Endothelium-derived nitric oxide metabolites and soluble intercellular adhesion molecule-1 in diabetic and normal pregnancies.

OBJECTIVE: Endothelial dysfunction has been demonstrated in adult subjects with diabetes. We studied if maternal diabetes is associated with altered endothelial function in the fetus, as this might shed light on mechanisms by which adult diseases are programmed in utero. STUDY DESIGN: Total nitrate/nitrite (NOx) concentration was measured spectrophotometrically with the Griess reagent method. Soluble intercellular adhesion molecule-1 (sICAM-1) concentration was measured by enzyme-linked immunoassay. RESULTS: Venous cord serum NOx concentration at birth was highest in pregnancies complicated by type 1 diabetes (29.5+/-1.8 micromol/l, n=63) (P<0.0001 versus controls) and lowest in normal pregnancies (19.0+/-1.0 micromol/l, n=56). The concentration was intermediate in pregnancies complicated by gestational diabetes (23.9+/-2.7 micromol/l, n=24), but not significantly higher than in normal pregnancies (P=0.172). Venous cord serum sICAM-1 concentration did not differ between the three groups (P=0.191). Maternal serum NOx concentration in the third trimester was higher in pregnancies complicated by type 1 diabetes (22.9+/-3.4 micromol/l, n=22) than in normal pregnancies (15.4+/-1.4 micromol/l, n=21) (P=0.049). CONCLUSIONS: : Increased cord serum NOx but unaltered sICAM-1 concentration in diabetic pregnancies indicates that maternal diabetes does not cause a general alteration in fetal endothelial function. The increase in cord serum and maternal serum NOx concentration in diabetic pregnancies may be due to abnormalities in insulin-induced nitric oxide release or to a diminished reactivity of the vasculature to the effects of nitric oxide.

Sphincter rupture and anal incontinence after first vaginal delivery.

BACKGROUND: The aim of this prospective study was to establish the incidence of anal incontinence and sphincter defects after first vaginal delivery. METHODS: A total of 99 nulliparous and pregnant women were examined prospectively 4 weeks (mean) before delivery and 4 months (mean) after delivery. Of the study population, 75 (76%) women had vaginal delivery and 24 (24%) had cesarean section. Vacuum extraction was necessary in 20 (20%) cases. The symptoms of anal incontinence were asked about using a standard questionnaire. Clinical examination, endoanal ultrasound (EAUS) and anal manometry were performed before and after delivery. RESULTS: The symptoms of mild anal incontinence, mainly gas incontinence, increased after vaginal delivery more than after cesarean section (P < 0.032). Occult anal sphincter defects were noted in 17 (23%) of the 75 women after vaginal delivery by using EAUS. After vacuum extraction, anal sphincter defects were noted in nine (45%) out of 20 women. No new sphincter defects were found in the cesarean section group. The maximal squeezing pressures were significantly decreased in the patients with external anal sphincter (EAS) defects (P = 0.0025). Vacuum extraction leads to more sphincter defects but does not significantly increase anal incontinence or decrease mean anal sphincter pressures. CONCLUSIONS: The first vaginal delivery can result in occult sphincter defects and the use of vacuum extraction increases the risk.

Primary sphincter repair: are the results of the operation good enough?

PURPOSE: This study was designed to evaluate the clinical outcome of primary anal sphincter repair caused by obstetric tears and to analyze possible risk factors associated with sphincter rupture during vaginal delivery. METHODS: A total of 52 females with a third-degree or fourth-degree perineal laceration during vaginal delivery were examined. The symptoms of anal incontinence were obtained by a standard questionnaire. In addition to a clinical examination, endoanal ultrasound, anal manometry, and pudendal nerve terminal motor latency examinations were performed. A control group consisted of 51 primiparous females with no clinically detectable perineal laceration after vaginal delivery. RESULTS: After primary sphincter repair, 31 females (61 percent) had symptoms of anal incontinence. Fecal incontinence occurred in 10 females (20 percent). According to Hardcastle and Parks' and Jorge and Wexner's classifications, the study group had more severe symptoms of anal incontinence than the control group (P<0.001 in both classification groups). In endoanal ultrasound examination, a persistent defect of the external anal sphincter was found in 39 females (75 percent) in the rupture group compared with 10 females (20 percent) in the control group (P<0.001). Anal sphincter pressures were significantly lower in the rupture group than in the control group. An abnormal presentation was the only risk factor for anal sphincter rupture during vaginal delivery. CONCLUSIONS: After primary sphincter repair, persistent external anal sphincter defect and symptoms of anal incontinence are common in females who have had a primary sphincter repair after vaginal delivery. The means of improving the results of primary repair should be studied further.