Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Maternal anemia

Clark RL, Robertson RT, Minsker DH et al (1984) Diflunisal-induced maternal anemia as a cause of teratogenicity in rabbits. Teratology 30 319-332... [Pg.324]

The only recognized toxic effect in infants is anemia within the first 6 weeks of life, which is not associated with premature delivery, duration of maternal treatment, degree of maternal immunosuppression, or maternal anemia. An 18-month follow-up of 342 children born to mothers who had taken zidovudine or placebo during pregnancy has recently been reported (38). There were no differences in growth parameters or immune function in uninfected children. In addition, no childhood neoplasias were reported in either group. [Pg.3715]

Pregnancy complications, such as maternal anemia, maternal diabetes, and placental dysfunction are predictors of the development of anorexia nervosa in offspring.65 Maternal smoking during pregnancy is associated with bulimia nervosa in offspring, but not with anorexia nervosa.66... [Pg.231]

Heavy tobacco smoking is especially dangerous for the fetus. Maternal smoking of more than 20 cigarettes a day is associated with maternal anemia, fetal brain hypoxia, and fetal polyglobulia (an abnormal increase in circulating red blood cells).35... [Pg.277]

Reviews of large-scale iron-supplementation programs in developing countries have reported limited effectiveness in reducing maternal anemia. The limited effectiveness is often attributed to implementation constraints including low compliance, short intervention duration, inadequate supplement supply. [Pg.377]

The variant was found In a 22 year old woman with chronic hemolytic anemia characterized by a persistent retlculocytosls, development of gallstones requiring cholecystectomy, frequent episodes of jaundice, dark urine, and falling PCV value. Her mother, maternal grandfather, and sister have a similar clinical picture In all patients red cell enzymes are elevated with a retlculocytosls of about 10%, and 2,3-DPG levels are normal ... [Pg.41]

The hemolytic anemia caused in pregnant rabbits by diflunisal was severe enough to explain the concomitant axial skeletal malformations (Clark et ah, 1984). Acetazolamide-induced fetal malformations in mice are apparently related to maternal hypercapnia (Weaver and Scott, 1984a, b) and hypokalemia (Ellison and Maren, 1972). The increased resorption rate induced in rabbits by the antibiotic norfloxacin depends on exposure of the maternal gastrointestinal tract (Clark et ah,... [Pg.283]

Clark and colleagues (27) found evidence of maternal toxicity influencing fetal findings in studies with diflunisal in rabbits, in which fetal axial skeletal defects were observed. Diflunisal was found to produce severe maternal hemolytic anemia and greatly decreased erythrocyte ATP levels. The authors were able to demonstrate that the skeletal malformations resulted from maternal hypoxia secondary to anemia, rather than from a direct effect of the drug on the embryo or fetus. In addition, it was demonstrated that diflunisal had no effects on rat erythrocyte ATP levels, and the compound was categorized as not teratogenic in rats or mice. [Pg.319]

Folic acid deficiency, unlike vitamin B12 deficiency, is often caused by inadequate dietary intake of folates. Patients with alcohol dependence and patients with liver disease can develop folic acid deficiency because of poor diet and diminished hepatic storage of folates. Pregnant women and patients with hemolytic anemia have increased folate requirements and may become folic acid-deficient, especially if their diets are marginal. Evidence implicates maternal folic acid deficiency in the occurrence of fetal neural tube defects, eg, spina bifida. (See Folic Acid Supplementation A Public Health Dilemma.) Patients with malabsorption syndromes also frequently develop folic acid deficiency. Patients who require renal dialysis develop folic acid deficiency because folates are removed from the plasma during the dialysis procedure. [Pg.741]

A large number of disorders are associated with cobalamin deficiency in infancy or childhood. Of these, the most commonly encountered is the Imerslund-Graesbeck syndrome, a condition that is characterized by inability to absorb vitamin B,2, with or without IF, and proteinuria. It appears to be due to an inability of intestinal mucosa to absorb the vitamin B,2 IF complex. The second most common of these is congenital deficiency of gastric secretion of IF. Very rarely, congenital deficiency of vitamin B12 in a breast-fed infant is due to deficiency of vitamin B12 in maternal breast milk as a result of unrecognized pernicious anemia in the mother. This is rare because most women with undiagnosed and untreated pernicious anemia are infertile. Additionally, there are some rare methylmalonic acidemias (acidurias) caused by inborn errors in homocysteine and methionine metabolism that are responsible for disorders in vitamin B status. ... [Pg.1103]

For sensitized mothers with an at-risk fetus, serial titers are performed on maternal serum every month until 24 weeks gestation, then every 2 weeks thereafter. If a critical titer anti-D is detected, then ultrasound Doppler measurements are used to determine the peak velocity of blood flow in the fetal middle cerebral artery. Higher velocity is a strong indicator of fetal anemia. In addition, amniocentesis is performed to assess the bilirubin concentration in amniotic fluid. [Pg.2165]

The answer is c. (Murray, pp 627-661. Scriver, pp 3897—3964. Sack, pp 121-138. Wilson, pp 287-320.) Hemorrhagic disease of the newborn is caused by poor transfer of maternal vitamin K through the placenta and by lack of intestinal bacteria in the infant for synthesis of vitamin K. The intestine is sterile at birth and becomes colonized over the first few weeks. Because of these factors, vitamin K is routinely administered to newborns. Deficiencies of the fat-soluble vitamins A, E, D, and K can occur with intestinal malabsorption, but avid fetal uptake during pregnancy usually prevents infantile symptoms. Hypervltaminosis A can cause liver toxicity but not bleeding, and deficiencies of E (neonatal anemia) or C (extremely rare in neonates) have other symptoms besides bleeding. [Pg.263]


See other pages where Maternal anemia is mentioned: [Pg.155]    [Pg.1336]    [Pg.1336]    [Pg.442]    [Pg.489]    [Pg.244]    [Pg.860]    [Pg.550]    [Pg.363]    [Pg.363]    [Pg.155]    [Pg.1336]    [Pg.1336]    [Pg.442]    [Pg.489]    [Pg.244]    [Pg.860]    [Pg.550]    [Pg.363]    [Pg.363]    [Pg.152]    [Pg.75]    [Pg.722]    [Pg.101]    [Pg.707]    [Pg.708]    [Pg.1579]    [Pg.233]    [Pg.320]    [Pg.319]    [Pg.1625]    [Pg.60]    [Pg.320]    [Pg.599]    [Pg.151]    [Pg.142]    [Pg.544]    [Pg.21]    [Pg.538]    [Pg.2547]    [Pg.15]    [Pg.681]    [Pg.240]    [Pg.245]    [Pg.394]   
See also in sourсe #XX -- [ Pg.550 ]




SEARCH



Maternity

© 2024 chempedia.info