Laura DiGiovanni

Choroid plexus cysts: Infant and early childhood developmental outcome

Objective To determine the infant and early childhood developmental outcome associated with choroid plexus cysts diagnosed prenatally. Methods Between January 1990 and August 1995, 8270 women underwent second-trimester ultrasound examinations. All women whose fetuses were diagnosed as having choroid plexus cyst(s) underwent ultrasonographic detailed anatomy survey, were offered fetal karyotyping, and were followed with serial ultrasounds. Fetal karyotype, associated structural anomalies, maternal serum triple analyte screen, neonatal outcomes, and infant and early childhood developmental milestones were recorded. The children were followed subsequently, and developmental assessment was performed with a modified Denver II Developmental Screening Test. Results A diagnosis of choroid plexus cyst was made in 89 fetuses (1.1%). The mean (± standard deviation [SD]) gestational age at diagnosis was 18.2 ± 1.9 weeks (range 15–22). The cysts varied in size and laterality, with a mean (±SD) size of 5.9 ± 3.3 mm (range 1–23). Three of the 61 women who underwent testing for fetal karyotype (4.9%) had abnormal karyotypes identified. All three karyotypes were trisomy 18, and all three trisomy 18 fetuses had additional sonographic abnormalities. All 28 women who chose not to undergo fetal karyotypic analysis delivered phenotypically normal infants. Infant and childhood developmental follow-up was performed on 76 children with cysts diagnosed prenatally. The mean (±SD) length of childhood follow-up was 35.5 ± 16.2 months (range 12–82). All 76 children were found to be developmentally normal by the Denver II Developmental Screening Test. Conclusion These observations suggest that the finding of isolated choroid plexus cysts is not associated with delayed infant and early childhood development or an increased risk of abnormal karyotype. The presence of isolated choroid plexus cysts does not warrant intensive infant and early childhood follow-up.

West Nile virus encephalitis during pregnancy

BACKGROUND West Nile virus is an emerging pathogen in the United States. Although most cases are subclinical, serious infection can occur in the form of fulminant meningoencephalitis. CASE We present a case of West Nile virus meningoencephalitis complicating pregnancy. The patient presented in the second trimester with fever, nuchal rigidity, and mental status changes. The diagnosis was made by demonstrating the presence of immunoglobulin M antibody to West Nile virus in the cerebrospinal fluid. Gradual clinical improvement was noted after several days of supportive care. No obvious fetal consequences of infection were noted after birth. CONCLUSION Obstetricians and health care providers need to be mindful of West Nile virus infection in pregnant women presenting with fever and neurological signs, particularly in endemic areas.

STEROID HORMONE MODULATION OF cAMP PRODUCTION IN RESPONSE TO BETA ADRENERGIC RECEPTOR STIMULATION IN GENITAL TRACT MYOCYTES

Summaryβ-Adrenergic receptor stimulation results in smooth muscle relaxation through activation of adenylyl cyclase and subsequent cyclic AMP (cAMP) production. The present study was performed to evaluate the effects of steroid hormones (i.e. testosterone and hydrocortisone) onβ2-adrenergic receptors and their signal transduction in the DDT1 MF-2 genital tract myocyte. Radioligand binding studies demonstrated that these two steroid hormones produced a 70 to 80% increase in the density ofβ2-adrenergic receptors in these myocytes. Stimulation of theβ2-adrenergic receptors with isoproterenol resulted in a significant increase of cAMP in control myocytes; cells treated with testosterone for 24 h demonstrated a comparable response to isoproterenol, whereas hydrocortisone for 24 h resulted in a 50% greater cAMP response. In contrast to the response at 24 h, stimulation of myocytes after testosterone treatment for 48 h resulted in a cAMP response comparable to that seen in response to hydrocortisone at 24 h. Studies performed using theophylline demonstrated similar cAMP responses at 24 h between the control and testosterone-treated myocytes, thereby ruling out the possibility that the delayed increase of the cAMP response after testosterone was caused by stimulation of phosphodiesterase. Direct stimulation with forskolin resulted in greater cAMP production in the testosterone-treated myocytes compared to controls, thereby refuting the possibility that testosterone directly suppresses adenylyl cyclase activity at 24 h. These findings suggest that although both testosterone and hydrocortisone produce a twofold increase inβ2-adrenergic receptor density in the DDT1 myocytes,β2-adrenergic receptors expressed in response to hydrocortisone appear functional at 24 h resulting in increased cAMP production, whereas those expressed in response to testosterone require 48 h to demonstrate increased functional activity.