Four layer bandage compared with short stretch bandage for venous leg ulcers: systematic review and meta-analysis of randomised controlled trials with data from individual patients

<p><b>Objective:</b> To compare the effectiveness of two types of compression treatment (four layer bandage and short stretch bandage) in people with venous leg ulceration.</p> <p><b>Design:</b> Systematic review and meta-analysis of patient level data.</p> <p><b>Data:</b> sources Electronic databases (the Cochrane Central Register of Controlled Trials, the Cochrane Wounds Group Specialised Register, Medline, Embase, CINAHL, and National Research Register) and reference lists of retrieved articles searched to identify relevant trials and primary investigators. Primary investigators of eligible trials were invited to contribute raw data for re-analysis.</p> <p><b>Review:</b> methods Randomised controlled trials of four layer bandage compared with short stretch bandage in people with venous leg ulceration were eligible for inclusion. The primary outcome for the meta-analysis was time to healing. Cox proportional hazards models were run to compare the methods in terms of time to healing with adjustment for independent predictors of healing. Secondary outcomes included incidence and number of adverse events per patient.</p> <p><b>Results:</b> Seven eligible trials were identified (887 patients), and patient level data were retrieved for five (797 patients, 90% of known randomised patients). The four layer bandage was associated with significantly shorter time to healing: hazard ratio (95% confidence interval) from multifactorial model based on five trials was 1.31 (1.09 to 1.58), P=0.005. Larger ulcer area at baseline, more chronic ulceration, and previous ulceration were all independent predictors of delayed healing. Data from two trials showed no evidence of a difference in adverse event profiles between the two bandage types.</p> <p><b>Conclusions:</b> Venous leg ulcers in patients treated with four layer bandages heal faster, on average, than those of people treated with the short stretch bandage. Benefits were consistent across patients with differing prognostic profiles.</p&gt

A clinical and haemodynamic investigation into the role of calf perforating vein surgery in patients with venous ulceration and deep venous incompetence

Objective:To determine the clinical efficacy and local haemodynamic effects of perforating vein surgery in ulcerated limbs with combined deep and perforating vein incompetence.Design:Prospective, interventional study.Materials and methods:Seven ulcerated limbs with combined primary deep and perforating vein incompetence were studied. Clinical efficacy was determined by ultimate ulcer healing and reduction in ulcer area, local haemodynamics were assessed at three sites with photoplethysmographic 90% venous refilling times (PPG RT90); both assessments were performed pre- and 1-month postoperatively.Results:None of the ulcers healed following perforating vein surgery, the median (range) ulcer areas pre- and postoperatively were 31 (7–685) cm2 and 35.5 (7–796) cm2 (Wilcoxon p = 0.07). Preoperative PPG RT90 demonstrated a global abnormality of venous function at all sites examined that persisted after perforating vein surgery.Conclusion:In the presence of deep venous incompetence perforating vein surgery had no influence on venous function or ulcer healing. We conclude that perforating vein surgery is not indicated for the treatment of venous ulceration in limbs with primary deep venous incompetence

Why Operationism Doesn't Go Away: Extrascientific Incentives of Social-Psychological Research

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/69038/2/10.1177_004839318601600302.pd

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease