Cognitive dysfunction (CD) is a common yet often clinically subtle manifestation that considerably impacts the health-related quality of life in patients with systemic lupus erythaematosus (SLE). Given the inconsistencies in CD assessment and challenges in its attribution to SLE, the reported prevalence of CD differs widely, ranging from 3 to 88%. The clinical presentation of CD in SLE is non-specific and may manifest concurrently with overt neuropsychiatric illness such as psychosis or mood disorders or as isolated impairment of attention, working memory, executive dysfunction or processing speed. Despite the lack of standardized and sensitive neuropsychological tests and validated diagnostic biomarkers of CD in SLE, significant progress has been made in identifying pathogenic neural pathways and neuroimaging.Furthermore, several autoantibodies, cytokines, pro-inflammatory mediators and metabolic factors have been implicated in the pathogenesis of CD in SLE. Abrogation of the integrity of the blood-brain barrier (BBB) and ensuing autoantibody-mediated neurotoxicity, complement and microglial activation remains the widely accepted mechanism of SLE-related CD. Although several functional neuroimaging modalities have consistently demonstrated abnormalities that correlate with CD in SLE patients, a consensus remains to be reached as to their clinical utility in diagnosing CD. Given the multifactorial aetiology of CD, a multi-domain interventional approach that addresses the risk factors and disease mechanisms of CD in a concurrent fashion is the favourable therapeutic direction. While cognitive rehabilitation and exercise training remain important, specific pharmacological agents that target microglial activation and maintain the BBB integrity are potential candidates for the treatment of SLE-related CD.

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CorrigendumCorrigendum to "Does oral calcium intake or body habitus relate to the degree of valvular calcification and adverse events in patients with severe aortic stenosis?" [Int.The authors regret for the error occurred in Table 2 and the corrected version is provided below.The amendments are in red font. The first line in paragraph 6: "Patients with a low BMI health risk were 1.26 times likelier to have heavy AVC load (relative risk, P = 0.019)".The first line in paragraph 8: "Our study also found that patients with a low BMI health risk (BMI ≤ 22.9) were 1.26 times likelier (relative risk) to have heavy AVC."

Aims: To describe inflammatory arthritis (IA) patients initiating biologic diseasemodifying anti-rheumatic drugs (bDMARDs) who use complementary and alternative medicine (CAM), and determine the impact of CAM on predicting modified Health Assessment Questionnaire (mHAQ) at 6 months.Methods: This was a prospective inception cohort study of patients ≥21 years old initiating a bDMARD for IA after July 2016. Data were obtained via questionnaires and abstraction from medical records. Baseline characteristics between ever-CAM and CAM non-users were compared. CAM as a predictor of mHAQ ≥1 at 6 months after bDMARD initiation was analyzed using multivariate logistic regression, adjusting for other baseline characteristics.Results: We recruited 299 patients (36.2% male, mean age 49.0 years). There were 45.8% who had rheumatoid arthritis, 54.2% had a spondyloarthropathy, median disease duration of 1.1 years and median mHAQ of 0.4. Compared to CAM non-users, ever-CAM users had a lower mean body mass index, were less likely to speak English, and more likely to smoke and drink alcohol. There was no association of CAM use with high mHAQ and no interaction with smoking. Smoking (odds ratio [OR] 938.9; 95% CI 3.20-275 884.1), baseline mHAQ (OR 252.2; 95% CI 5.34-11 899.2) and Charlson's Comorbidity Index score ≥4 (OR 237.4;) independently predicted high mHAQ at 6 months.Conclusions: CAM use was not associated with high mHAQ at 6 months. Smoking was an independent predictor of residual functional disability at 6 months, even after adjusting for age, comorbidity and baseline mHAQ. Greater emphasis on smoking cessation may improve long-term functional outcomes in IA patients on bDMARDs.