Reproductive Endocrinology and Infertility

Shahla Nader, MD
Interim Division Director
(713) 500-6385

The Division of Reproductive Endocrinology and Infertility consists of two physicians, two nurses, and clinical support staff who work together as a team to provide complete services in infertility and women's health.

Our specialists treat all changes in a woman's reproductive cycle beginning with puberty and sexual development, continuing with disorders of ovulation, irregular menstrual bleeding and pelvic pain, and ending with modern management of premature ovarian failure and menopause.  In addition, we evaluate patients for fertility and give advice and offer a broad range of treatment options as appropriate.

Many of our patient referrals are women requiring specialized reproductive surgery utilizing pelviscopy, hysteroscopy and lasers for the treatment of endometriosis, pelvis adhesions and fibroids, as well as the performance of tubal reconstruction, laparoscopic assisted hysterectomy and endometrial ablation. Although there is currently a national emphasis on cost containment and centralized management, we believe that all women deserve "old-fashioned" personal attention and top quality medical care first.

One of the research interests in the Division of Reproductive Endocrinology and Infertility is the development of pre-implantation embryos.  We are interested in factor(s) that enhance the implantation potentials of pre-implantation embryos.  We hope these factors may be used to augment the success rates of human in-vitro fertilization (IVF).  Our findings regarding prostacyclin (prostaglandin I2 or PGI2) can be summarized as follow:

In 2000, we discovered that human oviducts produce abundant prostacyclin (Human Fallopian Tubes Express Prostacyclin (PGI) Synthase and Cyclooxygenases and Synthesize Abundant PGI).When prostacyclin was supplemented in the culture media, it enhanced the hatching of mouse embryos (Prostacylin enhances embryo hatching but not sperm motility).  When these embryos were transferred to gestational carriers, they had improved rates of implantation and live birth (Prostacyclin enhances the implantation and live birth potential of mouse embryos).

Recently we showed increased prostacyclin production by the oviducts corresponds to the development of embryos in the oviduct: peak prostacyclin production, associated with the induction of cyclooxygenase-2 (COX-2) gene, occurs in post-coitus days 2 and 3 mouse oviducts (Oviduct prostacyclin functions as a paracrine factor to augment the development of embryos).  These data suggest that oviduct-derived prostacyclin has physiological roles in the development of embryos.  Results from our other studies showed embryo-derived, endogenous prostacyclin also enhanced the hatching of pre-implantation embryos.  Mouse embryos express enzymes required to produce prostacyclin i.e. COX-1, COX-2 and prostacyclin synthase; COX-2 derived prostacyclin enhances mouse embryo hatching (Cyclooxygenase-2-derived endogenous prostacyclin enhances mouse embryo hatching).

The above results underscore the physiological functions of prostaglandins in the development of pre-implantation embryos.  Thus, supplementing embryo culture media with prostacyclin may enhance the developmental and implantation potentials of human embryos; the safety of non-steroidal anti-inflammatory drugs (NSAIDs) in women desiring fertility may need to be re-evaluated.