, and developmental delays. [Pg.31]

Identify the 10 most affected countries by natural and human-initiated disasters in the past year. Examine the perinatal mortality and GDP of these countries. What are your conclusions ... [Pg.585]

Shapiro S, Siskind V, Monson RR, Heinonen OP, Kaufman DW, Slone D. Perinatal mortality and birth-... [Pg.28]

Observations derived from nncontrolled stndies have shown an association between maternal nse of propranolol and intrauterine growth retardation, neonatal respiratory depression, bradycardia, hjrpoglycemia, and increased perinatal mortality. However, in randomized, placebo-controlled studies of metoprolol and oxprenolol, there was no evidence of effects on birth weight. [Pg.465]

An observational comparison in a rural Ghanaian hospital of 2083 pregnant women and 3084 historical controls showed no serious adverse events with chloroquine chemoprophylaxis (300 mg/week), but a high rate of pruritus (34). There was a decrease in anemia in pregnancy but no increase in perinatal mortality or birth weight in the chloroquine-treated mothers, although this was only in comparison with historical controls. [Pg.727]

Preeclamptic Toxemia. This condition is associated with increasing plasma uric acid concentration, probably caused by uteroplacental tissue breakdown and decreased kidney perfusion. Plasma urate measurement can be used as an indicator of the severity of preeclampsia. Redman et al noted that concentrations in excess of 6.0mg/dL (0.36mmol/L) at 32 weeks gestation are associated with a high perinatal mortality rate. [Pg.807]

Biomass exposure has also been shown to be associated with other health outcomes, including bhndness (cataracts), self-reported tuberculosis, reduced birth weight and increased perinatal mortality but the evidence for such associations is not as strong as what is available for ARI and chronic obstructive pulmonary disease. They are subject to even greater uncertainties in both the exposure and the health assessment components and the reader is referred to the references cited earlier for individual studies concerned with particular health risks. [Pg.234]

Increased perinatal mortality (stillbirths and newborn deaths) occurred in mice as a consequence of maternal treatment with 0.02 mg NDMA/kg/day in the drinking water (Anderson et al. 1978). The mice were treated for 75 days prior to mating and throughout pregnancy and lactation. Histological examinations of the stillborn fetuses and dead neonates showed no abnormalities. The 0.02 mg/kg/day dose represents a LOAEL for developmental effects due to intermediate duration exposure (Table 2-2 and Figure 2-2). [Pg.47]

Asthma affects 7% of pregnant women, making it potentially the most common serious medical condition to complicate pregnancy. Maternal asthma has been reported to increase the risk of perinatal mortality, preeclampsia, preterm birth, and low-birth-weight infants. More severe asthma is associated with increased risks, whereas better-controlled asthma is associated with decreased risks. [Pg.527]

Behavioral and neurotoxic effects in the offspring of rats exposed via inhalation have been reported. Perinatal mortality was shown to be dose related to prenatal carbon disulfide exposure levels (225 and 642 ppm) in rats (Lehotzky et al. 1985). Exposure to 642 ppm carbon disulfide throughout pregnancy for 2 hours daily produced no malformations of fetuses in rats or mice but did increase the death rates of the embryos at all stages of intrauterine development (Yaroslavski 1969). [Pg.62]

Centers for Disease Control and Prevention/NVSS. (2007). Fetal and perinatal mortality, United States, 2004. Nad. Vital Stat. Rep. 56(3)1-20. [Pg.338]

Fetus abortion, stillbirth, congenital anomalies, increased perinatal mortality, increased infant mortality, neurological cretinism (mental deficiency, deaf mutism, spastic deplegia, squint), hypothyroid cretinism (mental deficiency), psychomotor defects. [Pg.1484]


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