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Objectives: To characterize pain and exposure after Prolift placement and identify risk factors., Methods: A case series of women who underwent Prolift vaginal mesh were surveyed. Pain was assessed using a visual analog scale. Exposure was evaluated clinically., Results: Of 183 eligible patients, 160 completed the survey, and 45 returned for examination. Mean preoperative pain score was 0.97 and postoperative was 1.35 (P = 0.12). Pre- and postoperative pain scores by compartment were: anterior (1.34 vs 1.25, mean change -0.09, P = 0.84), posterior (1.30 vs 1.56, mean change 0.26, P = 0.72), and total (0.63 vs 1.34, mean change 0.71, P = 0.05). Graft exposure was confirmed in 23 of 183 patients (12.6%); however, because asymptomatic patients were not examined, the true exposure rate may be underestimated. Hematoma formation is independently associated with mesh exposure, adjusted odds ratio 18.4 (95% confidence interval 3.4-147.4, P = 0.01)., Conclusions: Although pain scores did not increase overall, there was a trend toward increased pain score in the patients with total (anterior and posterior) Prolift. Hematoma formation was significantly associated with mesh exposure.

Obliterative vaginal surgery is an appropriate management option for pelvic organ prolapse in women who do not desire future vaginal intercourse. When colpoclesis is not technically feasible, constricting repairs can be performed. Obliterative surgery in older women has the advantages of fewer complications and less surgical time than reconstructive procedures, especially in those with medical comorbidities. Age-related changes in physiology should be kept in mind along with the risk of postoperative delirium. Candidates should be counseled regarding high success and satisfaction rates.

Purpose: We tested the effects of a saw palmetto herbal blend in men with symptomatic benign prostatic hyperplasia (BPH) via a randomized, placebo controlled trial., Materials and Methods: We randomized 44 men 45 to 80 years old with symptomatic BPH into a trial of a saw palmetto herbal blend versus placebo. End points included routine clinical measures (symptom score, uroflowmetry and post-void residual urine volume), blood chemistry studies (prostate specific antigen, sex hormones and multiphasic analysis), prostate volumetrics by magnetic resonance imaging, and prostate biopsy for zonal tissue morphometry and semiquantitative histology studies., Results: Saw palmetto herbal blend and placebo groups had improved clinical parameters with a slight advantage in the saw palmetto group (not statistically significant). Neither prostate specific antigen nor prostate volume changed from baseline. Prostate epithelial contraction was noted, especially in the transition zone, where percent epithelium decreased from 17.8% at baseline to 10.7% after 6 months of saw palmetto herbal blend (p <0.01). Histological studies showed that the percent of atrophic glands increased from 25. 2% to 40.9% after treatment with saw palmetto herbal blend (p <0.01). The mechanism of action appeared to be nonhormonal but it was not identified by tissue studies of apoptosis, cellular proliferation, angiogenesis, growth factors or androgen receptor expression. We noted no adverse effects of saw palmetto herbal blend. When the study was no longer blinded, 41 men elected to continue therapy in an open label extension., Conclusions: Saw palmetto herbal blend appears to be a safe, highly desirable option for men with moderately symptomatic BPH. The secondary outcome measures of clinical effect in our study were only slightly better for saw palmetto herbal blend than placebo (not statistically significant). However, saw palmetto herbal blend therapy was associated with epithelial contraction, especially in the transition zone (p <0.01), indicating a possible mechanism of action underlying the clinical significance detected in other studies.

Objectives: To determine the long-term effects of finasteride treatment on prostate tissue composition; to relate these effects to clinical outcomes; and to test the hypothesis that finasteride exerts a selective or preferential action on the transition zone., Methods: Nineteen men with symptomatic benign prostatic hyperplasia (BPH) who completed a 6-month double-blind trial of finasteride were enrolled in a 24-month open-label extension study of drug responders. Magnetic resonance imaging and prostate biopsy for morphometric analysis were performed together 70 times: at baseline (n = 19), after treatment periods of intermediate duration (6 to 18 months, n = 32), and after long-term drug treatment (24 to 30 months, n = 19). At baseline, prostate volume averaged 51 cc, of which 57% was transition zone., Results: Decreases in symptom score, dihydrotestosterone and prostate-specific antigen levels, and prostate volume occurred at 6 months (P <0.01), stabilized, and were maintained without further long-term decreases. Prostate epithelium contracted progressively from baseline (19.2% tissue composition; 6.0-cc volume; 3.2 stroma/epithelial ratio) to intermediate (12.5%, 3.3 cc, and 5.6, respectively) to long-term treatment (6.4%, 2.0 cc, and 17.4, respectively, P <0.01 for all). Percent epithelial contraction was similar in the peripheral and transition zones (P = NS). The transition zone remained a relatively constant proportion (53% to 58%) of whole-prostate volume from baseline to long-term observation., Conclusions: Long-term finasteride treatment (24 to 30 months) results in a marked involution of the prostate epithelium, which continues to progress for many months after clinical effects stabilize. The effect on the epithelium is similar in the peripheral and transition zones for both morphometric and volumetric changes. Progressive contraction of the prostate epithelium appears to constitute the underlying mechanism for sustained action of finasteride.

Purpose: We sought to quantify prostate tissue changes induced by finasteride and to identify a predictor of finasteride response in men with symptomatic benign prostatic hyperplasia (BPH) via a randomized, placebo controlled, double-blind clinical trial., Materials and Methods: Men with symptomatic BPH (52 to 78 years old) were randomly assigned to 6 months of treatment with finasteride (26) or placebo (15). Outcome measures were clinical (urinary symptom score and flow rate), chemical (serum prostate specific antigen and dihydrotestosterone levels), volumetric (transrectal ultrasound, and magnetic resonance imaging for whole and zonal prostate volumes) and histological (morphometry of prostate sextant biopsies, separated into inner and outer gland segments, to measure the percent epithelium, stroma and glandular lumen)., Results: In the finasteride group we found a suggestion of decreasing symptom scores and increasing flow rates (not significant) with significant decreases (p < 0.01) in prostate specific antigen (48%), dihydrotestosterone (74%) and prostate volume (21%). Finasteride treatment induced a 55% decrease in inner gland epithelium (p < 0.01) with little effect on stroma or lumina. We also found a linear correlation between pretreatment inner gland epithelial content and prostate volume decrease induced by the drug (tau = 0.58, p = 0.01)., Conclusions: Finasteride treatment results in a major suppression of prostate epithelium, which is most pronounced in the inner gland. Moreover, a finasteride induced prostate volume decrease was predictable by quantification of epithelial tissues of the inner gland. These data lend additional support to the emerging concept of transition zone primacy in symptomatic BPH.

Two patients with infrahepatic interruption of the inferior vena cava (IVC) with azygos (hemiazygos) continuation were examined ultrasonographically and the findings compared to seven normal studies. Pathognomonic ultrasonographic features of this anomaly are easily demonstrated and include absence of the IVC at the level of the liver and independent drainage of the confluence of hepatic veins into the right atrium. Conventional venography can now be replaced by ultrasonic examination to establish this diagnosis. The embryology, anatomy and clinical implications of this entity are discussed.

Two cases are reported in which air refluxed from the bladder to the pelviocaliceal systems after voiding cystourethrography. We stress that this is a benign condition, which can indicate the presence and degree of ureteral reflux.

The procoagulant protein F.VIII:C is noncovalently bound to von Willebrand factor (vWF) to give the factor VIII macromolecular complex. New highly purified preparations of isolated human F.VIII:C, devoid of vWF and about 500,000-fold purified, were administered to hemophilia A and von Willebrand disease (vWD) dogs to determine their hemostatic effectiveness and survival in the circulation. Two preparations of F.VIII:C were used: peak 1, with active components of Mr 185,000-280,000, and peak 2, with a single component of Mr 170,000. In hemophilic dogs, with no plasma F.VIII:C but normal vWF, both preparations immediately elevated plasma F.VIII:C to expected levels, promptly stopped induced and spontaneous hemorrhages, and gave sustained plasma levels of F.VIII:C. The isolated F.VIII:C immediately complexed with endogenous vWF in hemophilic plasma and was eliminated exponentially, with a half-life (t1/2) of about 9 hr. Survival of peak 2 F.VIII:C was longer than that of peak 1 material. In contrast, F.VIII:C complexed to vWF in a therapeutic concentrate administered to hemophilic dogs was eliminated biexponentially with first-phase t1/2 of 3.2 hr and second-phase t1/2 of 9 hr. In vWD dogs with no vWF and reduced F.VIII:C levels, the isolated F.VIII:C produced supernormal levels of F.VIII:C without effect on induced bleeding. It was rapidly eliminated from plasma with a t1/2 of about 1 hr, as was the complexed F.VIII:C in the concentrate. These data indicate that isolated F.VIII:C promptly complexes with vWF and in this form is highly effective in controlling hemophilic hemorrhages with good survival in plasma. Without endogenous vWF with which to complex, the F.VIII:C is promptly eliminated.

Recombinant factor VIIa (rF.VIIa) is a two-chain procoagulant enzyme (Mr, approximately 50,000) active only when complexed with tissue factor in the extrinsic clotting system. We administered human rF.VIIa to hemophilic and von Willebrand disease (vWD) dogs to determine its hemostatic effectiveness and survival in the circulation. Hemophilia A dogs lacking factor VIII demonstrated an immediate increase in plasma rF. VIIa and prompt stoppage of hemorrhage at bleeding time (BT) sites. In seven studies in two dogs, the range of dose of rF. VIIa was 50-220 micrograms/kg, with an apparent 7- to 11-fold increase in plasma factor VII and a mean recovery in plasma of 34%. The t1/2 was 2.8 +/- 0.5 hr. The BT was normalized except in an animal given the minimum dose. In four studies in two hemophilia B dogs lacking factor IX, BT was normalized. The elevation in plasma factor VII was by a factor of 8-30, with a mean recovery of rF.VIIa in plasma of 44%. In two studies in a homozygous vWD dog lacking von Willebrand factor, which is needed for platelet function, BT was not corrected even though large doses of rF. VIIa were given. The human rF. VIIa protein was immunogenic for dogs. These studies indicate that factor VIIa corrects the hemostatic defect in dogs with hemophilia A and B, diseases primarily of the intrinsic clotting system, but does not correct the hemostatic defect in vWD.

Thrombotic thrombocytopenia with severe von Willebrand factor (vWF) depletion was induced in rats by intraperitoneal injection of botrocetin, a Bothrops factor requiring vWF for platelet aggregation. The vWF deficiency state with thrombocytopenia was produced in 12 animals by single or multiple injections of botrocetin. Single botrocetin injection (450 units/kg) reduced plasma vWF activity to less than 0.01 mu/ml for 24 hours and less than 0.2 units/ml up to 72 hours. During this period, multimeric analysis of plasma vWF:Ag revealed loss of intermediate and high molecular weight forms. A moderate reduction in vWF:Ag (Laurell) and FVIII:C was observed. Bleeding time remained prolonged during the deficiency state. Recovery of plasma vWF and platelet count occurred in 4 to 5 days. Multiple botrocetin injections (450 units/kg/injection) at 48-hour intervals produced a sustained severe vWF depletion (less than 0.2 units/ml) for 1 week. On the 8th day, vWF and platelet count had recovered to preinjection levels. Recovery was associated with the appearance of increased levels of very high molecular weight multimers of vWF:Ag in the plasma. After each botrocetin administration (single or repeat), a transient thrombocytopenia developed which was most severe at 1 to 5 hours postinjection. Another group of 10 animals was given a single botrocetin injection and specimens of lung, liver, kidney, and spleen were obtained at varying time intervals postinjection. Transmission electron micrographs of the lung and spleen 2 hours after botrocetin administration showed platelet aggregates and platelet microthrombi in the lung and spleen. The platelet thrombi in the lung had disappeared within 24 hours, and in the spleen by 48 hours. Liver sinusoids and kidney glomeruli were free of thrombi. A comparison is made of the thrombocytopenia and the ultrastructure of the platelet microthrombi induced by botrocetin with that of other agents.

Two adult cases of anomalous left pulmonary artery (pulmonary artery sling) are described. Findings on plain radiography, conventional pluridirectional tomography, and barium esophagography led to diagnosis. Computed tomography (CT), not previously described in this anomaly, was done in each case, confirming the diagnosis and excluding other mediastinal abnormalities. Pulmonary arteriography was incidentally performed in one patient and was diagnostic. Tracheobronchial anomalies were seen in both cases. The authors suggest the diagnosis of anomalous left pulmonary artery may be made by noninvasive conventional methods and CT without the need for pulmonary arteriography.