Vitamin D status and outcomes for hospitalised older patients with COVID-19.

PURPOSE: Older adults are more likely to be vitamin D deficient. The aim of the study was to determine whether these patients have worse outcomes with COVID-19. METHODS: We conducted a prospective cohort study between 1 March and 30 April 2020 to assess the importance of vitamin D deficiency in older patients with COVID-19. The cohort consisted of patients aged ≥65 years presenting with symptoms consistent with COVID-19 (n=105). All patients were tested for serum 25-hydroxyvitamin D (25(OH)D) levels during acute illness. Diagnosis of COVID-19 was confirmed via viral reverse transcriptase PCR swab or supporting radiological evidence. COVID-19-positive arm (n=70) was sub-divided into vitamin D-deficient (≤30 nmol/L) (n=39) and -replete groups (n=35). Subgroups were assessed for disease severity using biochemical, radiological and clinical markers. Primary outcome was in-hospital mortality. Secondary outcomes were laboratory features of cytokine storm, thoracic imaging changes and requirement of non-invasive ventilation (NIV). RESULTS: COVID-19-positive arm demonstrated lower median serum 25(OH)D level of 27 nmol/L (IQR=20-47 nmol/L) compared with COVID-19-negative arm, with median level of 52 nmol/L (IQR=31.5-71.5 nmol/L) (p value=0.0008). Among patients with vitamin D deficiency, there was higher peak D-dimer level (1914.00 µgFEU/L vs 1268.00 µgFEU/L) (p=0.034) and higher incidence of NIV support and high dependency unit admission (30.77% vs 9.68%) (p=0.042). No increased mortality was observed between groups. CONCLUSION: Older adults with vitamin D deficiency and COVID-19 may demonstrate worse morbidity outcomes. Vitamin D status may be a useful prognosticator.

Drug-induced liver injury: a comprehensive review.

Drug-induced liver injury (DILI) remains a challenge in clinical practice and is still a diagnosis of exclusion. Although it has a low incidence amongst the general population, DILI accounts for most cases of acute liver failure with a fatality rate of up to 50%. While multiple mechanisms of DILI have been postulated, there is no clear causal relationship between drugs, risk factors and mechanisms of DILI. Current best practice relies on a combination of high clinical suspicion, thorough clinical history of risk factors and timeline, and extensive hepatological investigations as supported by the international Roussel Uclaf Causality Assessment Method criteria, the latter considered a key diagnostic algorithm for DILI. This review focuses on DILI classification, risk factors, clinical evaluation, future biomarkers and management, with the aim of facilitating physicians to correctly identify DILI early in presentation.

Snapping ankles: peroneal tendon subluxation and dislocation.

Peroneal tendon dislocation or subluxation is an orthopaedic condition that usually occurs as a result of injury to the superior peroneal retinaculum. The peroneal muscles are located in the lateral compartment of the leg, and their tendons run in the retromalleolar groove anchored by the superior peroneal retinaculum. Peroneal instability is usually classified using the Eckert and Davies classification, which was modified by Oden into a four-point grading system. The mechanism of injury is typically sudden forced dorsiflexion, resulting in aggressive tautness of the peroneal tendons, combined with a forced eversion of the hindfoot. Plain X-ray, ultrasound and magnetic resonance imaging are useful for imaging of the injury and in planning for surgery. Operative management has high success rates and there are multiple surgical techniques available, including superior peroneal retinaculum repair, tenoplasty, bone block procedures, groove deepening and endoscopic approaches, with little variation in outcome found between the approaches.

Inflammation across tissues: can shared cell biology help design smarter trials?

Immune-mediated inflammatory diseases (IMIDs) are responsible for substantial global disease burden and associated health-care costs. Traditional models of research and service delivery silo their management within organ-based medical disciplines. Very often patients with disease in one organ have comorbid involvement in another, suggesting shared pathogenic pathways. Moreover, different IMIDs are often treated with the same drugs (including glucocorticoids, immunoregulators and biologics). Unlocking the cellular basis of these diseases remains a major challenge, leading us to ask why, if these diseases have so much in common, they are not investigated in a common manner. A tissue-based, cellular understanding of inflammation might pave the way for cross-disease, cross-discipline basket trials (testing one drug across two or more diseases) to reduce the risk of failure of early-phase drug development in IMIDs. This new approach will enable rapid assessment of the efficacy of new therapeutic agents in cross-disease translational research in humans.

Lessons of the month 1: Polytrauma in a geriatric patient resulting in reactivation of cytomegalovirus infection and secondary cold agglutinin disease-induced haemolytic anaemia.

Haemolysis is a rare but serious complication of cytomegalovirus (CMV) infection, described mostly in immunocompromised patients, the pathogenesis of which is yet to be fully elucidated. We describe a case of Coombs-positive haemolytic anaemia in an older Caucasian immunocompetent woman after polytrauma, resulting from suspected reactivation of CMV infection and secondary cold agglutinin disease. Clinicians should consider CMV infection in the differential diagnosis of haemolytic anaemia in immunocompetent older adults who are admitted with significant musculoskeletal trauma. Early treatment with B-cell depletion therapy to halt cold agglutinin production can be life-saving.