Functional outcome after perineal stapled prolapse resection for external rectal prolapse.

BACKGROUND: A new surgical technique, the Perineal Stapled Prolapse resection (PSP) for external rectal prolapse was introduced in a feasibility study in 2008. This study now presents the first results of a larger patient group with functional outcome in a mid-term follow-up. METHODS: From December 2007 to April 2009 PSP was performed by the same surgeon team on patients with external rectal prolapse. The prolapse was completely pulled out and then axially cut open with a linear stapler at three and nine o'clock in lithotomy position. Finally, the prolapse was resected stepwise with the curved Contour Transtar stapler at the prolapse's uptake. Perioperative morbidity and functional outcome were prospectively measured by appropriate scores. RESULTS: 32 patients participated in the study; median age was 80 years (range 26-93). No intraoperative complications and 6.3% minor postoperative complications occurred. Median operation time was 30 minutes (15-65), hospital stay 5 days (2-19). Functional outcome data were available in 31 of the patients after a median follow-up of 6 months (4-22). Preoperative severe faecal incontinence disappeared postoperatively in 90% of patients with a reduction of the median Wexner score from 16 (4-20) to 1 (0-14) (P < 0.0001). No new incidence of constipation was reported. CONCLUSIONS: The PSP is an elegant, fast and safe procedure, with good functional results. TRIAL REGISTRATION: ISRCTN68491191.

The role of CFTR and SPINK-1 mutations in pancreatic disorders in HIV-positive patients: a case-control study.

OBJECTIVE: Pancreatic disorders in HIV-positive patients are frequent. CFTR and SPINK-1 mutations have been reported to increase the risk of pancreatitis, but no data are available in HIV-positive patients. This study will evaluate the frequency of CFTR mutations and SPINK-1 polymorphisms in HIV-positive patients with clinical pancreatitis or asymptomatic elevation of serum pancreatic enzymes. METHOD: Cases (patients with hyperamylasemia) were identified during a toxicity study conducted in August 1999 among 1152 participants of the Swiss HIV Cohort Study. We designed a case-control study in which each case was matched one to one to an HIV-infected control according to sex, age, CD4 cell count, viraemia and medication use. CFTR mutations and SPINK-1 polymorphisms were studied using polymerase chain reaction techniques. RESULTS: Fifty-one HIV-positive patients with hyperamylasemia were detected among 1152 participants in the toxicity study (4.4%). There were 13 carriers of CFTR and SPINK-1 mutations (12.7%). Amylase levels were 316 +/- 130 U/l for the group with mutations, and 135 +/- 18 U/l for non-carriers (P = 0.79). However, among patients with hyperamylasemia, those with CFTR or SPINK-1 mutations had 648 +/- 216 U/l amylase levels compared with 232 +/- 28 U/l for those without (P = 0.025). Ten patients had acute pancreatitis, four of whom had CFTR mutations or SPINK-1 polymorphisms (40%) compared with seven of the control patients (14%) (P = 0.01). CONCLUSION: CFTR mutations and SPINK-1 polymorphisms are frequent among HIV-positive patients suffering from acute pancreatitis. These mutations may increase the susceptibility to pancreatitis when exposed to environmental risk factors.

A convenient HPLC assay for the determination of fructosamine-3-kinase activity in erythrocytes.

Fructosamine-3-kinase (FN3K) mediates the regeneration of lysine from fructosamines formed on proteins as a result of the 'early' Maillard reaction. As fructosamines and advanced glycation endproducts derived therefrom are supposed to play an adverse role in the development of diabetic complications, FN3K is discussed as a protein-repairing enzyme. In this study, a method for the determination of FN3K activity in erythrocyte lysate is described which overcomes the complexity of currently known assays. The assay is based on the FN3K-dependent conversion of the synthetic UV-active fructosamine Nalpha-hippuryl-Nepsilon-(1-deoxy-D-fructosyl)lysine (BzGFruK) to Nalpha-hippuryl-Nepsilon-(phosphofructosyl)lysine (BzGpFruK). The FN3K activity was quantified by measuring the formation of BzGpFruK using RP-HPLC with UV detection. Identification of the metabolite BzGpFruK was achieved by means of UV and mass spectroscopy. The results are related to the content of haemoglobin for standardisation. First activity measurements with a chosen number of normoglycaemic subjects confirmed the convenient applicability of the method and showed distinctly different individual activities, as already discovered recently. The new established assay needs only the equipment of a routine laboratory with HPLC instrumentation. This should facilitate further studies about a possible relationship between the FN3K activity and the development of diabetic complications.

Antiretroviral therapy reduces markers of endothelial and coagulation activation in patients infected with human immunodeficiency virus type 1.

We investigated the effect of antiretroviral therapy on vascular activation in 41 human immunodeficiency (HIV)--infected patients receiving a regimen that included either at least 1 protease inhibitor (PI; n = 21) or a nonnucleoside reverse-transcriptase inhibitor (NNRTI; n = 20). A control group of 21 healthy subjects was included for comparison. Levels of endothelial markers (soluble vascular cell adhesion molecule [sVCAM]--1, soluble intercellular adhesion molecule--1, and von Willebrand factor) were higher in HIV-infected persons before treatment than in control subjects and decreased significantly after 5--13 months of treatment. Levels of sVCAM-1 and von Willebrand factor correlated significantly with initial virus load. d-dimer concentrations also decreased significantly after initiation of treatment. PI- and NNRTI-containing regimens had similar effects. Therapy did not reduce levels of the soluble platelet (sP) activation markers sP-selectin and CD40 ligand. The inhibition of markers of vascular activation may counterbalance sequelae of therapy-induced dyslipidemia and potentially prevent development of atherosclerosis in HIV-infected patients.

Prevalence of unsafe sexual behavior among HIV-infected individuals: the Swiss HIV Cohort Study.

Sexual contact is the major mode of HIV transmission. Increased sexual risk taking has been described in HIV-infected individuals receiving potent antiretroviral therapy. A new questionnaire on sexual behavior was introduced into the Swiss HIV Cohort Study on April 1, 2000. We evaluated sexual behavior in all individuals who completed the questionnaire for the first time within 1 year after its introduction. Our primary hypothesis was that self-reported unsafe sexual behavior would be more prevalent among individuals with optimal viral suppression. On April 1, 2000, 4948 individuals were registered in the study, and 4723 (95%) completed the questionnaire. Of these individuals, 12% reported unsafe sex, 78% received antiretroviral therapy, and 25% had optimal viral suppression (HIV RNA level always <50 copies/mL during the preceding 12 months). During the preceding 6 months, 55% of individuals had stable and 19% had occasional partners, and 6% had both types of partners. Sexual intercourse was reported by 82% of individuals with stable and 87% of individuals with occasional partners, and of those reporting sexual intercourse in each group, 76% and 86%, respectively, said that they always used condoms. After adjustment for covariates, reported unsafe sex was not associated with optimal viral suppression (odds ratio, 1.04; 95% confidence interval, 0.81-1.33) or antiretroviral therapy (odds ratio, 0.83; 95% confidence interval, 0.65-1.07), but it was associated with gender, age, ethnicity, HIV transmission group, HIV status of partner, having occasional partners, and living alone. There is no evidence that self-reported unsafe sexual behavior is more prevalent among HIV-infected individuals with optimal viral suppression. However, unsafe sex is associated with other factors.