Emeritus Faculty, Acad Council, Obstetrics & Gynecology
Gynecologic and obstetric infections.
This review highlights recent studies that refute the following hypothesis on the genesis of cerebral palsy: The risk factors that cause death are also risk factors for brain damage resulting in cerebral palsy, if they occur at lower intensity, less frequently, or for a shorter duration. Untested, unproved, and invalid theories that emerged in the 1950s stimulated the assembly of much data that are at odds with the notion that the pathways of causation for cerebral palsy and perinatal mortality are identical.
View details for Web of Science ID A1986C380800002
View details for PubMedID 3706452
These studies were designed to show that properly timed measurements of serum progesterone (P) can be conveniently used in the diagnosis and treatment of patients with recurrent and threatened abortion. Luteal phase serum P levels between 2 and 10 ng/ml and serum P levels below 15 ng/ml in the first 10 weeks of gestation were considered diagnostic of corpus luteum (CL) dysfunction. Patients were treated with clomiphene, gonadotropins, and/or progesterone suppositories in order to correct serum P levels, thus elevating the serum P into the normal range. When treatment of patients with subnormal P levels resulted in normalization of serum P, successful pregnancies occurred. CL dysfunctions, either before or after conception, were found in eight of the nine patients with histories of recurrent spontaneous abortions. Correction of serum P was associated with successful pregnancy in these eight patients. Twelve patients with threatened abortion were also found to have subnormal serum P levels. Progesterone suppositories corrected the serum P levels in nine of the eleven patients treated, and none of these patients aborted. Serum P measurements provide a means for evaluation of CL function during early gestation. Management of patients with CL dysfunction can also be monitored with serial serum P measurements, provided that progesterone is the therapeutic agent rather than synthetic progestins.
View details for Web of Science ID A1979HR63600006
View details for PubMedID 488424