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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A large number of congenital disorders are due to alcohol consumption during pregnancy. These anomalies are also known as the "fetal alcohol syndrome". Data available on this subject is very important and leaves no doubt in the disastrous effects of prenatal alcohol intake. Babies born with fetal alcohol syndrome present constant characteristics such as pre and post natal growth retardation, cranio-facial dysmorphism and central nervous system abnormalities. The mechanism by which alcohol produces these defects are linked to: 1. The alteration of essential aminoacid transfer. 2. Fetal hypoxia. 3. Central nervous system cellular proliferation and differentiation inhibition (mainly in the cerebellum and hippocampus). 4. Auto-immune reaction to S-100 protein. 5. Hormonal dysfunction. 6. Postnatal inhibition of response to growth hormones. The major risk is undoubtfully the excessive daily alcohol intake (2-6 consumptions/day). Social type of alcohol consumption brings more discrete effects and often these happen much later. Low birth weight and mental retardation may be seen with the absorption of 15 ml of alcohol per day (1 beer or 1 glass of wine or 40 ml of liquor) 52 mg/100 ml of blood alcohol has been identified as the fetal threshold activity concentration, while 140 mg/100 ml is associated with evident teratogenicity. Other factors such as maternal age and genetic predisposition also add to the risks of prenatal alcohol exposure.
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PMID:[alcohol and pregnancy: what is the level of risk?]. 220 63

Many newborns who appear normal at birth later manifest substantial neurologic and other disease. Pathologists are able to explain some of that sad enigma. Placental pathology frequently reveals the pathogenesis of cerebral palsy, mental retardation, and other neurodevelopmental disorders. This requires recognition of gross placental abnormalities and insightful light microscopic examination. Chorioamnionitis is now proven to be the major cause of premature onset of labor and prematurity. There is important need for investigation of pathogenetic processes associated with ascending intrauterine infection. Major complications therein include bacterially mediated fetal hypoperfusion resulting from placental and umbilical vasocontraction. Placentas of 10% of newborns have villitis of unknown etiology. The importance of villitis is incompletely known. The fetus may discharge meconium on more than one occasion, particularly so when the fetus is postmature. Clinicians may not recognize that fetal discharge has occurred if the event occurred 4 days or more prior to delivery. Intra-amniotic meconium associated with oligohydramnios probably causes placental and umbilical vasocontraction. Meconium probably thus contributes to the pathogenesis of pulmonary vasoconstriction, persistent fetal circulation, necrotizing enterocolitis, and damage of the fetal brain, liver, and kidneys. Fetal hypoxia and asphyxia may be acutely or chronically acquired. Major placental lesions associated with neonatal asphyxia include chronic ischemic change, nucleated red blood cells, intravillous hemorrhages, intimal vascular fibrin cushions, meconium staining, and intervillous fibrin.
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PMID:Some placental considerations related to neurodevelopmental and other disorders. 844 76

The early-onset type (onset earlier than 28 gestational weeks) of pregnancy induced hypertension (PIH) has the clinical characteristics of a high incidence of intrauterine growth retardations (IUGR), fetal distress, neonatal hypoglycemia and hypertensive disposition. Moreover, the infants from early-onset type of PIH mothers showed a statistically significant higher incidence of neurological handicap (cerebral palsy, mental retardation and epilepsy) than late onset type. The infants with a neurological handicap had severe IUGR and intractable hypoglycemia in the early neonatal period, probably due to low storage of glucose in the liver and fetal hypoxia. Appropriate perinatal management, including proper evaluation of fetal well-being and good timing of delivery, could improve the outcome of infants from early-onset type of PIH mothers.
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PMID:Neonatal hypoglycemia in infants with intrauterine growth retardation due to pregnancy-induced hypertension. 920 Aug 79