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Low-grade chronic inflammation has been suggested to play a role in uncomplicated asymptomatic and symptomatic diverticular disease. However, population-based studies are lacking. We investigated whether community participants with diverticulosis, with or without symptoms, would have colonic inflammation on histology and serology. In a nested case-control study of 254 participants from the population-based colonoscopy (PopCol) study, colonic histological inflammatory markers and serological C-reactive protein levels were analyzed in cases with diverticulosis and controls without diverticulosis. Statistical methods included logistic and linear regression models. Background variables including age (P = 0.92), sex (P = 1.00), body mass index (P = 0.71), smoking (P = 0.34), and recent antibiotic exposure (P = 0.68) were similar between cases and controls. Cases reported more abdominal pain (P = 0.04) and diarrhea symptoms (mushy and high-frequency stools) than controls (P = 0.01 and P = 0.03, respectively) but were otherwise similar. The median C-reactive protein levels were similar among cases and controls [1.05 mg/L (0.3, 2.7) vs 0.8 (0.4, 2.2), P = 0.53]. There was a trend of increased numbers of cecal lymphoid aggregates in cases vs controls (P = 0.07), but no other associations between diverticulosis and inflammatory markers on histology were found. Similarly, no serological or mucosal inflammation was associated with symptomatic cases of diarrhea or abdominal pain vs asymptomatic controls. In a general community sample, both asymptomatic and symptomatic diverticulosis are not associated with colonic mucosal inflammation. Other explanations for symptomatic colonic diverticulosis need to be identified.

Aims. It is currently unknown whether an association exists between polypropylene mesh and urethral diverticulum formation following placement of polypropylene midurethral slings (MUS) for the treatment of stress urinary incontinence (SUI). We aimed to examine the literature associating MUS with the occurrence of urethral diverticula. Methods. Multiple online research databases, including PubMed, Google Scholar, EBSCOhost, and the Cochrane Library, were searched, from January 2019 to February 2019, for evidence related to the occurrence of urethral diverticula following polypropylene MUS procedures. Results. Four case reports were published demonstrating the occurrence of urethral diverticula following the use of polypropylene mesh for surgical treatment of SUI. Subjects of these cases were menopausal and had an elevated body mass index (BMI), recurrent urinary tract infections (UTIs), autoimmune conditions, or prior pelvic floor surgeries. A thorough urologic workup, including imaging prior to sling placement, was not always performed. Conclusion. No clear association exists between polypropylene MUS placement and subsequent urethral diverticulum formation. Factors that diminish polypropylene mesh biocompatibility include elevated BMI, menopause, recurrent UTIs, prior pelvic surgeries, and preexisting medical conditions. Symptoms associated with urethral diverticula should prompt a complete urologic workup prior to MUS placement.

Zenker's diverticulum is an outpouching of the mucosa through the Killian's triangle. The etiology of Zenker's diverticulum is not well understood. It is thought to be due to the incoordination or incomplete relaxation of the cricopharyngeal muscle. Most patients are men who present with symptoms of dysphagia between the seventh and eighth decades of life. The diagnosis is made with a dynamic contrast swallowing study. Treatment options include open surgical diverticulectomy and diverticulopexy with myotomy or myotomy alone using flexible or rigid endoscopes. Rigid endoscopic treatment is currently the preferred initial choice for Zenker's diverticulum of any size. The flexible endoscopic technique is used when there is a high risk of general anesthesia, or neck extension is contraindicated. Some centers use flexible endoscopy as the initial treatment option. Due to a lack of prospective studies, the treatment choice should be tailored to the individual patient and local expertise.

Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor known to promote the survival and maintenance of neurons not only in the developing but also in the adult enteric nervous system. As diverticular disease (DD) is associated with reduced myenteric neurons, alterations of the GDNF system were studied in asymptomatic diverticulosis (diverticulosis) and DD. Morphometric analysis for quantifying myenteric ganglia and neurons were assessed in colonic full-thickness sections of patients with diverticulosis and controls. Samples of tunica muscularis (TM) and laser-microdissected myenteric ganglia from patients with diverticulosis, DD and controls were analyzed for mRNA expression levels of GDNF, GFRA1, and RET by RT-qPCR. Myenteric protein expression of both receptors was quantified by fluorescence-immunohistochemistry of patients with diverticulosis, DD, and controls. Although no myenteric morphometric alterations were found in patients with diverticulosis, GDNF, GFRA1 and RET mRNA expression was down-regulated in the TM of patients with diverticulosis as well as DD. Furthermore GFRA1 and RET myenteric plexus mRNA expression of patients with diverticulosis and DD was down-regulated, whereas GDNF remained unaltered. Myenteric immunoreactivity of the receptors GFRα1 and RET was decreased in both asymptomatic diverticulosis and DD patients. Our data provide evidence for an impaired GDNF system at gene and protein level not only in DD but also during early stages of diverticula formation. Thus, the results strengthen the idea of a disturbed GDNF-responsiveness as contributive factor for a primary enteric neuropathy involved in the pathogenesis and disturbed intestinal motility observed in DD.

Background The aim of this study was to develop and validate an individualized score based on preoperative parameters to predict patient outcomes after vaginal repair of cesarean section diverticulum. Methods This is a retrospective cohort study (Canadian Task Force classification II-2). Patients were enrolled between Jun 11, 2012, to May 27, 2016. Multivariable logistic regression analyses were used to construct the predictive model. Then, we generated a nomogram to assess the individualized risk of poor prognosis after operation. This prediction model included information from 167 eligible patients diagnosed with cesarean section diverticulum who underwent vaginal repair. Class-A healing group was defined as CSD patients who had menstruation duration of no more than 7 days and a thickness of the remaining muscular layer of no less than 5.8 mm after vaginal repair according to conferences. Others were included in the non-class-A healing group. A final nomogram was computed using a multivariable logistic regression model. Results The factors contained in the individualized prediction nomogram included the depth/ the thickness of the remaining muscular layer ratio, number of menstruation days before surgery, White blood cell and fibrinogen. This model demonstrated adequate discrimination and calibration (C-index = 0.718). There was a significant difference in the number of postmenstrual spotting days (12.98 ± 3.86 VS 14.46 ± 2.86, P  = 0.022) and depth/ the thickness of the remaining muscular layer ratio (2.81 ± 1.54 VS 4.00 ± 3.09, P  = 0.001) between two groups. Decision curve analysis showed that this nomogram was clinically useful. Conclusions This cesarean section diverticulum score can predict the outcomes of cesarean section diverticulum and can be useful for counseling patients who are making treatment decisions.

Background There is no consensus between urologists on the diagnosis and treatment of female urethral diverticula. Once the diagnosis has been established, the most common treatment approach is surgical excision and reconstruction. Whether a staged procedure or simultaneous management is more appropriate for treating concomitant urethral diverticula and stress urinary incontinence remains controversial. Case presentation A 63-year-old woman was hospitalized for repeated frequent urination, urgent urination, odynuria, and dysuria accompanied by intermittent overflow urinary incontinence for over 10 years. She had a 5 year history of urinary stress incontinence prior to onset of these symptoms and had had four urethral caruncles resected on four separate occasions. There was visible leakage of urine when abdominal pressure was increased during physical examination and urodynamic studies. Additionally, turbid urine was discharged when the anterior vaginal wall was squeezed. Cystourethrography showed circumferential filling with contrast and multiple bladder diverticulae in the mid plane of the pubic symphysis. Urethrocystoscopy showed an orifice to a diverticulum at 7 o’clock in the proximal urethra, into which an F19.8 urethroscope could be inserted, enabling examination of most of the diverticulae. The urethral diverticulae were resected, followed by mesh reconstruction of the urethra. During a 20-month follow-up, the treatment outcomes were satisfactory. Conclusion We here report a case of a giant circumferential urethral diverticulum combined with stress urinary incontinence that was successfully managed by an uncommon surgical reconstructive technique: a minimally invasive “Sandwich” mesh repair procedure utilizing synthetic mesh wrap in the midurethral region.

Zenker's diverticulum is a rare and generally benign condition. Its occurrence in a hemodialysis patient has therapeutic and prognostic implications and is a risk factor for mortality and morbidity due to its complications, such as protein-energy malnutrition and pneumonitis. We here report a case of Zenker's diverticulum diagnosed in a chronic haemodialysis patient. The study involved a 61-year-old female patient admitted with upper gastrointestinal bleeding associated with dysphagia. Physical examination showed alteration of general condition and the patient reported an average weight loss of 5 kg in 3 months. Esophagogastroduodenal transit was characterized by dilatation of the cervical esophagus, appearing as a large heterogeneous niche whose upper pole was at the level of the pharyngoesophageal junction. The diagnosis of Zenker's diverticulum was retained. Diverticulectomy by cervical incision was performed. The patient died due to inhalational lung disease in the early postoperative period. Zenker diverticulum is a rare, generally benign disease, but in patients undergoing chronic haemodialysis, it increases mortality and morbidity.

Background. Although air cells within temporal bone may play an important role in the transmission of pulsatile tinnitus (PT) noise, it has not been studied systematically. Purpose. To evaluate the difference in temporal bone pneumatization between PT patients with sigmoid sinus diverticulum and/or dehiscence (SSDD) and healthy people. Material and Methods. A total of 199 unilateral persistent PT patients with SSDD and 302 control subjects underwent dual-phase contrast-enhanced CT (DP-CECT), to assess the grade of temporal bone pneumatization in each ear. Results. In the bilateral temporal bone of 302 controls, 16 ears were grade I, 53 were grade II, 141 were grade III, and 394 were grade IV. Among the affected ears of 199 PT cases, 1 ear was grade I, 18 were grade II, 53 were grade III, and 127 were grade IV. There was no significant difference in the pneumatization grade between the affected PT ear and either ear in the healthy subjects ( p > 0.05 ) . Conclusion. Although air cells within the temporal bone are an important factor in the occurrence of PT, its severity does not differ significantly from the pneumatization of healthy people.

Juxtapapillary duodenal diverticula (JPD) are observed in around 10–20% of patients undergoing endoscopic retrograde cholangiopancreatography (ERCP). They are acquired extraluminal outpouchings of the duodenal wall through ‘locus minoris resistance’ and their incidence increases with age. They have been studied mainly with regard to their association with pancreatobiliary disease. Choledocholithiasis is considered to be strongly associated with JPD, but the role of JPD in the development of cholecystolithiasis and pancreatitis is still disputable. Since JPD are located in the vicinity of the papilla of Vater, they not only cause mechanical compression of the bile duct but also induce dysfunction of the sphincter of Oddi. They are considered to lead to bile stasis and to allow reflux from the duodenum into the bile duct, which results in an ascending infection of β-glucuronidase-producing bacteria. The ERCP procedure can be hampered by JPD, although recent papers have reported no difference in the successful cannulation rate or complications between patients with JPD and those without JPD. Disorders caused by JPD are amenable to appropriate therapy, e.g. endoscopic sphincterotomy and surgical intervention.

Absence of glial cell line-derived neurotrophic factor (GDNF) leads to intestinal aganglionosis. We recently demonstrated that patients with diverticular disease (DD) exhibit hypoganglionosis suggesting neurotrophic factor deprivation. Thus, we screened mRNA expression pattern of the GDNF system in DD and examined the effects of GDNF on cultured enteric neurons. Colonic specimens obtained from patients with DD (n = 21) and controls (n = 20) were assessed for mRNA expression levels of the GDNF system (GDNF, GDNF receptors GFRα1 and RET). To identify the tissue source of GDNF and its receptors, laser-microdissected (LMD) samples of human myenteric ganglia and intestinal muscle layers were analyzed separately by qPCR. Furthermore, the effects of GDNF treatment on cultured enteric neurons (receptor expression, neuronal differentiation and plasticity) were monitored. mRNA expression of GDNF and its receptors was significantly down-regulated in the muscularis propria of patients with DD. LMD samples revealed high expression of GDNF in circular and longitudinal muscle layers, whereas GDNF receptors were also expressed in myenteric ganglia. GDNF treatment of cultured enteric neurons increased mRNA expression of its receptors and promoted neuronal differentiation and plasticity revealed by synaptophysin mRNA and protein expression. Our results suggest that the GDNF system is compromised in DD. In vitro studies demonstrate that GDNF enhances expression of its receptors and promotes enteric neuronal differentiation and plasticity. Since patients with DD exhibit hypoganglionosis, we propose that the observed enteric neuronal loss in DD may be due to lacking neurotrophic support mediated by the GDNF system.