Functional outcome after perineal stapled prolapse resection for external rectal prolapse

<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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) (<it>P </it>< 0.0001). No new incidence of constipation was reported.</p> <p>Conclusions</p> <p>The PSP is an elegant, fast and safe procedure, with good functional results.</p> <p>Trial registration</p> <p>ISRCTN68491191</p

Is epsilon 4 allele of apolipoprotein E associated with more severe end-organ damage in essential hypertension?

The aim of the present study comparing patients with mild to moderate hypertension with controls, was to explore a possible association between hypertension-related target organ damage and evaluation found in the gene encoding apolipoprotein E (apo E) genotype. Detailed medical history was recorded and physical examination was per-formed for all patients in the study (88 hypertensives, 63 normotensive controls). PCR (Polymerase Chain Reaction), RFLP (Restriction Fragment Length Polymorphism), and agarose gel electrophoresis techniques were used to determine the apo E genotypes. The frequencies of apo epsilon2, apo epsilon3, and apo epsilon4 alleles were 3.97, 88.06, and 9.95%, respectively in the hypertensive group. The frequencies of apo epsilon2, apo epsilon3, and apo epsilon4 alleles were 5.5, 92.0, and 2.38%, respectively in the control group. There were about twice as many individuals in the heterozygote hypertensive group who had apo E3/4 as compared to the control group (7.30 vs. 2.38%) (p = 0.07). The hypertensive patients who were carriers of the apo epsilon4 had significantly higher organ damage (left ventricular hypertrophy (p < 0.001). dilated left atrium (p < 0.05), retinopathy (p < 0.05)) as compared to those who were not carriers of apo epsilon4. These results showed a trend for the epsilon4 allele to be associated with a higher prevalence of target organ damage in patients with mild to moderate hypertension. Copyright (C) 2001 John Wiley & Sons, Ltd

CCR2-64I is a risk factor for development of bladder cancer

Chemokines are potent proinflammatory cytokines that are implicated in numerous inflammatory diseases. Proinflammatory gene polymorphisms lead to variations in the production and concentration of inflammatory proteins. We investigated a possible association between polymorphisms in chemokine and chemokine receptor genes (MCP-1 A-2518G and CCR2-V64I) and bladder cancer risk. Genotypes were determined by PCR-RFLP assays in 72 bladder cancer patients and 76 unrelated age-matched healthy controls. There were significant differences in the frequencies of the MCP-1 A-2518G (P = 0.012) and CCR2-V64I genotypes (P = 0.004) between the controls and patients. The MCP-1 A-2518G GG genotype frequencies for controls and cases were 0.039 and 0.11, respectively; individuals who had the GG genotype had a 3-fold increased risk of bladder cancer (P = 0.08). The CCR2-64I/64I genotype frequencies for controls and cases were 0.02 and 0.13, respectively; subjects carrying the 64I/64I genotype had a 5.9-fold increased risk of bladder cancer compared to the other genotypes. Individuals carrying the CCR2-V64I heterozygote or homozygous variant genotype (64I/64I + wt/64I) had a 2.9-fold increased risk of bladder cancer compared with the wild-type genotype (wt/wt). CCR2-V64I heterozygote or homozygous wild-type genotype (wt/wt + wt/64I) frequencies were significantly decreased in the patient group compared with controls. We conclude that CCR2-64I is a new risk factor for bladder cancer

ACE I/D gene polymorphism in primary FSGS and steroid-sensitive nephrotic syndrome

The role of angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism in various renal disorders has been investigated. We evaluated the association between the clinical characteristics and ACE genotypes of Turkish children with primary focal segmental glomerulosclerosis (FSGS) and steroid-sensitive nephrotic syndrome (SSNS). Patients with FSGS (n=30) were classified into two groups: one with remission together with stable renal function (n=22) and the other without remission and with impaired renal function (n=8). We classified children with SSNS (n=43) that were followed for at least 4 years into two subgroups as having more frequent (n=19) and less frequent relapses (n=11). The DD genotype was more frequent in the SSNS group than that in controls (37% vs. 17%, chi(2)=4.98, P=0.025). However, among SSNS subgroups, the frequency of the DD genotype was not different. The distribution of ACE genotype was similar among patients with FSGS and SSNS. There was no difference in the ACE I/D distribution between children with FSGS and normal controls (II 10%, ID 60%, DD 30% vs. II 13%, ID 70%, DD 17%). The frequency of the DD genotype was higher in FSGS patients with declining renal function (63%) than in those with stable renal function (18%) (P=0.031). Progressive renal impairment was significantly more frequent in patients with FSGS with the homozygous D allele compared with FSGS patients with ID and II genotypes. Our results indicate that the DD genotype may be a risk factor for the development of progressive renal impairment in children with FSGS; however, larger studies are required to confirm this