SummaryBackground and objectives Endothelial dysfunction is an early manifestation of vascular injury and contributes to the development of atherosclerotic cardiovascular disease. Recent studies have implicated hyperuricemia as a risk factor for cardiovascular disease. We hypothesized that lowering uric acid in subjects with asymptomatic hyperuricemia with allopurinol might improve endothelial dysfunction, BP, estimated GFR (eGFR), and inflammatory markers.Design, setting, participants, & measurements Subjects with asymptomatic hyperuricemia and no history of gout and 30 normouricemic control subjects were enrolled in this 4-month randomized prospective study. Thirty hyperuricemic patients received 300 mg/d allopurinol and were compared with 37 hyperuricemic patients and 30 normouricemic subjects in matched control groups. Flow-mediated dilation (FMD), eGFR, ambulatory BP monitoring, spot urine protein-creatine ratio, and highly sensitive C-reactive protein were measured at baseline and at 4 months.Results Age, gender, lipid profile, eGFR, hemoglobin, glucose, and level of proteinuria were similar in hyperuricemic subjects and controls at baseline. As expected, hyperuricemic patients had higher levels of highly sensitive C-reactive protein and lower FMD compared with normouricemic patients. Allopurinol treatment resulted in a decrease in serum uric acid, a decrease in systolic BP, an increase in FMD, and an increase in eGFR compared with baseline. No significant difference was observed in the control hyperuricemic and normouricemic groups. In a multiple regression analysis, FMD levels were independently related to uric acid both before (beta ϭ Ϫ0.55) and after (beta ϭ Ϫ0.40) treatment.Conclusions Treatment of hyperuricemia with allopurinol improves endothelial dysfunction and eGFR in subjects with asymptomatic hyperuricemia.

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In this study, confirmed COVID-19 cases of Denmark,

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RESULTSA total of 330 stenoses were found in 228 patients. PTA was technically successful in 96.3% of the stenoses (n=319). Clinical success was achieved in 97.2% (n=321). Early dysfunction (within six months) was positively correlated with patient age (P < 0.001) and diabetes (P < 0.005). Older age (P < 0.001) and diabetes (P = 0.002) were associated with a lower primary patency rate. Patient age (P < 0.001), presence of diabetes (P = 0.023), length of stenosis (P = 0.003), early recurrence (P = 0.003) and presence of residual stenosis (P = 0.014) were associated with a lower secondary patency rate. CONCLUSION Patency of dysfunctional hemodialysis fistulas can be maintained safely with continuous follow-up and repeated interventions without shortening the venous segment by surgical revision. Percutaneous approach to hemodialysis access stenosis is an alternative to the conventional surgical approach and PTA is an effective treatment method for dysfunctional AVF.H emodialysis, and therefore patent hemodialysis access, is of great importance to patients with end-stage renal disease (ESRD). The preferred type of access in patients undergoing hemodialysis is an arteriovenous fistula (AVF) (1). The Kidney Disease Outcomes Quality Initiative provides evidence-based clinical practice guidelines for all stages of ESRD and reports autogenous AVF as the reference standard for primary vascular access, due to their longevity and low infection rates (2, 3). Sands et al. (4) and Schwab et al. (5) demonstrated a 10-fold increase in thrombosis rate of synthetic polytetrafluoroethylene (PTFE) accesses when compared to AVFs. Despite proven advantages of AVF over PTFE, both types of access eventually fail and contribute to multiple hospital admissions, radiological and surgical interventions, and overall morbidity associated with chronic hemodialysis. Significant stenosis causing access dysfunction is a frequent complication in hemodialysis and requires repeated percutaneous transluminal balloon angioplasty (PTA) to maintain patency (6-9). The patency of PTA is limited, however, with first year primary patency rates ranging between 26% and 62% (6-8). Many factors influencing the patency rate have been studied in previously reported series (7,8). Our study is the first to investigate the effect of early recurrence on secondary patency. MethodsThe records of 228 patients (129 men, 99 women; mean age, 56.8±14.6 years) who underwent first time PTA for a dysfunctional native AVF between January 2007 and January 2011 were retrospectively reviewed. Inclusion criteria were presence of a dysfunctional native AVF referred for fistulography and treatment, no previous history of stenosis or thrombosis, and only stenosis of the AVFs on fistulography. Patients who had synthetic dialysis, composite grafts, or autogenous fistulas that were already thrombosed were excluded from our study. Indications for fistulography included decreased flow rate, difficult cannulation, increased venous pressure, edema of the upper extremity, or pain during dialy...

Dysphagia is a common presenting complaint in otolaryngology practice, and there are many causes. Forestier syndrome is a rare cause of dysphagia. It is also known as diffuse idiopathic skeletal hyperostosis (DISH) syndrome or vertebral ankylosing hyperostosis. Forestier syndrome consists of anterolateral perivertebral ligament calcification. It was first described by Forestier and Rotes-Querol in 1950; diagnosis is primarily radiological and the etiology is unknown. In addition to dysphagia Forestier syndrome has been reported to cause laryngeal stridor, dyspnea, snoring and hoarseness. Other important symptoms associated with Forestier syndrome are stiffness and pain in the back, pain related to tendinitis, myelopathy related to core compression associated with the ossification of the posterior longitudinal ligament, and pain related to vertebral complications such as fracture or subluxation. We report six cases of Forestier syndrome as an etiologic factor in dysphagia and present clinical and radiological findings.

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