The Role of Micronutrients in the Pathogenesis of Alcohol-Related Liver Disease.

AIMS: Chronic alcohol consumption may result in liver injury and chronic liver disease, but other factors are likely to influence disease progression. Malnutrition, specifically micronutrient deficiency, is frequently associated with both alcohol use disorder and chronic liver disease. We hypothesize that micronutrient deficiencies may affect the progression of liver disease in this population. METHODS: Systematic integrative review of the medical literature; electronic search of MEDLINE 1950-2021; studies investigating role of any micronutrient in the acceleration of alcohol-related liver injury in humans or animals. Studies which specifically related to alcoholic hepatitis were excluded. Outcomes were extracted and recorded in tabulated form and discussed narratively. RESULTS: We identified 46 studies investigating the role of micronutrient deficiencies in the pathogenesis of alcohol-related liver disease. Specific micronutrients which were identified included folic acid or related B vitamins (n = 9 studies), Vitamin D (n = 9 studies), magnesium (n = 8 studies), zinc (n = 8 studies) and selenium (n = 12 including one systematic review). Observational evidence suggests a potential role of magnesium deficiency in accelerating alcohol-related liver injury with weak or negative evidence for other micronutrients. CONCLUSIONS: Magnesium deficiency may increase the risk of alcohol-related liver injury and adverse liver outcomes. However, currently, there is insufficient evidence to support magnesium supplementation except for clinically relevant magnesium deficiency. Long-term prospective cohort studies assessing the impact of micronutrients on liver disease progression in patients with alcohol use disorder are lacking and may help determine whether there is a causal role for micronutrient deficiencies in alcohol-related liver injury.

Improving the quality of weekend medical handover on non-receiving medical hospital wards.

INTRODUCTION: Handover is the system by which the responsibility for immediate and ongoing care is transferred between healthcare professionals and can be an area of risk. The Royal College of Physicians (RCP) has recommended improvement and standardisation of handover. Locally, national training surveys have reported poor feedback regarding handover at Glasgow Royal Infirmary. AIM: To improve and standardise handover from weekday to weekend teams. METHODS: The Plan-Do-Study-Act (PDSA) quality improvement framework was used. Interventions were derived from a driver diagram after consultation with relevant stakeholders. Four PDSA cycles were completed over a 4-month period:PDSA cycle 1-Introduction of standardised paper form on three wards.PDSA cycle 2-Introduction of electronic handover system on three wards.PDSA cycle 3-Expansion of electronic handover to seven wards.PDSA cycle 4-Expansion of electronic handover to all non-receiving medical wards.The outcome of interest was the percentage of patients with full information handed over based on a six-point scale derived from the RCP. Data were collected weekly throughout the study period. RESULTS: 18 data collection exercises were performed including 525 patients. During the initial phase there was an improvement in handover quality with 0/28 (0%) at baseline having all six points completed compared with 13/48 (27%) with standardised paper form and 21/42 (50%) with the electronic system (p<0.001). When the electronic handover form was expanded to all wards, the increased quality was maintained, however, to a lesser extent compared with the initial wards. CONCLUSION: A standardised electronic handover system was successfully introduced to downstream medical wards over a short time period. This led to an in improvement in the quality of handover in the initial wards involved. When expanded to a greater number of wards there was still an improvement in quality but to a lesser degree.

Models of care for chronic kidney disease: A systematic review.

AIM: Chronic kidney disease (CKD) is common and presents an increasing burden to patients and health services. However, the optimal model of care for patients with CKD is unclear. We systematically reviewed the clinical effectiveness of different models of care for the management of CKD. METHODS: A comprehensive search of eight databases was undertaken for articles published from 1992 to 2016. We included randomized controlled trials that assessed any model of care in the management of adults with pre-dialysis CKD, reporting renal, cardiovascular, mortality and other outcomes. Data extraction and quality assessment was carried out independently by two authors. RESULTS: Results were summarized narratively. Nine articles (seven studies) were included. Four models of care were identified: nurse-led, multidisciplinary specialist team, pharmacist-led and self-management. Nurse and pharmacist-led care reported improved rates of prescribing of drugs relevant to CKD. Heterogeneity was high between studies and all studies were at high risk of bias. Nurse-led care and multidisciplinary specialist care were associated with small improvements in blood pressure control. CONCLUSION: Evidence of long term improvements in renal, cardiovascular or mortality endpoints was limited by short follow up. We found little published evidence about the effectiveness of different models of care to guide best practice for service design, although there was some evidence that models of care where health professionals deliver care according to a structured protocol or guideline may improve adherence to treatment targets.

Fracture risk calculation tool enhances dual-energy X-ray absorptiometry scan referral pathway in cirrhosis patients.

OBJECTIVES: Liver cirrhosis is associated with osteoporosis leading to an increased risk of fractures. We aimed to establish whether a risk stratification strategy using a fracture risk calculation tool (FRAX) to determine which patients should receive a dual-energy X-ray absorptiometry (DXA) scan is effective in reducing scan rates without compromising sensitivity for detecting osteoporosis. METHODS: A retrospective analysis of 252 patients with liver cirrhosis attending hepatoma surveillance clinics. Receiver operating characteristic analysis was performed to assess sensitivity and specificity at 10-year fracture risk thresholds of 5, 10 and 15%. RESULTS: DXA scans were performed among 252 patients. Mean age was 61.6±10.2 years, of which 53.2% were male. Cirrhosis aetiology was largely a result of alcohol excess (n=33.3%), chronic hepatitis C virus infection (n=20.2%) and nonalcoholic fatty liver disease (n=15.9%). The majority of patients were in good prognostic groups (87.4% Child-Pugh A, 11.3% Child-Pugh B, 1.3% Child-Pugh C). Osteoporosis was present in 19.0% of those who underwent DXA scanning. The optimum 10-year fracture risk threshold was found to be 10% using the FRAX tool. This retained a high sensitivity of 95.8%, specificity 64.7%, and negative predictive value 98.5%. Introduction of a 10% FRAX threshold would result in a reduction of the DXA scanning rate to 46.8% of the current rate. CONCLUSION: A risk stratification strategy for DXA scanning using a fracture risk assessment tool (FRAX) and a 10-year fracture risk threshold of 10% leads to a significant reduction in scan rates without compromising osteoporosis detection rates.

Elevated expression of the chemokine-scavenging receptor D6 is associated with impaired lesion development in psoriasis.

D6 is a scavenging-receptor for inflammatory CC chemokines that are essential for resolution of inflammatory responses in mice. Here, we demonstrate that D6 plays a central role in controlling cutaneous inflammation, and that D6 deficiency is associated with development of a psoriasis-like pathology in response to varied inflammatory stimuli in mice. Examination of D6 expression in human psoriatic skin revealed markedly elevated expression in both the epidermis and lymphatic endothelium in "uninvolved" psoriatic skin (ie, skin that was more than 8 cm distant from psoriatic plaques). Notably, this increased D6 expression is associated with elevated inflammatory chemokine expression, but an absence of plaque development, in uninvolved skin. Along with our previous observations of the ability of epidermally expressed transgenic D6 to impair cutaneous inflammatory responses, our data support a role for elevated D6 levels in suppressing inflammatory chemokine action and lesion development in uninvolved psoriatic skin. D6 expression consistently dropped in perilesional and lesional skin, coincident with development of psoriatic plaques. D6 expression in uninvolved skin also was reduced after trauma, indicative of a role for trauma-mediated reduction in D6 expression in triggering lesion development. Importantly, D6 is also elevated in peripheral blood leukocytes in psoriatic patients, indicating that upregulation may be a general protective response to inflammation. Together our data demonstrate a novel role for D6 as a regulator of the transition from uninvolved to lesional skin in psoriasis.