title: Are myo-inositol, glucose and zinc concentrations in amniotic fluid of fetuses with spina bifida different from controls?
abstract: OBJECTIVE
  Associations are reported between myo-inositol, glucose, zinc and the occurrence of spina bifida. To gain more insight into the pathogenesis of spina bifida, the concentrations of myo-inositol, glucose and zinc were determined in amniotic fluids from pregnancies with a spina bifida or unaffected control fetus.
  
  
  METHODS
  Amniotic fluids of 27 pregnancies complicated by spina bifida and 49 controls were collected at the Department of Obstetrics and Gynecology of the University Medical Center Nijmegen in the Netherlands. Myo-inositol, glucose and zinc concentrations were determined. By indication, the samples were taken at different gestational ages. Therefore, the data were evaluated using multiple linear regression analysis to adjust for gestational age.
  
  
  RESULTS
  Amniocentesis was performed at a more advanced gestational age in the spina bifida group than in controls. In the spina bifida group, amniotic fluid myo-inositol, glucose and zinc concentrations gradually declined throughout pregnancy. At a gestational age of 15 weeks, the estimated mean amniotic fluid glucose and zinc concentrations in the spina bifida group were, respectively, significantly lower (p< or =0.5) and higher (p< or =0.5) compared with the control group. At the same gestational age, the estimated mean myo-inositol concentrations were comparable in both groups. At a gestational age of 38 weeks, the estimated mean myo-inositol, glucose and zinc concentrations were not significantly different in the spina bifida compared with the control group.
  
  
  CONCLUSIONS
  This study may suggest that a derangement in zinc and glucose transfer or metabolism is associated with spina bifida. Since compounds in amniotic fluid are only a very crude marker of the actual fetal condition, studies that focus on the metabolism of these compounds on tissue or even cellular level should be performed to clarify their role in the pathogenesis and future prevention of spina bifida.
authors.affiliation: Department of Epidemiology and Biostatistics, University Medical Center Nijmegen, 6500 HB Nijmegen, The Netherlands.
authors.forename: Pascal M W
authors.initials: PM
authors.lastname: Groenen
authors.forename: Ron A
authors.initials: RA
authors.lastname: Wevers
authors.forename: Fokje S M
authors.initials: FS
authors.lastname: Janssen
authors.forename: Joep H A M
authors.initials: JH
authors.lastname: Tuerlings
authors.forename: Johannes M W M
authors.initials: JM
authors.lastname: Merkus
authors.forename: Régine P M
authors.initials: RP
authors.lastname: Steegers-Theunissen
mesh_terms: D000328:Adult; D000653:Amniotic Fluid / Q000737:chemistry / Q000378:metabolism*; D005260:Female; D005865:Gestational Age; D005947:Glucose / Q000032:analysis / Q000378:metabolism*; D006801:Humans; D007294:Inositol / Q000032:analysis / Q000378:metabolism*; D008423:Maternal Age; D011247:Pregnancy; D018566:Pregnancy, High-Risk; D013054:Spectrophotometry, Atomic; D016135:Spinal Dysraphism / Q000209:etiology / Q000378:metabolism*; D015032:Zinc / Q000032:analysis / Q000378:metabolism*
chemical_list: D007294:Inositol; D005947:Glucose; D015032:Zinc