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OBJECTIF: Fournir aux professionnels des soins primaires un aperçu actualisé du trouble de l’accès hyperphagique (TAH), qui comporte des recommandations pertinentes. QUALITÉ DES DONNÉES: Une recension a été effectuée dans PubMed, PsycInfo et Google Scholar, sans restrictions temporelles, à l’aide des expressions clés en anglais binge eating disorder, treatment, review, guidelines, psychotherapy, primary care et pharmacotherapy. Le niveau des données probantes pour toutes les recommandations varie de I à III. MESSAGE PRINCIPAL: Le trouble de l’accès hyperphagique est associé à une grande détresse et à une incapacité considérable chez le patient, ainsi qu’à des comorbidités médicales et psychiatriques; il a été ajouté dans la 5(e) édition du Manuel diagnostique et statistique des troubles mentaux, en 2013. Les médecins de soins primaires sont bien placés pour le dépistage, le diagnostic et l’amorce du traitement du TAH. Une approche par étapes du traitement commence par un développement personnel guidé, suivi par l’ajout ou le changement de la pharmacothérapie, ou par une psychothérapie individuelle, au besoin. Les psychothérapies dont l’efficacité est le plus corroborée par la recherche sont la thérapie cognitivo-comportementale, la thérapie interpersonnelle et la thérapie comportementale dialectique. CONCLUSION: Cet aperçu présente des conseils sur le dépistage, le diagnostic et les approches thérapeutiques fondés sur les données probantes actuellement disponibles, de même les avis d’un groupe diversifié d’experts, pour aider à orienter les cliniciens lorsque les données probantes sont limitées.

OBJECTIVE: To provide an updated overview of binge eating disorder (BED) that includes recommendations relevant for primary care practitioners. QUALITY OF EVIDENCE: PubMed, Google Scholar, and PsycInfo were searched with no time restriction using the subject headings binge eating disorder, treatment, review, guidelines, psychotherapy, primary care, and pharmacotherapy. Levels of evidence for all treatment recommendations ranged from I to III. MAIN MESSAGE: Binge eating disorder is associated with considerable patient distress and impairment, as well as medical and psychiatric comorbidities, and was added to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, in 2013. Primary care practitioners are well suited to screen, diagnose, and initiate treatment for BED. A stepped-care approach to treatment starts with guided self-help, adding or moving to pharmacotherapy or individual psychotherapy as needed. The psychotherapies with the most research support include cognitive behaviour therapy, interpersonal therapy, and dialectical behaviour therapy. In terms of pharmacotherapy, evidence supports the use of lisdexamfetamine, antidepressant medications, and anticonvulsant medications. CONCLUSION: This overview provides guidance on screening, diagnosis, and treatment approaches based on the currently available evidence, as well as expert opinions of a diverse group of experts to help guide clinicians where evidence is limited.

Background: Frailty is a known predictor of mortality and poor outcomes during hospital admission. In this large renal retrospective cohort study, we investigated whether frailer COVID-19 positive renal patients had worse outcomes. Design: All SARS-Cov-2 positive renal patients aged ≥18 years who presented to the emergency department at the Royal Free Hospital or at the satellite dialysis centres from 10th of March until the 10th of May 2020, with recent data on frailty, were included. The follow up was until 26th of May 2020. Age, gender, ethnicity, body mass index, chronic kidney disease stage, modality of renal replacement therapy, co-morbidities, Rockwood clinical frailty score (CFS), C reactive protein and the neutrophil-to-lymphocyte count were collected at presentation. The primary outcome was the overall mortality rate following COVID-19 diagnosis. Secondary outcomes included the need for hospital admission. Results: A total of 200 renal patients were SARS-Cov-2 positive. In the 174 patients who had a CFS recorded, the age was 65.4 years ± 15.8 (mean ± SD) and 57,5% were male. At the end of follow up, 26% had died. Frail patients (CFS 5-7) were more than three times more likely to die compared to less frail patients (CFS of 1-4) (odds ratio (OR) 3.3, 95% confidence interval (CI) 1.0-10.6). 118 patients (68%) required admission, but there was no difference in hospital admission rates for frail vs non-frail patients (OR 0.6, CI 0.3-1.7). Conclusions: Frailty is a better predictor of mortality than age and co-morbidities in COVID-19 positive renal patients.

Characteristics of studies. (PDF 224 kb)

Medline search strategy. (PDF 61.2 kb)

Funnel plots. (PDF 259 kb)

Chronic kidney disease (CKD) is a major public health problem affecting 10-15% of the adult population. Outcomes of CKD include not only progression to end stage kidney disease (ESKD) but also complications from reduced kidney function and treatments for ESKD, and increased risk of cardiovascular disease. In chapter 1, outcome reporting practices for core outcomes in trials of primary immunosuppression in kidney transplant recipients are described through systematic review of randomised trial data, with an emphasis on identifying potential sources of reporting bias. Despite people with CKD being at increased risk of stroke, the magnitude of stroke risk, the effect of traditional and novel risk factors for stroke, and prognosis following stroke in CKD and ESKD are unclear. Chapter 2 uses systematic review of randomised trial and observational study data to establish estimates of stroke risk in people with CKD. Chapters 3 and 4 use cohort data from the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA), the New South Wales Admitted Patient Data Collection and the New South Wales Registry of Births Deaths and Marriages to establish estimates of stroke risk and identify risk factors for stroke in people with ESKD. Chapter 5 uses data from a cohort study of people presenting to hospital with an ischaemic stroke followed-up at 90 days to establish how CKD affects prognosis following a stroke. People with CKD and ESKD have a 65-80% greater risk of having cognitive impairment than age-matched people without kidney disease, but whether cognition improves after a kidney transplant is relatively unclear. The final chapter uses systematic review of observational study data to examine the effect of kidney transplantation on cognitive function. The overarching purpose of each study was to underpin the theme of the thesis: improving outcomes for people with CKD and ESKD.

Background Most people who receive a kidney transplant die from either cardiovascular disease or cancer before their transplant fails. The most common reason for someone with a kidney transplant to lose the function of their transplanted kidney necessitating return to dialysis is chronic kidney transplant scarring. Immunosuppressant drugs have side effects that increase risks of cardiovascular disease, cancer and chronic kidney transplant scarring. Belatacept may provide sufficient immunosuppression while avoiding unwanted side effects of other immunosuppressant drugs. However, high rates of post‐transplant lymphoproliferative disease (PTLD) have been reported when belatacept is used in particular kidney transplant recipients at high dosage. Objectives 1) Compare the relative efficacy of belatacept versus any other primary immunosuppression regimen for preventing acute rejection, maintaining kidney transplant function, and preventing death. 2) Compare the incidence of several adverse events: PTLD; other malignancies; chronic transplant kidney scarring (IF/TA); infections; change in blood pressure, lipid and blood sugar control. 3) Assess any variation in effects by study, intervention and recipient characteristics, including: differences in pre‐transplant Epstein Barr virus serostatus; belatacept dosage; and donor‐category (living, standard criteria deceased, or extended criteria deceased). Search methods We searched the Cochrane Renal Group's Specialised Register to 1 September 2014 through contact with the Trials' Search Co‐ordinator using search terms relevant to this review. Selection criteria Randomised controlled trials (RCT) that compared belatacept versus any other immunosuppression regimen in kidney transplant recipients were eligible for inclusion. Data collection and analysis Two authors independently extracted data for study quality and transplant outcomes and synthesized results using random effects meta‐analysis, expressed as risk ratios (RR) and mean differences (MD), both with 95% confidence intervals (CI). Subgroup analyses and univariate meta‐regression were used to investigate potential heterogeneity. Main results We included five studies that compared belatacept and calcineurin inhibitors (CNI) that reported data from a total of 1535 kidney transplant recipients. Of the five studies, three (478 participants) compared belatacept and cyclosporin and two (43 recipients) compared belatacept and tacrolimus. Co‐interventions included basiliximab (4 studies, 1434 recipients); anti‐thymocyte globulin (1 study, 89 recipients); alemtuzumab (1 study, 12 recipients); mycophenolate mofetil (MMF, 5 studies, 1509 recipients); sirolimus (1 study, 26 recipients) and prednisone (5 studies, 1535 recipients). Up to three years following transplant, belatacept and CNI‐treated recipients were at similar risk of dying (4 studies, 1516 recipients: RR 0.75, 95% CI 0.39 to 1.44), losing their kidney transplant and returning to dialysis (4 studies, 1516 recipients: RR 0.91, 95% CI 0.61 to 1.38), and having an episode of acute rejection (4 studies, 1516 recipients: RR 1.56, 95% CI 0.85 to 2.86). Belatacept‐treated kidney transplant recipients were 28% less likely to have chronic kidney scarring (3 studies, 1360 recipients: RR 0.72, 95% CI 0.55 to 0.94) and also had better graft function (measured glomerular filtration rate (GFR) (3 studies 1083 recipients): 10.89 mL/min/1.73 m², 95% CI 4.01 to 17.77; estimated GFR (4 studies, 1083 recipients): MD 9.96 mL/min/1.73 m², 95% CI 3.28 to 16.64) than CNI‐treated recipients. Blood pressure was lower (systolic (2 studies, 658 recipients): MD ‐7.51 mm Hg, 95% CI ‐10.57 to ‐4.46; diastolic (2 studies, 658 recipients): MD ‐3.07 mm Hg, 95% CI ‐4.83 to ‐1.31, lipid profile was better (non‐HDL (3 studies 1101 recipients): MD ‐12.25 mg/dL, 95% CI ‐17.93 to ‐6.57; triglycerides (3 studies 1101 recipients): MD ‐24.09 mg/dL, 95% CI ‐44.55 to ‐3.64), and incidence of new‐onset diabetes after transplant was reduced by 39% (4 studies (1049 recipients): RR 0.61, 95% CI 0.40 to 0.93) among belatacept‐treated versus CNI‐treated recipients. Risk of PTLD was similar in belatacept and CNI‐treated recipients (4 studies, 1516 recipients: RR 2.79, 95% CI 0.61 to 12.66) and was no different among recipients who received different belatacept dosages (high versus low dosage: ratio of risk ratios (RRR) 1.06, 95% CI 0.11 to 9.80, test of difference = 0.96) or among those who were Epstein Barr virus seronegative compared with those who were seropositive before their kidney transplant (seronegative versus seropositive; RRR 1.49, 95% CI 0.15 to 14.76, test for difference = 0.73). The belatacept dose used (high versus low), type of donor kidney the recipient received (extended versus standard criteria) and whether the kidney transplant recipient received tacrolimus or cyclosporin made no difference to kidney transplant survival, incidence of acute rejection or estimated GFR. Selective outcome reporting meant that data for some key subgroup comparisons were sparse and that estimates of the effect of treatment in these groups of recipients remain imprecise. Authors' conclusions There is no evidence of any difference in the effectiveness of belatacept and CNI in preventing acute rejection, graft loss and death, but treatment with belatacept is associated with less chronic kidney scarring and better kidney transplant function. Treatment with belatacept is also associated with better blood pressure and lipid profile and a lower incidence of diabetes versus treatment with a CNI. Important side effects (particularly PTLD) remain poorly reported and so the relative benefits and harms of using belatacept remain unclear. Whether short‐term advantages of treatment with belatacept are maintained over the medium‐ to long‐term or translate into better cardiovascular outcomes or longer kidney transplant survival with function remains unclear. Longer‐term, fully reported and published studies comparing belatacept versus tacrolimus are needed to help clinicians decide which patients might benefit most from using belatacept.