Delayed diagnosis of endometriosis

When following current pelvic pain management algorithms, appropriate counseling may lessen emotional and social issues associated with endometriosis-associated pelvic pain.     

Composition of the extracellular matrix of the peritoneum.

OBJECTIVE: To localize the extracellular matrix proteins collagen I, collagen IV, fibronectin, and laminin in the peritoneal membrane. STUDY DESIGN: Peritoneal biopsies (n = 13) from the anterior abdominal wall and the uterine serosa (n = 3) were incubated with antibodies to collagen IV, laminin, collagen I, and fibronectin. Specimens were examined using light and confocal laser scanning microscopy. RESULTS: All of the extracellular matrix (ECM) proteins were present immediately under the mesothelium. Collagen (Col) IV and laminin (LM) were seen in the smooth muscle of microvascular structures, in the subendothelial basement membrane, and were present in a fascicular pattern in the peritoneal stroma. Collagen I was distributed diffusely in the peritoneal stroma. Fibronectin was also present in the subendothelial basement membrane. CONCLUSIONS: The resolution of the confocal microscope allowed for localization of extracellular matrix proteins in relation to the mesothelium. The presence of collagen IV, laminin, collagen I, and fibronectin under the mesothelium suggests that cells invading the peritoneum must have the ability to degrade and remodel this matrix.     

Surgically induced endometriosis does not alter peritoneal factors in the rabbit model

OBJECTIVE: It was the purpose of this study to examine the cause and effect relationship between alterations in peritoneal factors and the presence of ectopic endometrium in the rabbit model. DESIGN: Forty rabbits had autologous endometrial or omental (control) tissue surgically implanted. Peritoneal fluid (PF) volume, macrophage number, and macrophage activation, as well as the number of implants with adhesions, were compared with values obtained during the initial surgery. The effect of hormonal treatment on these factors was evaluated at a third laparotomy. RESULTS: There was a significant increase (P less than 0.05) of adhesions in animals with endometrial implants. Peritoneal fluid volume, macrophage number, or macrophage activation were not increased in rabbits with endometrial implants as compared with controls, nor was there a response to hormonal manipulation. CONCLUSIONS: These results demonstrate that PF volume, macrophage number, and macrophage activation are not altered by endometrial implants in the rabbit model. This suggests that the increase in these peritoneal factors in women with endometriosis may not be caused exclusively by the presence of ectopic endometrial tissue.     

Cocaine impairs gonadotropin secretion in oophorectomized monkeys.

OBJECTIVE: Our objective was to determine whether cocaine alters gonadotropin secretion in oophorectomized monkeys. STUDY DESIGN: Oophorectomized monkeys with elevated gonadotropin levels were chronically cannulated to allow blood sampling every 15 minutes. Monkeys received either saline solution or 2 or 4 mg/kg cocaine hydrochloride as an intravenous bolus. Other oophorectomized monkeys were pretreated with either saline solution or 4 mg/kg cocaine 2 hours before bolus gonadotropin-releasing hormone administration, and plasma luteinizing hormone and follicle-stimulating hormone levels were measured every 15 minutes for 3 hours. Monkeys were also given either saline solution or 4 mg/kg of cocaine with gonadotropin-releasing hormone simultaneously, and plasma gonadotropin levels were measured every 15 minutes for 3 hours. Serum luteinizing hormone and follicle-stimulating hormone levels were measured by radioimmunoassay. RESULTS: Both doses of cocaine resulted in a significant decrease in luteinizing hormone levels compared with controls. Follicle-stimulating hormone levels were significantly decreased only with the 4 mg/kg dose of cocaine. There was no difference in luteinizing hormone and follicle-stimulating hormone responses to gonadotropin-releasing hormone in the cocaine-treated monkeys compared with saline solution-treated monkeys by using repeated-measures analysis of variance. CONCLUSION: These findings demonstrate that acute cocaine administration to oophorectomized primates inhibits basal luteinizing hormone-follicle-stimulating hormone secretion but not gonadotropin-releasing hormone-stimulated luteinizing hormone and follicle-stimulating hormone release. In the absence of an effect on gonadotropin-releasing hormone-stimulated gonadotropin release, we conclude that the impaired luteinizing hormone-follicle-stimulating hormone secretion after cocaine administration is due in part to a direct effect of cocaine on gonadotropin-releasing hormone neurons or on hypothalamic neurotransmitter modulation of gonadotropin-releasing hormone release.     

Response of mouse Lewis lung carcinoma to variation in dietary retinyl esters

The effect of manipulating dietary concentrations of retinyl acetate or retinyl palmitate on the growth of subcutaneous murine Lewis lung carcinoma was studied. Both deficiencies and excesses of vitamin A resulted in slowed tumor growth. An optimal intermediate level of dietary vitamin A for solid tumor growth was established. Although previous studies have suggested that established subcutaneous Lewis tumors were responsive to various forms of chemotherapy, a significant increase in the efficacy of BGNU therapy was observed when drug treatment was coupled with either deficient or excessive amounts of dietary retinyl esters.     

Treatment of premature labor with beta sympathomimetics: results with isoxsuprine

This prospective study presents a protocol for the treatment of premature labor with beta sympathomimetics and the results when isoxsuprine was used. Seventy-two patients from 25 to 36 weeks' gestation were treated. All patients were placed at bed rest, hydrated, and given parenteral sedation prior to the intravenous use of isoxsuprine. Treatment was continued via the intramuscular and oral routes until the thirty-seventh week of gestation. Three patients (4.2%) were delivered of infants during the initial infusion, and 15 (20.2%) were delivered of infants within 2 weeks after the onset of therapy. Forty-nine (68%) were delivered of infants after 37 weeks' gestation, and their infants weighed more than 2,500 grams. Maternal side effects were common, but none necessitated termination of therapy. There were six neonatal deaths, the causes of which were respiratory distress syndrome in two infants, necrotizing enterocolitis in one, group B streptococcal sepsis in one, congenital anomalies with sepsis in one, and multiple congenital anomalies in one.     

Follicle-stimulating hormone blocks estrogen-positive feedback during the early follicular phase in monkeys

Normally cycling rhesus monkeys were treated with 12.5 IU of follicle-stimulating hormone (FSH; n = 9) or saline (n = 9) on cycle days 1 to 4, 1 to 6, or 1 to 8 and 50 micrograms/kg estradiol benzoate (E2B, intramuscularly) on day 1, 3, or 5, respectively. Blood was collected daily, then every 8 hours for 96 hours after E2B treatment. Serum was assayed for FSH and luteinizing hormone (LH) by radioimmunoassay. Laparoscopy and serum E2 levels were used to assess ovarian follicular development. Eight of nine FSH-treated monkeys failed to demonstrate typical LH surges in response to E2B. One monkey treated with E2B on day 1 had an attenuated LH surge. All nine control monkeys demonstrated typical threefold LH increases within 72 hours after E2B treatment. Supraphysiologic ovarian stimulation was not visibly evident until 5 days after initiation of FSH treatment. These results suggest that the FSH-induced blockade of estrogen-positive feedback for the LH surge antecedes overt ovarian hyperstimulation.