Dear Barbara,

Here is some information that might help you.  I've just recently come across another article, that also talks to this issue.  It is particularly interesting in that it addresses the issue of genetic typing as it relates to the decision to treat prenatally or not.  Will pass that along, when I get the chance, as well.   Sorry I have not had dex treatment myself, so can't share anything from personal experience.  Good luck with your pregnancy.

From http://www.aap.org/policy/re0027.html

Prenatal Treatment of CAH Attributable to 21-OH Deficiency

Prenatal treatment of CAH to prevent the virilization of an affected female fetus has been considered desirable by a number of investigators.^2,30-33 Because masculinization of the external genitalia begins at about 6 to 7 weeks of gestation (8 to 9 weeks after the last menstrual period),^34,35 suppression of the fetal pituitary-adrenal axis at no later than 6 weeks of gestation theoretically could prevent ambiguity of the external genitalia in the female fetus with classic CAH, whereas therapy after that time would prevent progression of virilization.

Successful prenatal treatment to ameliorate or prevent virilization of a female fetus with classic CAH attributable to 21-OH deficiency was first reported in 1984.³⁶ In 2 pregnancies at risk for classic salt-wasting CAH, the mothers were treated with hydrocortisone and dexamethasone, respectively. Subsequent amniocentesis demonstrated that both infants were girls and had HLA types identical to those of their affected siblings, and treatment was continued to term. At birth, the external genitalia were normal in the infant whose mother was given dexamethasone and minimally virilized in the infant whose mother received hydrocortisone. Postnatally, the diagnosis of 21-OH deficiency was confirmed in both infants.³⁶ There are reports of >50 affected female infants in whom prenatal treatment with dexamethasone has been attempted. The dose of dexamethasone has ranged between 0.5 and 2 mg/d in 1 to 4 divided doses. Treatment was begun as early as the 4th week of pregnancy to as late as the 16th week. In some cases, treatment was interrupted for 5 to 7 days before amniocentesis, and, in a few cases, treatment was discontinued at 21 to 26 weeks.^{18,21-23,37-53}

Fetal Outcome

Of the total number of cases for which data are available, treatment was considered successful for almost three fourths of the female infants; approximately one third had normal genitalia, and two thirds were described as being mildly virilized with clitoromegaly, partial labial fusion, or both. In slightly more than one fourth of all female infants treated, therapy was unsuccessful, and the infants had marked genital virilization.

The variability of the results has been attributed to a number of factors: inadequate dosage, interruption of treatment, delay in initiating treatment, variability in maternal metabolic clearance, and variability of placental metabolism of the administered glucocorticoid.^23,50 Variability in onset of fetal sexual differentiation and maternal noncompliance to therapy also must be considered.^23,50

Spontaneous abortion, fetal demise during late pregnancy, intrauterine growth retardation, liver steatosis, hydrocephalus, agenesis of the corpus callosum, and hypospadias with unilateral cryptorchidism⁵¹ have been reported occasionally when mothers received short-term treatment in unaffected pregnancies, as well as in affected pregnancies in which the mother received prolonged corticosteroid treatment. These events generally have not been considered related to the treatment or to the disease itself.^17,45,49,50 In a report of intrauterine growth retardation in an infant treated successfully for CAH, however, it was concluded that intrauterine growth retardation still should be considered "a possible fetal complication of treatment."⁴⁶ In long-term follow-up of most infants treated throughout the pregnancy or treated prenatally until midgestation,^17,44-50 development seems to be normal, and growth has been consistent with the family pattern and that of the other affected siblings.^{17,41,42,44,45} Rare adverse events, including failure to thrive and psychomotor and psychosocial delay in development, have been observed.⁵¹ Long-term follow-up is limited, however, and detailed neuropsychological evaluations have not been reported.

In a preliminary report, cognitive and behavioral development of young children aged 6 months to 5.5 years treated prenatally with dexamethasone because of risk for CAH was assessed by standard questionnaires completed by the mothers. The development of those children was compared with the development of children from untreated pregnancies at risk for CAH.⁵² No significant differences in cognitive abilities or behavior problems were identified.⁵⁰ However, the demonstration of an increased frequency of neurologically silent white matter abnormalities and temporal lobe atrophy in children and adults with CAH indicates that the long-term effects of glucocorticoids on the central nervous system are not fully known and must be evaluated carefully.⁵⁴ Although experimental treatment given to animals cannot be directly extrapolated to humans, high doses of dexamethasone administered to rhesus monkeys toward the end of gestation were associated with abnormalities of the fetal brain consisting of neuronal degeneration of hippocampal, pyramidal, and dentate regions.⁵⁵ Other animal studies have focused on long-term cardiovascular risks of prenatal dexamethasone treatment. Intrauterine growth retardation, lower kidney weight, oligonephronia, and the development of hypertension in adulthood have been demonstrated in rat pups whose mothers received dexamethasone prenatally.^56-58 These studies underscore the need for careful long-term outcome studies of prenatal dexamethasone treatment, in which treated mothers and infants are followed up to determine possible ill effects in later adult life.