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Background: Patients with solid cancers and hematopoietic malignancy can experience systemic symptoms compatible with adult-onset Still’s disease (AOSD). The newly described VEXAS, associated with somatic UBA1 mutations, exhibits an overlap of clinical and/or biological pictures with auto inflammatory signs and myelodysplastic syndrome (MDS). Objectives: To describe a cohort of patients with signs of undifferentiated systemic autoinflammatory disorder (USAID) concordant with AOSD and MDS/chronic myelomonocytic leukemia (CMML) and the prevalence of VEXAS proposed management and outcome. Methods: A French multicenter retrospective study from the MINHEMON study group also used for other published works with the support of multidisciplinary and complementary networks of physicians and a control group of 104 MDS/CMML. Results: Twenty-six patients were included with a median age at first signs of USAID of 70.5 years with male predominance (4:1). Five patients met the criteria for confirmed AOSD. The most frequent subtypes were MDS with a blast excess (31%) and MDS with multilineage dysplasia (18%). Seven patients presented with acute myeloid leukemia and twelve died during a median follow-up of 2.5 years. Six out of 18 tested patients displayed a somatic UBA1 mutation concordant with VEXAS, including one woman. High-dose corticosteroids led to a response in 13/16 cases and targeted biological therapy alone or in association in 10/12 patients (anakinra, tocilizumab, and infliximab). Azacytidine resulted in complete or partial response in systemic symptoms for 10/12 (83%) patients including 3 VEXAS. Conclusion: Systemic form of VEXAS syndrome can mimic AOSD. The suspicion of USAID or AOSD in older males with atypia should prompt an evaluation of underlying MDS and assessment of somatic UBA1 mutation.

There is an established association between air pollution and cardiovascular disease (CVD), which is likely to be mediated by systemic inflammation. The present study evaluated links between long-term exposure to ambient air pollution and high-sensitivity C reactive protein (hs-CRP) in an older Chinese adult cohort (n = 7915) enrolled in the World Health Organization (WHO) study on global aging and adult health (SAGE) China Wave 1 in 2008–2010. Multilevel linear and logistic regression models were used to assess the associations of particulate matter (PM) and nitrogen dioxide (NO2) on log-transformed hs-CRP levels and odds ratios of CVD risk derived from CRP levels adjusted for confounders. A satellite-based spatial statistical model was applied to estimate the average community exposure to outdoor air pollutants (PM with an aerodynamic diameter of 10 μm or less (PM10), 2.5 μm or less (PM2.5), and 1 μm or less (PM1) and NO2) for each participant of the study. hs-CRP levels were drawn from dried blood spots of each participant. Each 10 μg/m3 increment in PM10, PM2.5, PM1, and NO2 was associated with 12.8% (95% confidence interval; (CI): 9.1, 16.6), 15.7% (95% CI: 10.9, 20.8), 10.2% (95% CI: 7.3, 13.2), and 11.8% (95% CI: 7.9, 15.8) higher serum levels of hs-CRP, respectively. Our findings suggest that air pollution may be an important factor in increasing systemic inflammation in older Chinese adults.

BackgroundLong-term exposure to ambient air pollution leads to respiratory morbidity and mortality; however, the evidence of the effect on lung function and chronic obstructive pulmonary disease (COPD) in older adult populations is inconsistent.ObjectiveTo address this knowledge gap, we investigated the associations between particulate matter (PM), nitrogen dioxide (NO2) exposure and lung function, as well as COPD prevalence, in older Chinese adults.MethodsWe used data from the WHO Study on global AGEing and adult health (SAGE) China Wave 1, which includes 11, 693 participants from 64 townships in China. A cross-sectional analysis explored the association between satellite-based air pollution exposure estimates (PM with an aerodynamic diameter of ≤10 µm [PM10], ≤2.5 µm [PM2.5] and NO2) and forced expiratory volume in one second (FEV1), forced vital capacity (FVC), the FEV1/FVC ratio and COPD (defined as post-bronchodilator FEV1/FVC <70%). Data on lung function changes were further stratified by COPD status.ResultsHigher exposure to each pollutant was associated with lower lung function. An IQR (26.1 µg/m3) increase in PM2.5 was associated with lower FEV1 (−71.88 mL, 95% CI –92.13 to –51.64) and FEV1/FVC (−2.81, 95% CI −3.37 to –2.25). For NO2, an IQR increment of 26.8 µg/m3 was associated with decreases in FEV1 (−60.12 mL, 95% CI –84.00 to –36.23) and FVC (−32.33 mL, 95% CI –56.35 to –8.32). A 31.2 µg/m3 IQR increase in PM10 was linked to reduced FEV1 (−8.86 mL, 95% CI −5.40 to 23.11) and FEV1/FVC (−1.85, 95% CI −2.24 to –1.46). These associations were stronger for participants with COPD. Also, COPD prevalence was linked to higher levels of PM2.5 (POR 1.35, 95% CI 1.26 to 1.43), PM10 (POR 1.24, 95% CI 1.18 to 1.29) and NO2 (POR 1.04, 95% CI 0.98 to 1.11).ConclusionAmbient air pollution was associated with lower lung function, especially in individuals with COPD, and increased COPD prevalence in older Chinese adults.

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