Transabdominal repair of cystocele by wedge colpectomy during combined abdominal-vaginal surgery

The aim of the study was to evaluate the effectiveness of transabdominal wedge colpectomy as surgical treatment for cystocele. One hundred and sixty-three women with either first or second-degree cystocele (Beecham classification), rectocele and concomitant stress urinary incontinence or benign pelvic masses were submitted for a combined operation. Transabdominal repair of the cystocele was performed by wedge colpectomy employing two different absorbable sutures, Vicryl and PDS. The choice of suture was not random but depended on the period at which surgery was performed. Data obtained were analyzed with Student’st-test and Fisher’s exact test. The cystocele cure rate was 90.2% (110 out of 122) at 3-year follow-up and was significantly associated with the preoperative degree, being 95.5% and 76.5% in first and in second degree, respectively (P=0.003). At 1-year follow-up the cure rate was significantly associated with the type of the suture employed (P=0.01). At 2-year follow-up rectocele cure rate was 97.2% and vaginal vault prolapse appeared in 3.5% of cases. Stress urinary incontinence relapsed in 10% of patients after Burch colposuspension. After the operation 94.1% of the women declared normal coitus. In the present series wedge colpectomy was found to be effective in repairing first-degree cystocele, whereas a high incidence of relapse was observed when second-degree cystocele was present preoperatively. The suture material employed influenced the cure rate. EDITORIAL COMMENT: Wedge colpectomy of the anterior vaginal wall has been described by Weinstein and Roberts (1949), Macer (1978) and Drutz (1991) as a means of abdominally correcting anterior vaginal wall relaxation. Although the present authors did not find as high a success rate with the procedure as the previous investigators, they do show that an abdominal approach to cystocele repair is feasible. There are instances when such an approach would be advantageous to avoid repositioning for a vaginal anterior wall repair. The danger of abdominal anterior wedge colpectomy lies in the dissection of the bladder base from the underlying vaginal wall. Dissection in this area must proceed carefully to avoid trauma to the bladder, ureters and, more distally, to the urethrovesical junction. Performed carefully, with attention directed at avoiding these structures, the abdominal wedge colpectomy is a potentially useful procedure to add to the armamentarium of the urogynecologic surgeon.     

High tidal volume ventilation induces proinflammatory signaling in rat lung endothelium

Alveolar overdistension during mechanical ventilation causes leukocyte sequestration, leading to lung injury. However, underlying endothelial cell (EC) mechanisms are undefined. In a new approach, we exposed isolated blood-perfused rat lungs to high tidal volume ventilation (HV) for 2 h, then obtained fresh lung endothelial cells (FLEC) by immunosorting at 4 degrees C. Immunoblotting experiments indicated that as compared with FLEC derived from lungs ventilated at low volume (LV), HV markedly enhanced tyrosine phosphorylation (TyrP). The tyrosine kinase blocker, genistein, inhibited this response. HV also induced focal adhesion (FA) formation in FLEC, as detected by immunofluorescent aggregates of the alpha(v)beta(3) integrin that co-localized with aggregations of focal adhesion kinase (FAK). Immunoprecipitation and blotting experiments revealed that HV increased TyrP of the FA protein, paxillin. In addition, HV induced a paxillin-associated P-selectin expression on FLEC that was also inhibited by genistein. However, HV did not increase lung water. These results indicate that in HV, EC signaling in situ causes FA formation and induces TyrP-dependent P-selectin expression. These signaling mechanisms may promote leukocyte-mediated responses in HV.     

Results of a study to correlate serum prostate specific antigen and reproductive hormone levels in patients with localized prostate cancer.

This cross-sectional study was undertaken to determine whether serum hormones (free testosterone, androstenedione, luteinizing hormone, or prolactin) have any influence on serum prostate specific antigen (PSA) levels in patients with stage A-C prostate cancer. Blood samples were collected prior to any treatment in 36 patients; in 19 (group 1), three blood samples were collected 10 minutes apart between 9:00 AM and 9:30 AM for each patient and pooled together to avoid diurnal and episodic variation in serum testosterone values. In the remaining patients, only one sample could be collected (group 2). Free testosterone, androstenedione, luteinizing hormone, prolactin, and PSA levels were determined with appropriate radioimmunoassay techniques. Statistical analyses were performed separately for groups 1 and 2, and then with pooled data. None of the hormones in any of the analyses showed any association to serum PSA values except for prolactin for the pooled data and for group 2. This statistical significance for prolactin disappeared on multivariate analysis. There were 21 African-American men and 15 whites in the study; no racial differences in hormonal levels were found except for lower luteinizing hormone levels in African Americans in group 2 and pooled data. No differences were found between group 1 and group 2 in the mean serum prolactin and luteinizing hormone values. Serum free testosterone, androstenedione, and luteinizing hormone appeared to have no influence on serum PSA values in nonmetastatic cancer patients. Serum prolactin values were inversely associated with PSA values in univariate analysis for the pooled data; this disappeared in multivariate analysis. Unlike other studies that found higher serum testosterone levels in African-American college students than whites, no such differences were seen in this age group. Luteinizing hormone was lower in African-American men than in whites in the pooled study population. Further studies are needed to clarify our findings.     

Splenomegalia haemolytica mit interkurrentem acholischen Ikterus

Ohne ZusammenfassungÜbersetzt von Dr. C. Davidsohn.     

Octanediol treatment of glutaraldehyde fixed bovine pericardium: evidence of anticalcification efficacy in the subcutaneous rat model

OBJECTIVE: Anticalcification strategies of glutaraldehyde-fixed xenograft tissue aim to extract lipids or to neutralize toxic aldehyde residuals. The purpose of this study was to evaluate the efficacy of octanediol compared to standard treatments of glutaraldehyde-fixed bovine pericardium in the subdermal rat model. Octanediol treatment is an ethanolic solution (40%) containing a long chain aliphatic alcohol (5% 1,2-octanediol) that removes lipids without diminishing the stability of collagen. METHODS: Octanediol and standard glutaraldehyde fixed bovine pericardium were both implanted in 24 Sprague-Dawley rats, explanted after 30-75 days (12 animals each) and submitted to X-ray (score 0-4), histology, electron microscopy and elemental analysis by spectroscopy (Ca and P content). Unimplanted octanediol and standard glutaraldehyde fixed pericardium served as control. RESULTS: At 30 days octanediol-treated pericardium showed calcium content of 0.20+/-0.1 vs 20.07+/-36.79 mg/g dry weight for standard pericardium. The difference was also evident at 75 days: calcium content of 2.36+/-7.38 mg/g dry weight for octanediol vs 165.61+/-23.35 mg/g dry weight for standard (p<0.0001). Differences were also detected at X-ray (mean score 0.7+/-0.6 octanediol vs 3.8+/-0.4 standard at 75 days). Equally, mean P content was 11.69+/-21.33 mg/g dry weight for standard vs 0.60+/-1.45 mg/g dry weight for octanediol samples at 30 days, and 90.90+/-12.61 mg/g dry weight for standard vs 1.42+/-4.34 mg/g dry weight for octanediol at 75 days (p<0.0001). At electron microscopy collagen appeared well preserved regardless of the type of treatment; in octanediol treated pericardium cell membranes almost disappeared and only few profiles of endoplasmic reticulum and rare mitochondria were visible. CONCLUSIONS: Treatment with octanediol strongly prevents calcification of glutaraldehyde fixed bovine pericardium in rat subdermal model, even in the long-term. Evidence of octanediol efficacy may entail important implications for new generation bioprosthetic valves.     

Coronary cardiac allograft vasculopathy versus native atherosclerosis: difficulties in classification

Cardiac allograft vasculopathy is regarded as a progressive and diffuse intimal hyperplastic lesion of arteries and veins that leads to insidious vessel narrowing and to allograft ischemic disease, such as acute myocardial infarction or sudden cardiac death. The coronary lesions in transplanted hearts are considered as a particular type of arteriosclerosis with many similarities but also significant differences compared to native coronary atherosclerosis. It is particularly difficult for pathologists to systematically classify the lesions and to elucidate their origins, since over time, the allograft immune responses cause vascular pathology characterized by not only the onset of de novo fibrocellular lesions but also remodeling of already-existing native atherosclerotic lesions in the donor heart. Intraplaque hemorrhages, which result from newly formed leaky microvessels, may cause rapid increase of stenosis and generate a substrate for plaque destabilization. Comparing cardiac allograft vasculopathy from explanted hearts at autopsy with native coronary atherosclerosis from hearts removed at transplantation has revealed that ongoing intraplaque hemorrhages are also an important feature of cardiac allograft vasculopathy and may be important factors in the rapid progression of cardiac allograft vasculopathy.