5366 research outputs found
Sort by
Preface to the October 2020 issue of : can the raw data from military submissions ever be fully accessible?
No full textThe influence of time to adrenaline administration in the Paramedic 2 randomised controlled trial
No full text
Nursing workforce-fit for practice: an overview of the RCN education and training directory.
No full textClinical utility of fractional exhaled nitric oxide (FeNO) in severe asthma management.
No full textAsthma is a chronic inflammatory disease of the airways, affecting over 350 million people worldwide and placing a significant burden on healthcare providers and wider society. Approximately 5-10% of asthma patients are diagnosed with severe asthma and typically are associated with increased risk of hospitalisation from exacerbations, increased morbidity, mortality and higher asthma-associated healthcare costs. Nitric oxide (NO) is an important regulator of immune responses and is a product of inflammation in the airways that is over-produced in asthma. Fractional exhaled NO (FeNO) is predominantly used as a predictor of response to inhaled corticosteroids (ICSs), to monitor adherence and as a diagnostic tool in ICS-naïve patients. In the UK, the National Institute for Health and Care Excellence (NICE) guidelines recommend the use of FeNO for the initial diagnosis of patients with suspected asthma. In the US, the American Thoracic Society (ATS) guidelines recommend FeNO as part of the initial diagnosis of asthma and for monitoring of airway inflammation. FeNO has also been shown to be a predictive factor for asthma exacerbations, with higher levels being associated with a greater number of exacerbations. In addition, higher levels of FeNO have been shown to be associated with a decline in lung function. FeNO testing is a cost-effective procedure and has been shown to improve patient management when combined with standard assessment methods. Recent evidence suggests that FeNO may also be useful as a surrogate biomarker for the assessment and management of severe asthma and to predict responsiveness to some biological therapies
Sarcopenia in Non-alcoholic Fatty Liver Disease: New challenges for clinical practice.
No full text: Sarcopenia is increasingly recognised in patients with non-alcoholic liver disease (NAFLD). Initially recognised as a consequence of advanced liver disease, there is now emerging evidence that sarcopenia may be a novel risk factor for the development of NAFLD, with a role in fibrosis and disease progression.: This review examines the epidemiology, pathogenesis and complex interplay between NAFLD and sarcopenia. Furthermore, the authors discuss the challenges with diagnosis of sarcopenia in the clinic and the evidence-based management of sarcopenia in patients with NAFLD. A MEDLINE and PubMed search was undertaken using the terms; "sarcopenia", "frailty", "muscle", "obesity", "non-alcoholic fatty liver disease", "non-alcoholic steatohepatitis" and "cirrhosis" up to 31 September 2019.: Sarcopenia may be masked by the co-existence of morbid obesity, which is most notable in patients with NAFLD. Sarcopenia is a key indicator of adverse outcomes in patients with cirrhosis, such as hepatic decompensation, poor quality of life and premature mortality. Patients with NAFLD and advanced fibrosis/cirrhosis should undergo anthropometric measures (hand grip strength), dry body mass index and measures of physical frailty (including muscle function, not just mass) to enable targeted early interventions of nutrition (low fat, 1.5g/kg/day protein intake, 2-3 hourly food intake) and exercise (combined resistance and aerobic)
UK-based dermatologist online survey on the current practice and training in the management of melasma and post-inflammatory hyperpigmentation.
No full textSkin hyperpigmentary disorders, commonly including melasma and post-inflammatory hyperpigmentation, are frequent dermatologic problems with higher prevalence in people with darker Fitzpatrick skin type. The current gold standard treatment is triple combination cream containing hydroquinone, retinoid and topical steroids but concerns over its long-term use including exogenous ochronosis, along with the lack of guidelines on the management of hyperpigmentary disorders, have contributed to the inconsistent practice amongst dermatologists
The impact of mode of subsequent birth after obstetric anal sphincter injury on bowel function and related quality of life: a cohort study.
No full textINTRODUCTION AND HYPOTHESIS
The objective was to assess the impact of mode of subsequent birth on bowel function and related quality of life (QoL) in pregnant women with previous obstetric anal sphincter injury (OASI).
METHODS
A prospective cohort study, designed, undertaken and reported using the Strengthening the Reporting of Observational Studies in Epidemiology statement and checklist. All pregnant women with previous OASI recruited at a specialist antenatal OASI clinic in a tertiary hospital to discuss mode of subsequent birth, between 1 January 2014 and 31 October 2015. Women are counselled in line with local guidelines based on Royal College of Obstetricians and Gynaecologists Green-top recommendations. In addition to routine endoanal ultrasound scan (EAUS), women recruited to the study were asked to complete the validated Manchester Health Questionnaire (MHQ) at both 34 weeks' gestation and 6 months postnatally.
RESULTS
Of the 175 study participants, 125 (71.4%) completed follow-up at 6 months. There was no significant change in frequency of bowel symptoms or QoL domain scores in women who had a subsequent vaginal birth compared with caesarean section. Multivariate analysis showed the odds of having poor "incontinence impact" (OR 2.91, 95% CI 1.03-8.21) and "physical limitations" (OR 4.56, 95% CI 1.02-20.45) were significantly higher for women who had a subsequent caesarean section.
CONCLUSIONS
For women with previous OASI, a subsequent vaginal birth is suitable for those with no bowel symptoms and normal EAUS and caesarean section is reasonable for women who do not have normal bowel function and/or normal EAUS findings; however, for some of these women bowel symptoms and QoL may be worsened
Efficacy of Upadacitinib in a Randomized Trial of Patients With Active Ulcerative Colitis.
No full textBACKGROUND & AIMS
We evaluated the efficacy and safety of upadacitinib, an oral selective inhibitor of Janus kinase 1, as induction therapy for ulcerative colitis (UC).
METHODS
We performed a multicenter, double-blind, phase 2b study of 250 adults with moderately to severely active UC and an inadequate response, loss of response, or intolerance to corticosteroids, immunosuppressive agents, and/or biologic therapies. Patients were randomly assigned to groups that received placebo or induction therapy with upadacitinib (7.5 mg, 15 mg, 30 mg, or 45 mg, extended release), once daily for 8 weeks. The primary endpoint was the proportion of subjects who achieve clinical remission according to the Adapted Mayo score at week 8. No multiplicity adjustments were applied.
RESULTS
At week 8, 8.5%, 14.3%, 13.5%, and 19.6% of patients receiving 7.5 mg, 15 mg, 30 mg, or 45 mg upadacitinib, respectively, achieved clinical remission compared with none of the patients receiving placebo (P = .052, P = .013, P = .011, and P = .002, compared with placebo, respectively). Endoscopic improvement at week 8, defined as endoscopic subscore ≤ 1, was achieved in 14.9%, 30.6%, 26.9%, and 35.7% of patients receiving upadacitinib 7.5 mg, 15 mg, 30 mg, or 45 mg, respectively compared with 2.2% receiving placebo (P = .033, P < .001, P < .001, P < .001, compared with placebo, respectively). One event of herpes zoster and 1 subject with pulmonary embolism and deep venous thrombosis (diagnosed 26 days after treatment discontinuation) were reported in the group that received upadacitinib 45 mg once daily. Increases in serum lipid levels and creatine phosphokinase with upadacitinib were observed.
CONCLUSION
In a phase 2b trial, 8 weeks treatment with upadacitinib was more effective than placebo for inducing remission in patients with moderately to severely active UC. ClinicalTrials.gov no: NCT02819635