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Haemochromatosis is defined as systemic iron overload of genetic origin, caused by a reduction in the concentration of the iron regulatory hormone hepcidin, or a reduction in hepcidin-ferroportin binding. Hepcidin regulates the activity of ferroportin, which is the only identified cellular iron exporter. The most common form of haemochromatosis is due to homozygous mutations (specifically, the C282Y mutation) in HFE, which encodes hereditary haemochromatosis protein. Non-HFE forms of haemochromatosis due to mutations in HAMP, HJV or TFR2 are much rarer. Mutations in SLC40A1 (also known as FPN1; encoding ferroportin) that prevent hepcidin-ferroportin binding also cause haemochromatosis. Cellular iron excess in HFE and non-HFE forms of haemochromatosis is caused by increased concentrations of plasma iron, which can lead to the accumulation of iron in parenchymal cells, particularly hepatocytes, pancreatic cells and cardiomyocytes. Diagnosis is noninvasive and includes clinical examination, assessment of plasma iron parameters, imaging and genetic testing. The mainstay therapy is phlebotomy, although iron chelation can be used in some patients. Hepcidin supplementation might be an innovative future approach.

Background and objectives In Australia, mortality rates for hepatocellular carcinoma (HCC) are rising. Targeted surveillance is recommended to increase early diagnosis. The aim of this study was to synthesise evidence regarding HCC surveillance in primary care and identify barriers and facilitators to surveillance. Methods A systematic review was performed, with searches conducted in five biomedical databases, the Centre for Reviews and Dissemination website and the grey literature. Study quality was assessed using the National Institute for Heath and Care Excellence (NICE) quality appraisal checklists. Results In all, 32 studies, focusing on viral hepatitis and cirrhosis patients, were included in the review. HCC surveillance rates were lower for patients managed by primary care providers (PCPs) than for those managed by gastroenterologists/hepatologists. HCC surveillance rates increased when additional support was provided to PCPs (eg reminder systems, nurse follow-up). Key barriers were a lack of awareness of HCC risks and surveillance recommendations, as well as competing priorities PCPs must address when working with patients with multimorbidity. Discussion HCC surveillance programs in primary care should be accompanied by additional support for PCPs and strategies to increase awareness of clinical recommendations. [ABSTRACT FROM AUTHOR]

Background and Objective: Little is known about the association between ambient air pollution and idiopathic pulmonary fibrosis (IPF) in areas with lower levels of exposure. We aimed to investigate the impact of air pollution on lung function and rapid progression of IPF in Australia. Methods: Participants were recruited from the Australian IPF Registry (n = 570). The impact of air pollution on changes in lung function was assessed using linear mixed models and Cox regression was used to investigate the association with rapid progression. Results: Median (25th–75th percentiles) annual fine particulate matter (<2.5 μm, PM2.5) and nitrogen dioxide (NO2) were 6.8 (5.7, 7.9) μg/m3 and 6.7 (4.9, 8.2) ppb, respectively. Compared to living more than 100 m from a major road, living within 100 m was associated with a 1.3% predicted/year (95% confidence interval [CI] −2.4 to −0.3) faster annual decline in diffusing capacity of the lungs for carbon monoxide (DLco). Each interquartile range (IQR) of 2.2 μg/m3 increase in PM2.5 was associated with a 0.9% predicted/year (95% CI −1.6 to −0.3) faster annual decline in DLco, while there was no association observed with NO2. There was also no association between air pollution and rapid progression of IPF. Conclusion: Living near a major road and increased PM2.5 were both associated with an increased rate of annual decline in DLco. This study adds to the evidence supporting the negative effects of air pollution on lung function decline in people with IPF living at low‐level concentrations of exposure. [ABSTRACT FROM AUTHOR]

Aims: To quantify the incremental direct medical costs in people with diabetes from the healthcare system perspective; and to identify trends in the incremental costs. Methods: This was a matched retrospective cohort study based on a linked data set developed for investigating chronic kidney disease in Tasmania, Australia. Using propensity score matching, 51,324 people with diabetes were matched on age, sex and residential area with 102,648 people without diabetes. Direct medical costs (Australian dollars 2020–2021) due to hospitalisation, Emergency Department visits and pathology tests were included. The incremental costs and cost ratios between mean annual costs of people with diabetes and their controls were calculated. Results: On average, people with diabetes had healthcare costs that were almost double their controls ($2427 [95% CI 2322–2543]; ratio 1.87 [95% CI 1.85–1.91]; pooled from 2007–2017). While in the first year of follow‐up, the costs of a person with diabetes were $1643 (95% CI 1489–1806); ratio 1.83 (95% CI 1.76–1.92) more than their control, this increased to $2480 (95% CI 2265–2680); ratio 1.69 (95% CI 1.62–1.77) in the final year. Although the incremental costs were higher in older age groups (e.g., ≥70: $2498 [95% CI 2265–2754]; 40–49: $2117 [95% CI 1887–2384]), the cost ratios were higher in younger age groups (≥70: 1.52 [95% CI 1.48–1.56]; 40–49: 2.37 [95% CI 2.25–2.61]). Conclusions: Given the increasing burden that diabetes imposes, our findings will support policymakers in future planning for diabetes and enable targeting sub‐groups with higher long‐term costs for possible cost savings for the Tasmanian healthcare system. [ABSTRACT FROM AUTHOR]