While the benefits of real-time digital clinical data at micro level for AKI management have been evident for some time, their application at meso and macro levels is emergent therefore limiting progress towards establishing LHSs. Lack of progress is due to digital maturity, system design, human factors and policy levers.

Future approaches need to harness the potential of interoperability, data analytical advances and include multiple stakeholder perspectives to develop effective digital LHSs in order to gain benefits across the system.

Future approaches need to harness the potential of interoperability, data analytical advances and include multiple stakeholder perspectives to develop effective digital LHSs in order to gain benefits across the system.

Liver disease, a major cause of death worldwide, affects younger people compared with other major causes of death. Onvansertib in vivo Palliative and end-of-life care for these patients are often overlooked. Guidelines are emerging on what good end-of-life care in liver disease should look like, but there is a dearth of research into patients’ perspectives even though they are most affected by these guidelines.

To explore current knowledge and understanding of patients’ lived experiences, perspectives and expectations in relation to palliative and end-of-life care in advanced liver disease.

Systematic review with thematic synthesis complying to the enhancing transparency in reporting the synthesis of qualitative research (ENTREQ) statement.

Database searches (Ovid Medline, 1946-2021 and Web of Science, 1970-2021) to identify qualitative studies exploring patients’ perspectives of palliative and end-of-life care in advanced liver disease.

Only eight articles met all criteria. Themes demonstrated repeated hospital admisse primary research from diverse population is needed to improve palliative care and end-of-life care in end-stage liver disease.

Tumour necrosis factor α (TNF-α) is pivotal in sarcoid granuloma formation, and inhibitors of TNF-α offer an attractive third-line treatment option in sarcoidosis. The sarcoid inflammation is characterised by an exaggerated T helper 1 response, and evidence indicates a contribution of dysregulated and/or deficient NK (natural killer) cells, CD56+ T cells and B cells.

Insight into how TNF-α inhibitors influence these cells may provide more information on inflammatory mechanisms in sarcoidosis and improve understanding of such treatment. We therefore evaluated treatment effects of the TNF-α inhibitor infliximab on lung and peripheral blood (PB) NK, CD56+ T cells and B cells.

Fifteen patients were assessed with PB samples, spirometry and CT scan, and 11 of them also underwent bronchoalveolar lavage (BAL) close to start of infliximab treatment. These investigations were repeated after 6 months of treatment.

Twelve out of 15 patients disclosed a clinical improvement at follow-up. Median percentage of BAL fluid (BALF) CD56+ T cells increased while a decrease was seen in PB (p<0.05 and 0.005, respectively). No significant changes were observed for NK cells. There was a trend towards increased median percentage of PB B cells (p=0.07), and a negative correlation was observed between PB and BALF B cells after treatment (p<0.05).

In conclusion, 6 months of infliximab treatment in patients with sarcoidosis, of whom the majority benefited from the treatment, influenced immune cells in the lung and circulation differently, highlighting the importance of investigating several compartments concomitantly when evaluating treatment effects on the inflammatory activity.

In conclusion, 6 months of infliximab treatment in patients with sarcoidosis, of whom the majority benefited from the treatment, influenced immune cells in the lung and circulation differently, highlighting the importance of investigating several compartments concomitantly when evaluating treatment effects on the inflammatory activity.

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease (ILD) with a poor prognosis. Early diagnosis and treatment of IPF may increase lifespan and preserve quality of life. Chest CT is the best test to diagnose IPF, but it is expensive and impractical as a screening test. Fine crackles on chest auscultation may be the only best to screen for IPF.

We prospectively assessed the presence and type of crackles on chest auscultation in all patients referred to the ILD Clinic at the Kingston Health Sciences Center in Ontario, Canada. Clinicians with varying levels of experience recorded the presence of fine crackles, coarse crackles or both independently and unaware of the final diagnosis. We applied multinomial logistic regression to adjust for ILD severity and factors that could affect the identification of crackles.

We evaluated 290 patients referred to the ILD Clinic. On initial presentation, 93% of patients with IPF and 73% of patients with non-IPF ILD had fine crackles on auscultation. In patients with IPF, fine crackles were more common than cough (86%), dyspnoea (80%), low diffusing capacity (87%), total lung capacity (57%) and forced vital capacity (50%). There was 90% observer agreement in identifying fine crackles at a subsequent visit. In multiple regression analysis, the identification of fine crackles was unaffected by lung function, symptoms, emphysema, chronic obstructive pulmonary disease, obesity or clinician experience (p>0.05).

Fine crackles on chest auscultation are a sensitive and robust screening tool that can lead to early diagnosis and treatment of patients with IPF.

Fine crackles on chest auscultation are a sensitive and robust screening tool that can lead to early diagnosis and treatment of patients with IPF.

Large retrospective case-control studies have reported an association between chronic obstructive pulmonary disease (COPD), reduced lung function and an increased risk of Alzheimer’s disease. However, it remains unclear if these diseases are causally linked, or due to shared risk factors. Conventional observational epidemiology suffers from unmeasured confounding and reverse causation. Additional analyses addressing causality are required.

To examine a causal relationship between COPD, lung function and Alzheimer’s disease.

Using two-sample Mendelian randomisation, we used single nucleotide polymorphisms (SNPs) identified in a genome wide association study (GWAS) for lung function as instrumental variables (exposure). Additionally, we used SNPs discovered in a GWAS for COPD in those with moderate to very severe obstruction. The effect of these SNPs on Alzheimer’s disease (outcome) was taken from a GWAS based on a sample of 24 807 patients and 55 058 controls.

We found minimal evidence for an effect of either lung function (OR 1.