Results of the tension-free vaginal tape procedure for stress incontinence: Patient''s perspective

BACKGROUND: To evaluate the results of the tension-free vaginal tape procedure (TVT) from a patient's perspective. METHODS: Between May 1999 and January 2002, 90 patients underwent a TVT for genuine stress incontinence (GSI) and mixed incontinence. Prior to the procedure, GSI was confirmed by clinical examination and urodynamic studies. Results were then audited from patient notes and the same patients were sent questionnaires to examine results from a patient perspective. RESULTS: Overall response rate to the questionnaire was 70 (77%). The mean age of the patients was 50.4 years (range 31-83 years). Sixty-one patients had spinal anesthesia, seven had general anesthesia and two had local anesthesia. Mean hospital stay was 3.36 days (range 2-14 days) and mean period from the operation to the time of the survey and audit was 16.34 months (range 3-28; SD 6.92). Thirty-nine (56%) of the 70 patients who answered said that the operation had cured their incontinence, 16 (23%) had an improvement in their symptoms, 7 (10%) had worsening of their symptoms and 8 (11%) felt that the operation did not make any difference. The overall success rate according to the patients' perspective was 79%, whereas our audit showed an overall success rate of 86% (77% and 82%, respectively, when we compared only the 66 patients who had both notes and replies available for analysis). CONCLUSION: Although a patient's perception regarding the success of TVT tends to differ from that of a clinician, it was not found to be statistically significant (P = 0.22, McNemar test). The TVT is a very successful operation, but realistic cure rates should be offered to patients.     

Hodgkin disease: CT of the thymus

The computed tomography (CT) scans in two groups of patients with Hodgkin disease were reviewed to determine the frequency of thymic enlargement. In 50 CT scans from 50 patients with evidence of thoracic disease on CT scans who were examined for primary staging, the thymus was enlarged in 15 of 50 (30%). Fifty CT scans were obtained from 44 patients at the time of 50 separate episodes of known or suspected relapse. Relapse occurred in the mediastinum in 12 episodes, lung parenchyma in five, and both sites in one. Thymic enlargement thought to be due to involvement by disease was present in seven of 18 (38%). Mediastinal disease was associated with thymic enlargement in all but one patient in whom a thymic cyst developed after radiation therapy. Differentiation of thymic enlargement from enlarged superior mediastinal lymph nodes was easily made in all but two patients. Thymic enlargement in the absence of lymph node enlargement may indicate a different disease, since isolated Hodgkin disease of the thymus is uncommon. Primary thymic tumor should be considered initially, whereas after treatment, rebound hyperplasia of the thymus may be the cause of enlargement.     

Solid and papillary epithelial neoplasms of the pancreas: CT findings

Five female patients and one male patient with solid and papillary epithelial neoplasms of the pancreas were examined with computed tomography (CT). The mean age of the patients was 27 years (range, 13-46 years). All cases showed well-encapsulated, round or lobulated masses consisting of both cystic and solid areas. Cystic portions showed CT numbers that suggested hemorrhagic necrosis. There were no internal septations within the masses. In three tumors located in the head of the pancreas, dilatation of the biliary tree was absent or minimal, although the masses were large. Two tumors contained calcifications. One tumor demonstrated metastatic deposits in liver and lymph nodes. Metastatic masses appeared similar to the primary pancreatic mass. Solid and papillary neoplasm of the pancreas should be the primary diagnostic consideration when characteristic CT findings are detected in a young female patient.     

Variable selection under multiple imputation using the bootstrap in a prognostic study

Background  

Missing data is a challenging problem in many prognostic studies. Multiple imputation (MI) accounts for imputation uncertainty that allows for adequate statistical testing. We developed and tested a methodology combining MI with bootstrapping techniques for studying prognostic variable selection.     

The (α2→8)-Linked Polysialic Acid Capsule and Lipooligosaccharide Structure Both Contribute to the Ability of Serogroup B Neisseria meningitidis To Resist the Bactericidal Activity of Normal Human Serum

The molecular basis for the resistance of serogroup B Neisseria meningitidis to the bactericidal activity of normal human sera (NHS) was examined with a NHS-resistant, invasive serogroup B meningococcal isolate and genetically and structurally defined capsule-, lipooligosaccharide (LOS)-, and sialylation-altered mutants of the wild-type strain. Expression of the (α2→8)-linked polysialic acid serogroup B capsule was essential for meningococcal resistance to NHS. The very NHS-sensitive phenotype of acapsular mutants (99.9 to 100% killed in 10, 25, and 50% NHS) was not rescued by complete LOS sialylation or changes in LOS structure. However, expression of the capsule was necessary but not sufficient for a fully NHS-resistant phenotype. In an encapsulated background, loss of LOS sialylation by interrupting the α2,3 sialyltransferase gene, lst, increased sensitivity to 50% NHS. In contrast, replacement of the lacto-N-neotetraose α-chain (Galβ1-4GlcNAcβ1-3Galβ1-4Glc) with glucose extensions (Glc_N) in a galE mutant resulted in a strain resistant to killing by 50% NHS at all time points. Encapsulated meningococci expressing a Hep₂(GlcNAc)→KDO₂→lipid A LOS without an α-chain demonstrated enhanced sensitivity to 50% NHS (98% killed at 30 min) mediated through the antibody-dependent classical complement pathway. Encapsulated LOS mutants expressing truncated Hep₂→KDO₂→lipid A and KDO₂→lipid A structures were also sensitive to 50% NHS (98 to 100% killed at 30 min) but, unlike the wild-type strain and mutants with larger oligosaccharide structures, they were killed by hypogammaglobulinemic sera. These data indicate that encapsulation is essential but that the LOS structure contributes to the ability of serogroup B N. meningitidis to resist the bactericidal activity of NHS.Serogroup B Neisseria meningitidis (the meningococcus) is an obligate human pathogen and remains a leading cause of fulminant septicemia and meningitis. In addition to sporadic outbreaks, large epidemics of serogroup B meningococcal disease continue to occur in many parts of the world, including South America, the United States Pacific Northwest, Western Europe, and New Zealand (4, 22). After penetrating upper respiratory tract mucosal surfaces, N. meningitidis must survive and multiply in the bloodstream to cause sepsis, meningitis, and other manifestations of invasive meningococcal disease. A major mechanism inhibiting or preventing the multiplication of meningococci in the blood is the complement-mediated bactericidal activity of human sera (17, 39). The importance of this activity in the prevention of systemic meningococcal disease is reinforced by host factors that alter bactericidal activity and increase the risk for development of invasive disease. These factors include the absence of bactericidal antibodies against meningococci (17, 18, 45), deficiencies in the complement cascade (13), and the presence of blocking immunoglobulin A antibodies that inhibit the bactericidal activity of human sera (19). The bactericidal activity of human sera against meningococci is also used as a surrogate marker for assessing meningococcal vaccine efficacy.Meningococci have evolved mechanisms that protect them from the bactericidal activity of human sera. Invasive serogroup B meningococcal strains recovered from blood and cerebrospinal fluid often resist being killed by human sera (48). The molecular basis for resistance has been attributed to the expression by this organism of an (α2→8)-linked polysialic acid capsule and a short-chained lipooligosaccharide (LOS) with terminal sialic acid residues (23, 34, 35). Meningococci isolated from the bloodstream in invasive disease, in contrast to nasopharyngeal isolates, are heavily encapsulated (9) and express the L3,7,9 LOS immunotypes (28). These immunotypes have a lacto-N-neotetraose originating from HepI of the inner core, which may be terminally sialylated (34, 62). However, the experimental data defining the precise contributions of the capsule, LOS sialylation, and LOS structure to the ability of serogroup B meningococci to resist the bactericidal activity of human sera is conflicting (11, 15, 20, 21, 27, 37, 63–65).LOS epitopes are immunogenic in infants and children and induce protective bactericidal antibodies in convalescent sera (10, 12). These bactericidal LOS antibodies appear to be directed at conserved low-molecular-weight LOS epitopes (10, 12). LOS is also a component of new serogroup B outer membrane vesicle (OMV) vaccines and is proposed as a basis for other new meningococcal vaccines (1–3, 50). Although changes in the structure of LOS are known to influence the amount and epitopes of bactericidal and other functional antibodies elicited by OMV vaccines (2), the precise LOS structure(s) to include in these and other LOS-containing meningococcal vaccines is uncertain.To help understand the basis for meningococcal survival following mucosal invasion and to facilitate development of meningococcal vaccines which may contain LOS, we created a series of genetically and structurally defined capsule-, sialylation-, and LOS-altered mutants of the serogroup B meningococcal strain NMB. We used these mutants to study the contributions of the capsule, LOS sialylation, and changes in LOS structure to meningococcal resistance to the bactericidal activity of normal human sera (NHS).     

Clinical and genetic features of variegate porphyria in a Chinese patient

Acute porphyria is rare in orientals. We describe a Chinese woman with recurrent generalised tonic-clonic seizures and abdominal pain. Genomic DNA studies identified a heterozygous base substitution from guanine to adenine at nucleotide position 503, resulting in substitution of arginine by histidine at position 168 of the protein (R168H). This genetic abnormality is similar to the mutation reported in Caucasians with variegate porphyria. To the best of our knowledge, this is the first report in the English literature a Chinese patient with variegate porphyria with an identifiable mutation. A brief review of porphyria is presented.     

Suppression of hepatic fatty acid oxidation and food intake in men

We investigated the effects of the fatty acid oxidation inhibitor etomoxir (ETO) on food intake and on fat and carbohydrate metabolism in two double-blind crossover studies in male, normal-weight subjects. In study 1, ETO (75 mg [+]-racemate) or placebo was given orally 30 min after completion of a standardized, fat-enriched (total energy: 2698 kJ, 40% from fat) lunch. The subjects (n = 15) were isolated from external time cues and free to choose when to eat dinner from an oversized serving (total energy: 6656 kJ, 60% from fat). In study 2, subjects (n = 13) were selected for habitually high fat intake (mean: 44% of energy intake). ETO (150 mg) or placebo was given after an overnight fast, 2.5 h before offering an oversized high fat breakfast (6960 kJ, 72% from fat). In both studies, blood samples were taken and the respiratory quotient (RQ) was measured several times during each test period. In study 1, ETO (75 mg) did not affect the timing and size of the dinner or subjective feelings of hunger and satiety. Although ETO (75 mg) did not affect the RQ, it decreased plasma beta-hydroxybutyrate (BHB) and increased plasma lactate compared with placebo. Plasma triacylglycerols (TG), free fatty acids (FFA), glucose, and insulin were not affected by ETO. In study 2, ETO (150 mg) enhanced hunger feelings and increased the size of the breakfast by 22.7%. ETO did not affect the RQ, but baseline RQ was lower in study 2 than in study 1 (0.83 versus 0.89, P < 0.01). Compared with placebo, ETO (150 mg) decreased plasma BHB and increased plasma FFA and plasma lactate. Baseline plasma concentrations of BHB, FFA, and lactate were higher in study 2 than in study 1 (BHB: 242 versus 81 mumol/L, P < 0.001; FFA: 0.674 versus 0.406 mmol/L, P < 0.01; lactate: 1.08 versus 0.74 mmol/L, P < 0.05). Plasma concentrations of TG, glucose, and insulin were not affected by ETO. The results suggest that inhibition of hepatic fatty acid oxidation stimulates eating in men when baseline fatty acid oxidation is sufficiently high and markedly suppressed by the treatment.     

Oral presentations

SSIEM 33rd Annual Symposium Cardiff, 10th–13th September 1996 Abstracts

Oral presentations