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Background and Aim: People with inflammatory bowel disease (IBD) have an increased risk of cardiovascular disease, including in younger adulthood. This may arise in part from chronic, systemic low‐grade inflammation. The process of atherosclerosis may begin in childhood. We sought to determine whether pediatric IBD is associated with adverse changes in arterial structure and function as a marker of early increased cardiovascular risk. Methods: We performed a case–control study comparing children with IBD for a median disease duration of 2.49 (interquartile range 1.23, 4.38) years with healthy children. In a single visit, we collected baseline clinical and anthropometric data, and measured blood pressure, pulse wave velocity, carotid artery distensibility, and aortic and carotid intima‐media thickness. High‐sensitivity C‐reactive protein and fasting lipids were measured. Results: We enrolled 81 children with IBD (40 with Crohn's disease, 40 with ulcerative colitis, and 1 with unspecified IBD) and 82 control participants. After adjusting for age, sex, body mass index z‐score, blood pressure, and low‐density lipoprotein cholesterol, there was no difference in measures of arterial structure and function in children with IBD compared with controls, nor between those with Crohn's disease or ulcerative colitis. Conclusion: We did not show any differences in arterial structure and function in children with a history of IBD for less than 5 years compared with healthy controls. IBD diagnosed in childhood may provide a window of opportunity to actively reduce standard cardiovascular risk factors and improve future cardiovascular outcomes. [ABSTRACT FROM AUTHOR]

Background Aim Methods Results Conclusion The frequency of EoE has been increasing in Northern Hemisphere cohorts, yet there is a scarcity of data in our region. Regional climatic factors, and lifestyle habits may influence the presentation of EoE, and appropriate management is crucial to prevent complications. WIth this is mind we undertook the first comprehensive multisite study of EoE in Australasian children.To determine the incidence, prevalence, clinical characteristics and management of eosinophilic esophagitis (EoE) in Australasian children.Retrospective audit of endoscopic records, histology reports and case notes (ICD code) over a 10‐year period (1 January 2008 to 31 December 2018). Cases were defined as having >15 eosinophils per high‐power field (HPF) at endoscopy and oesophageal biopsy, while treatment response was defined as <5 eosinophils per HPF. Included were patients aged 0–18 years presenting to tertiary paediatric hospitals in seven capital cities (Adelaide, Auckland, Brisbane, Christchurch, Melbourne, Perth and Sydney), while those with conditions that could cause eosinophilia (organ transplantation, hyper‐eosinophilic syndrome) or taking medications that may influence tissue eosinophilia (systemic corticosteroids immunosuppressants) were excluded. Australian Bureau of Statistics and Stats NZ were used to define comparative population data. Demographics (age at diagnosis, gender, country of birth, race) comorbidities (atopic conditions, e.g. asthma, seasonal rhinitis, eczema) and treatment (diet, steroids, proton pump inhibitors) were noted.The prevalence of EoE ranged from 15 to 54 per 100 000 children, where cases were more common in Adelaide than other localities. Incidence increased significantly in all sites across the 10 years, with peak incidence in Adelaide of 6.4 per 100 000 children in 2017. EoE was most frequent in males (male:female ratio = 3:1) and >90% were white Caucasian. Polynesian racial background in Auckland (10%) and middle eastern racial background in Sydney (10%) were the next most frequent. Treatment choice varied across sites, and greater than 30% of patients did not undergo endoscopy to assess initial treatment success.The prevalence of EoE in Australasian children is comparable to that observed elsewhere, and the incidence is increasing significantly. Regional differences in disease frequency, management practices and access to endoscopy warrant further study. [ABSTRACT FROM AUTHOR]

The challenges of human space exploration produce some of humanity's greatest technological and scientific advances, not excluding innovations in medicine. The microgravity environment causes a host of physiological changes, and exposure to dust on the Moon caused considerable pulmonary distress to astronauts during the Apollo missions. As the National Aeronautics and Space Administration and other organizations prepare for long-duration exploration missions to Mars, the hazards and consequences of the Martian surface need to be accounted for. This review investigates how substances analogous to hazardous components of Martian dust have caused disease in people on Earth. Because of its small grain size, dust on Mars is more likely to cause lung irritation, absorb into the bloodstream, and lead to diseases in astronauts. Toxic components of martian dust include perchlorates, silica, nanophase iron oxides, and gypsum in addition to trace amounts of toxic metals whose abundances are debated: chromium, beryllium, arsenic, and cadmium. Predicted effects of dust exposure ranges from asymptomatic to life-threatening, with many substances being carcinogenic and most damage impacting the pulmonary system. The longer transit time for astronauts to return home makes the operations of performing emergency medical treatment more difficult and increases both the likelihood and consequences of developing chronic disease. Exposure mitigation needs to be prioritized; however, supplements may be taken to prevent disease from breakthrough exposures, and treatment regimens could lessen morbidity and mortality. Treatments and equipment need to be carefully considered and transported with the astronauts to be prepared for all possible scenarios., Competing Interests: The authors declare no conflicts of interest relevant to this study., (© 2025 The Author(s). GeoHealth published by Wiley Periodicals LLC on behalf of American Geophysical Union.)

Aim: To determine the utility of anti-tissue transglutaminase IgA antibodies (tTG-IgA) and anti-deaminated gliadin peptide IgG antibodies (DGP-IgG) in detecting coeliac disease (CD) and whether DGP-IgG can replace anti-endomysial IgA antibody in the European Society for Paediatric Gastroenterology Hepatology and Nutrition no-biopsy approach in diagnosing CD., Methods: Children aged < 19 years who had paired tTG-IgA and DGP-IgG performed and had a gastroscopy with biopsies between 1 March 2016 and 31 October 2020 were retrospectively reviewed., Results: Of 1206 patients who fulfilled the study criteria, 298 (24.7%) patients were diagnosed with CD. Fifteen patients with IgA deficiency were excluded from any tTG-IgA analysis. tTG-IgA had sensitivity and specificity of 93.5% and 92.0%, respectively, in detecting CD, while DGP-IgG had sensitivity of 97.0% and specificity of 86.7%. tTG-IgA ≥ 10x upper limit of normal (ULN) alone had a specificity of 99.3% and a positive predictive value (PPV) of 96.8%. An optimal DGP-IgG threshold was identified to be 70 U/mL (3.5x ULN) based on > 99% specificity in detecting CD. When tTG-IgA ≥ 10x ULN was combined with DGP-IgG ≥ 3.5 ULN, the PPV in diagnosing CD was 98.5%. DGP-IgG performed well in detecting CD in 126 children aged < 3 years, with all patients with CD having an elevated DGP-IgG (sensitivity 100%)., Conclusions: Combined tTG-IgA ≥ 10x ULN and DGP-IgG ≥ 3.5x ULN provided a high PPV (98.5%) in diagnosing CD. DGP-IgG testing can potentially replace EMA testing in those children with tTG-IgA ≥ 10x ULN. Future studies should evaluate DGP-IgG testing as a sequential test., (© 2025 The Author(s). Journal of Paediatrics and Child Health published by John Wiley & Sons Australia, Ltd on behalf of Paediatrics and Child Health Division (The Royal Australasian College of Physicians).)