The role of occupational and environmental exposures in the aetiology of acquired severe aplastic anaemia: a case control investigation

Aplastic anaemia is a rare but serious disorder with a high morbidity and mortality rate. The causes of aplastic anaemia are, for the most part, unknown. We report on the hypothesis that aplastic anaemia may be caused by occupational and/or environmental exposures to certain chemicals. The UK Aplastic Anaemia Study was an interview-based case-control study covering the whole of Great Britain. Those patients diagnosed between 1 July 1993 and 20 October 1997, aged < or =75 years and born and diagnosed in the UK were eligible for the study. Two hundred eligible cases of aplastic anaemia were compared with 387 age- and sex-matched controls. A number of occupational exposures showed increases in risk. In a multivariate model of these exposures the odds ratios (ORs) for solvents/degreasing agents, pesticides and radiation were >2 and statistically significant. Reported chemical treatment of houses within 5 years of diagnosis had a significantly raised risk for adults [OR = 2.51, 95% confidence interval (CI) 1.02-12.01], particularly for woodworm treatment (OR = 5.1, 95% CI 1.5-17.4). This study identified significant risks associated with self-reported exposure to solvents, radiation and pesticides in the workplace. Self-reported chemical treatment of houses was also associated with an increased risk of developing aplastic anaemia, in keeping with previous literature.     

Our contemporary understanding of the aetiology of pressure ulcers/pressure injuries

In 2019, the third and updated edition of the Clinical Practice Guideline (CPG) on Prevention and Treatment of Pressure Ulcers/Injuries has been published. In addition to this most up‐to‐date evidence‐based guidance for clinicians, related topics such as pressure ulcers (PUs)/pressure injuries (PIs) aetiology, classification, and future research needs were considered by the teams of experts. To elaborate on these topics, this is the third paper of a series of the CPG articles, which summarises the latest understanding of the aetiology of PUs/PIs with a special focus on the effects of soft tissue deformation. Sustained deformations of soft tissues cause initial cell death and tissue damage that ultimately may result in the formation of PUs/PIs. High tissue deformations result in cell damage on a microscopic level within just a few minutes, although it may take hours of sustained loading for the damage to become clinically visible. Superficial skin damage seems to be primarily caused by excessive shear strain/stress exposures, deeper PUs/PIs predominantly result from high pressures in combination with shear at the surface over bony prominences, or under stiff medical devices. Therefore, primary PU/PI prevention should aim for minimising deformations by either reducing the peak strain/stress values in tissues or decreasing the exposure time.     

Investigation into cases of hepatitis of unknown aetiology among young children,Scotland, 1 January 2022 to 12 April 2022

On 31 March 2022, Public Health Scotland was alerted to five children aged 3–5 years admitted to hospital with severe hepatitis of unknown aetiology. Retrospective investigation identified eight additional cases aged 10 years and younger since 1 January 2022. Two pairs of cases have epidemiological links. Common viral hepatitis causes were excluded in those with available results. Five children were adenovirus PCR-positive. Other childhood viruses, including SARS-CoV-2, have been isolated. Investigations are ongoing, with new cases still presenting.     

Background factors of molar-incisor hypomineralization in a group of Finnish children

Objective. Molar-Incisor Hypomineralization (MIH) is a common developmental enamel defect characterized by demarcated opacities in permanent molars and incisors. Its etiology still remains unclear. The aim of this retrospective cohort study was to assess if the socioeconomic environment of the child is associated with MIH. Materials and methods. The study was located in two rural towns and three urban cities in Finland. A total of 818 children, between 7–13 years old, were examined for MIH using the evaluation criteria in line with those of the European Academy of Paediatric Dentistry, but excluding opacities smaller than 2 mm in diameter. The mothers filled in a questionnaire which included questions related to the family’s way of living (e.g. area of residency, farming, day care attendance) and socioeconomic status (family income, number of mother’s school years, level of maternal education). Results. The prevalence of MIH in the study population was 17.1%. Family income, urban residency and day care attendance were associated with MIH in the univariate analysis. In the multivariate analysis using binary logistic regression, only urban residency during a child’s first 2 years of life remained associated with MIH. The prevalence of MIH in urban areas was 21.3% and in rural areas 11.5% (OR = 2.18, CI = 1.35–3.53, p = 0.001). Conclusions. The prevalence of MIH was related to urban residency and could not be explained by any other factor included in the study.