Rogersnapier3027

Patients with sepsis-induced cardiomyopathy with cardiogenic shock have a high mortality. This study assessed venoarterial extracorporeal membrane oxygenation (VA-ECMO) support for sepsis-induced cardiogenic shock refractory to conventional treatments.

In this retrospective, multicentre, international cohort study, we compared outcomes of 82 patients (aged ≥18 years) with septic shock who received VA-ECMO at five academic ECMO centres, with 130 controls (not receiving ECMO) obtained from three large databases of septic shock. All patients had severe myocardial dysfunction (cardiac index 3 L/min per m

or less or left ventricular ejection fraction [LVEF] 35% or less) and severe haemodynamic compromise (inotrope score at least 75 μg/kg per min or lactic acidaemia at least 4 mmol/L) at time of inclusion. The primary endpoint was survival at 90 days. A propensity score-weighted analysis was done to control for confounders.

At baseline, patients treated with VA-ECMO had more severe myocardial dysfunction (mk treated with VA-ECMO had a large and significant improvement in survival compared with controls not receiving ECMO. However, despite the careful propensity-weighted analysis, we cannot rule out unmeasured confounders.

None.

None.Persistent depressive disorder is a chronic mood disorder that is common and often more disabling than episodic major depression. In DSM-5, the term subsumes several chronic depressive presentations, including dysthymia with or without superimposed major depressive episodes, chronic major depression, and recurrent major depression without recovery between episodes. Dysthymia can be difficult to detect in psychiatric and primary care settings until it intensifies in the form of a superimposed major depressive episode. Although information is scarce concerning the cause of persistent depressive disorder including dysthymia, the causation is likely to be multifactorial. In this narrative Review, we discuss current knowledge about the nosology and neurobiological basis of dysthymia and persistent depressive disorder, emphasising a dimensional perspective based on course for further research. We also review new developments in psychotherapy and pharmacotherapy for persistent depressive disorder, and propose a tailored, modular approach to accommodate its multifaceted nature.

Maternal depression has a recurring course that can influence offspring outcomes. Evidence on how to treat maternal depression to improve longer-term maternal outcomes and reduce intergenerational transmission of psychopathology is scarce, particularly for task-shifted, low-intensity, and scalable psychosocial interventions. We evaluated the effects of a peer-delivered, psychosocial intervention on maternal depression and child development at 3 years postnatal.

40 village clusters in Pakistan were randomly allocated using a computerised randomisation sequence to receive a group-based, psychosocial intervention and enhanced usual care for 36 months, or enhanced usual care alone. Pregnant women (≥18 years) were screened for moderate or severe symptoms of depression (patient health questionnaire-9 [PHQ-9] score ≥10) and were recruited into the trial (570 participants), and a cohort without depression (PHQ-9 score <10) was also enrolled (584 participants). Including the non-depressed dyads enabled us to deamong the outcomes of this trial). Early intervention efforts might need to rely on multiple models (eg, collaborative care), be of greater intensity, and potentially targeted at mothers who are at high risk for depression to reduce the intergenerational transmission of psychopathology from mothers to children.

National Institutes of Health.

National Institutes of Health.

People with schizophrenia have higher rates of smoking than the general population, and lower quit rates. Several randomised controlled trials have investigated the effectiveness of pharmacological interventions for smoking cessation over the past 20 years. We did a systematic review and pairwise and network meta-analysis of smoking abstinence to guide decision making in offering pharmacological interventions for smoking cessation for people with schizophrenia spectrum disorders.

We systematically reviewed PubMed, Embase, Cochrane Central Register of Controlled Trials, PsycINFO, and China National Knowledge Infrastructure from inception to Sept 30, 2019, for randomised controlled trials of varenicline, bupropion, and nicotine replacement therapy for smoking cessation for people with schizophrenia spectrum disorders or psychotic disorders who were smokers at the time of study recruitment. Data were extracted from published studies on smoking abstinence outcomes and psychotic symptoms. We did pairwise and nrenicline was superior to bupropion (RR 2·02, 95% CI 1·04-3·93; p=0·038) but no significant difference was found between varenicline and nicotine replacement therapy, or bupropion and nicotine replacement therapy. No agents were associated with changes in psychiatric symptoms, but varenicline was associated with higher rates of nausea than was placebo.

We found evidence to support use of pharmacological agents for smoking cessation for people with psychosis. Varenicline might be superior to bupropion; however, additional direct testing and combination trials of pharmacological agents for smoking cessation are required to inform clinical decision making for people with psychosis.

None.

None.

Most individuals with schizophrenia-spectrum disorders have relapses, which increase the risk of morbidity and mortality. Because non-adherence to antipsychotic maintenance treatment could affect more than half of individuals with schizophrenia-spectrum disorders, psychosis relapse can often be confounded by unnoticed treatment interruption. Research of relapse during confirmed antipsychotic exposure has basic clinical and neurobiological implications, but data are scarce. We aimed to generate reliable estimates of incidence and predictors of relapse during assured antipsychotic treatment.

We did a systematic review and individual participant data (IPD) meta-analysis of clinical trials of long-acting injectable antipsychotics (LAIs) for psychosis relapse-prevention, following IPD-PRISMA guidelines. Datasets were identified by searching relevant repositories from inception to Aug 1, 2019. Each LAI group was reanalysed as a separate cohort, further identifying subcohorts of individuals with and without prosr of relapse was tardive dyskinesia at treatment onset (HR 2·39, 95% CI 1·05 to 5·42).

Despite the established efficacy of antipsychotics in preventing relapse, these data indicate that these drugs might not prevent subsequent exacerbations for a proportion of individuals whose illness is stabilised on continuous antipsychotic treatment. Tardive dyskinesia in particular might have pathophysiological implications for relapse.

Northwell Health.

Northwell Health.

We aimed to investigate the association between the different antiphospholipid antibodies (aPL) and both systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) manifestations.

Patients from the RELESSER registry, a Spanish retrospective, cross-sectional, forty-five hospital registry of adult SLE patients, were included.

Out of a total of 3,658 SLE patients, 1372 were aPL positive (555 of them fulfilled criteria for APS). All aPL types showed a negative association with cutaneous SLE manifestations. Lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) were both associated with haematological, ophthalmological and neuropsychiatric manifestations. IgG isotypes were associated with a higher risk of lupus manifestations compared with IgM. We found that the risk of neuropsychiatric and ophthalmological manifestations significantly increased with a higher number of positive aPL whereas the risk of cutaneous symptoms showed a negative correlation. All types of aPL, and more strongly LA, manifestations.

The aim of this study was to establish whether serum RANKL levels in early inflammatory arthritis (IA) were associated with rheumatoid arthritis (RA) diagnosis at follow-up, and to evaluate the added value of RANKL for RA diagnosis.

Serum from 298 patients was collected. Demographic and clinical (swollen/tender joint counts, CRP, DAS28-CRP, RF, ACPA and shared-epitope data were recorded. Baseline ultrasound of 26 joints was performed, including total power Doppler (PD). An ELISA was used to measure RANKL. Predictors of progression were identified using multivariable logistic regression analysis. Area under the receiver operating characteristics (AUROC) was used to assess the performance of the prediction models and quantify the added value of RANKL in RA diagnosis.

151 patients developed RA and 147 were non-RA (undifferentiated IA, other inflammatory diagnoses or non-persistent inflammation). RANKL levels were significantly higher in RA (median [IQR] 474.1 [270.8-1430.6]) than in non-RA (median [IQR] 301.0 [174.1-477.5]. selleck Three clinical factors (age, SJC and PD) were identified by multivariable logistic regression with model performance AUROC of 77.9% (95% CI 72.1-83.8%). Adding RANKL resulted in a relative increase of 6.5% in the model classification performance of an AUROC of 83.0% (95% CI 77.9-88.1%). In ACPA-negative patients, the model performance increased from 77.6% (95% CI 69.5-85.7%) with clinical data only to 81.9% (95% CI 73.7-89.8%) with added value of RANKL and imaging.

RANKL levels can predict RA diagnosis over clinical biomarkers alone, both seropositive and particularly in seronegative IA patients.

RANKL levels can predict RA diagnosis over clinical biomarkers alone, both seropositive and particularly in seronegative IA patients.

Metformin is a known therapeutic agent for diabetes. Recently, several reports suggested the possibility of improvement in autoimmune disease and malignancy conditions through the effect of metformin on the immune system. Although there have been reports on the therapeutic effects of metformin on mouse models of collagen-induced arthritis, simulating human rheumatoid arthritis (RA), the effect of metformin on human RA remains unknown. Therefore, we investigated the inhibitory effect of metformin on the pathogenesis of human RA in vitro.

Osteoclastogenesis was evaluated with or without metformin. through tartrate-resistant acid phosphatase staining, osteoclast-specific enzyme expression analysis, and a bone resorption assay. Human fibroblast-like synoviocyte MH7A cells were stimulated with TNF-α, and the expression of proinflammatory cytokines and protease and growth factor genes was evaluated with or without metformin. Metformin has been used to evaluate their potential modulatory effects on cells treated with TNF-α. Moreover, we examined angiogenesis by performing a tube formation assay using human umbilical vein endothelial cells (HUVECs) with or without metformin.

Osteoclastogenesis was suppressed in the presence of metformin, and the expression of osteoclast-specific genes was reduced. The TNF-α-induced expression of inflammatory cytokines and protease and growth factor genes in MH7A cells was downregulated by metformin. Additionally, the induced formation of tubular networks in HUVECs was also disrupted following treatment with metformin.

These results suggest that metformin might improve the pathogenesis of RA, including joint inflammation and destruction. Thus, metformin might be utilised as a potential therapeutic agent in the treatment of RA.

These results suggest that metformin might improve the pathogenesis of RA, including joint inflammation and destruction. Thus, metformin might be utilised as a potential therapeutic agent in the treatment of RA.