FACILITATING MIDWIFERY INVOLVEMENT IN MANAGING GESTATIONAL WEIGHT GAIN IN PREGNANT WOMEN LIVING WITH OBESITY

Overview: Pregnant women living with obesity are at increased risk of pregnancy complications, with risks rising as Body Mass Index (BMI) increases. Midwives are willing to support women with managing their gestational weight gain but lack confidence and access to supporting resources. In the UK there are no interventions that aim to change the intention and behaviour of midwives, to support women with managing their gestational weight gain. The Theory of Planned Behaviour (TPB) (Ajzen, 1985) was utilised to frame the design of a behaviour change intervention for midwives. This three-phase study conducted a qualitative needs assessment, intervention design, and a quantitative study of, intervention testing. Methods: Phase One: Interview data were thematically analysed and the TPB utilised to elicit participants’ salient beliefs, to inform intervention design. Phase Two: The design of the intervention, and the TPB scale, were informed by Phase One data. Midwives reviewed the intervention and participated in a pilot test of the scale. Phase Three: The intervention was tested in a before-and-after controlled trial, utilising the refined TPB scale. Results: Phase One: 4 key themes emerged: 1)The current state of affairs 2) Perspectives on an intervention: what may work 3) Influences on uptake and successful weight control 4) Taking things forward. Phase Two: An intervention to facilitate the involvement of community midwives in supporting weight management for pregnant women living with obesity; a booklet about weight management in pregnancy; and a TPB scale were designed. Recommendations from midwives were integrated into the final intervention resource, and pilot testing of the scale led to refinement for use in phase 3. Phase Three: Midwives in the intervention group increased their intention to offer weight management support to pregnant women living with obesity. Furthermore, midwives in the intervention group increased actual weight management support for pregnant women living with obesity, after participating in the intervention. Conclusions: This study made a unique contribution to new knowledge by developing and testing a novel intervention that was underpinned by health psychology theory, which increased the intention and behaviour of community midwives to support pregnant women living with obesity, with managing their gestational weight gain

Cystatin D (CST5):An ultra-early inflammatory biomarker of traumatic brain injury

Traumatic brain injury (TBI) is set to become the leading cause of neurological disability across all age groups. Currently, no reliable biomarkers exist to help diagnose the severity of TBI to identify patients who are at risk of developing secondary injuries. Thus, the discovery of reliable biomarkers for the management of TBI would improve clinical interventions. Inflammatory markers are particularly suited for biomarker discovery as TBI leads to very early alterations in inflammatory proteins. Using the Proseek Multiplex Inflammation assay, we measured in patients that had suffered mild TBI (n=10) or severe TBI (n=10) with extra-cranial injury or extracranial injury only (EC) (n=10), 92 inflammationassociated proteins in serum obtained: <1hr (within 1-hour), 4–12hr and 48–72hr post injury. Changes were compared to healthy volunteers (HV). Our results identified CST5, AXIN1 and TRAIL as novel early biomarkers of TBI. CST5 identified patients with severe TBI from all other cohorts and importantly was able to do so within the first hour of injury. AXIN1 and TRAIL were able to discriminate between TBI and HV at <1hr. We conclude that CST5, AXIN1 and TRAIL are worthy of further study in the context of a pre-hospital or pitch-side test to detect brain injur

Individual Health Trainers to support health and wellbeing for people under community supervision in the criminal justice system: the STRENGTHEN pilot RCT

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Multiorgan MRI findings after hospitalisation with COVID-19 in the UK (C-MORE): a prospective, multicentre, observational cohort study

Introduction: The multiorgan impact of moderate to severe coronavirus infections in the post-acute phase is still poorly understood. We aimed to evaluate the excess burden of multiorgan abnormalities after hospitalisation with COVID-19, evaluate their determinants, and explore associations with patient-related outcome measures. Methods: In a prospective, UK-wide, multicentre MRI follow-up study (C-MORE), adults (aged ≥18 years) discharged from hospital following COVID-19 who were included in Tier 2 of the Post-hospitalisation COVID-19 study (PHOSP-COVID) and contemporary controls with no evidence of previous COVID-19 (SARS-CoV-2 nucleocapsid antibody negative) underwent multiorgan MRI (lungs, heart, brain, liver, and kidneys) with quantitative and qualitative assessment of images and clinical adjudication when relevant. Individuals with end-stage renal failure or contraindications to MRI were excluded. Participants also underwent detailed recording of symptoms, and physiological and biochemical tests. The primary outcome was the excess burden of multiorgan abnormalities (two or more organs) relative to controls, with further adjustments for potential confounders. The C-MORE study is ongoing and is registered with ClinicalTrials.gov, NCT04510025. Findings: Of 2710 participants in Tier 2 of PHOSP-COVID, 531 were recruited across 13 UK-wide C-MORE sites. After exclusions, 259 C-MORE patients (mean age 57 years [SD 12]; 158 [61%] male and 101 [39%] female) who were discharged from hospital with PCR-confirmed or clinically diagnosed COVID-19 between March 1, 2020, and Nov 1, 2021, and 52 non-COVID-19 controls from the community (mean age 49 years [SD 14]; 30 [58%] male and 22 [42%] female) were included in the analysis. Patients were assessed at a median of 5·0 months (IQR 4·2–6·3) after hospital discharge. Compared with non-COVID-19 controls, patients were older, living with more obesity, and had more comorbidities. Multiorgan abnormalities on MRI were more frequent in patients than in controls (157 [61%] of 259 vs 14 [27%] of 52; p&lt;0·0001) and independently associated with COVID-19 status (odds ratio [OR] 2·9 [95% CI 1·5–5·8]; padjusted=0·0023) after adjusting for relevant confounders. Compared with controls, patients were more likely to have MRI evidence of lung abnormalities (p=0·0001; parenchymal abnormalities), brain abnormalities (p&lt;0·0001; more white matter hyperintensities and regional brain volume reduction), and kidney abnormalities (p=0·014; lower medullary T1 and loss of corticomedullary differentiation), whereas cardiac and liver MRI abnormalities were similar between patients and controls. Patients with multiorgan abnormalities were older (difference in mean age 7 years [95% CI 4–10]; mean age of 59·8 years [SD 11·7] with multiorgan abnormalities vs mean age of 52·8 years [11·9] without multiorgan abnormalities; p&lt;0·0001), more likely to have three or more comorbidities (OR 2·47 [1·32–4·82]; padjusted=0·0059), and more likely to have a more severe acute infection (acute CRP &gt;5mg/L, OR 3·55 [1·23–11·88]; padjusted=0·025) than those without multiorgan abnormalities. Presence of lung MRI abnormalities was associated with a two-fold higher risk of chest tightness, and multiorgan MRI abnormalities were associated with severe and very severe persistent physical and mental health impairment (PHOSP-COVID symptom clusters) after hospitalisation. Interpretation: After hospitalisation for COVID-19, people are at risk of multiorgan abnormalities in the medium term. Our findings emphasise the need for proactive multidisciplinary care pathways, with the potential for imaging to guide surveillance frequency and therapeutic stratification

Author Correction: Cystatin D (CST5)::An ultra-early inflammatory biomarker of traumatic brain injury

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper

Prehospital immune responses and development of multiple organ dysfunction syndrome following traumatic injury: A prospective cohort study

<div><p>Background</p><p>Almost all studies that have investigated the immune response to trauma have analysed blood samples acquired post-hospital admission. Thus, we know little of the immune status of patients in the immediate postinjury phase and how this might influence patient outcomes. The objective of this study was therefore to comprehensively assess the ultra-early, within 1-hour, immune response to trauma and perform an exploratory analysis of its relationship with the development of multiple organ dysfunction syndrome (MODS).</p><p>Methods and findings</p><p>The immune and inflammatory response to trauma was analysed in 89 adult trauma patients (mean age 41 years, range 18–90 years, 75 males) with a mean injury severity score (ISS) of 24 (range 9–66), from whom blood samples were acquired within 1 hour of injury (mean time to sample 42 minutes, range 17–60 minutes). Within minutes of trauma, a comprehensive leukocytosis, elevated serum pro- and anti-inflammatory cytokines, and evidence of innate cell activation that included neutrophil extracellular trap generation and elevated surface expression of toll-like receptor 2 and CD11b on monocytes and neutrophils, respectively, were observed. Features consistent with immune compromise were also detected, notably elevated numbers of immune suppressive CD16^BRIGHT CD62L^DIM neutrophils (82.07 x 10⁶/l ± 18.94 control versus 1,092 x 10⁶/l ± 165 trauma, <i>p</i> < 0.0005) and CD14⁺HLA-DR^low/− monocytes (34.96 x 10⁶/l ± 4.48 control versus 95.72 x 10⁶/l ± 8.0 trauma, <i>p</i> < 0.05) and reduced leukocyte cytokine secretion in response to lipopolysaccharide stimulation. Exploratory analysis via binary logistic regression found a potential association between absolute natural killer T (NKT) cell numbers and the subsequent development of MODS. Study limitations include the relatively small sample size and the absence of data relating to adaptive immune cell function.</p><p>Conclusions</p><p>Our study highlighted the dynamic and complex nature of the immune response to trauma, with immune alterations consistent with both activation and suppression evident within 1 hour of injury. The relationship of these changes, especially in NKT cell numbers, to patient outcomes such as MODS warrants further investigation.</p></div

A prospective, phase II, single-centre, cross-sectional, randomised study investigating Dehydroepiandrosterone supplementation and its Profile in Trauma:ADaPT

Introduction The improvements in short-term outcome after severe trauma achieved through early resuscitation and acute care can be offset over the following weeks by an acute systemic inflammatory response with immuneparesis leading to infection, multiorgan dysfunction/multiorgan failure (MOF) and death. Serum levels of the androgen precursor dehydroepiandrosterone (DHEA) and its sulfate ester DHEAS, steroids with immune-enhancing activity, are low after traumatic injury at a time when patients are catabolic and immunosuppressed. Addressing this deficit and restoring the DHEA(S) ratio to cortisol may provide a range of physiological benefits, including immune modulatory effects.Objective Our primary objective is to establish a dose suitable for DHEA supplementation in patients after acute trauma to raise circulating DHEA levels to at least 15 nmol/L. Secondary objectives are to assess if DHEA supplementation has any effect on neutrophil function, metabolic and cytokine profiles and which route of administration (oral vs sublingual) is more effective in restoring circulating levels of DHEA, DHEAS and downstream androgens.Methods and analysis A prospective, phase II, single-centre, cross-sectional, randomised study investigating Dehydroepiandrosterone supplementation and its profile in trauma, with a planned recruitment between April 2019 and July 2021, that will investigate DHEA supplementation and its effect on serum DHEA, DHEAS and downstream androgens in trauma. A maximum of 270 patients will receive sublingual or oral DHEA at 50, 100 or 200 mg daily over 3 days. Females aged ≥50 years with neck of femur fracture and male and female major trauma patients, aged 16–50 years with an injury severity score ≥16, will be recruited.Ethics and dissemination This protocol was approved by the West Midlands – Coventry and Warwickshire Research Ethics Committee (Reference 18/WM/0102) on 8 June 2018. Results will be disseminated via peer-reviewed publications and presented at national and international conferences.Trial registration This trial is registered with the European Medicines Agency (EudraCT: 2016-004250-15) and ISRCTN (12961998). It has also been adopted on the National Institute of Health Research portfolio (CPMS ID:38158).Trial progression The study recruited its first patient on 2 April 2019 and held its first data monitoring committee on 8 November 2019. DHEA dosing has increased to 100 mg in both male cohorts and remains on 50 mg in across all female groups

Illustrative odds ratios for development of MODS based on changes in values of NKT number.

<p>Illustrative odds ratios for development of MODS based on changes in values of NKT number.</p

Traumatic injury results in elevated percentages and absolute numbers of circulating CD14⁺HLA-DR^-/low immunosuppressive monocytes.

<p>(A) Representative flow cytometry plots depicting the percentage of CD14⁺HLA-DR^-/low monocytes (upper left quadrant) in a single HC and a trauma patient across time. (B–C) Prospective assessment of the percentage (B) and absolute number (C) of CD14⁺HLA-DR^-/low monocytes post-trauma. The number of samples analysed is indicated below each time point. The horizontal line for HC data depicts the median value. *<i>p</i> < 0.05, ***<i>p</i> < 0.0005 versus HC. HC, healthy control.</p

Serum cytokine and chemokine concentrations post-trauma.

<p>Serum concentrations of IL-6 (A), IL-8 (B), G-CSF (C), IL-1Ra (D), TNF-α (E), and IL-10 (F) across time post-trauma. The number of patient and HC samples analysed is indicated below each time point. The horizontal line for HC data depicts the median value. **<i>p</i> < 0.005, ***<i>p</i> < 0.0005 versus HCs. G-CSF, granulocyte-colony stimulating factor; HC, healthy control; IL, interleukin; IL-1Ra, interleukin-1 receptor antagonist; TNF- α, tumour necrosis factor-alpha.</p