Tung Wah Eastern Hospital is a hospital located at Causeway Bay and operated by the Tung Wah Group of Hospitals. The hospital was formerly called Indian General Hospital (IGH).Opened on 27 November 1929, the hospital is located in So Kon Po, Causeway Bay and became a public hospital in 1991. It is primarily for the rehabilitation of patients who are almost ready to be discharged from the hospital system. Thus, patients are typically not severely ill or injured. This is why there are no emergency or accident facilities.The rooftop garden, located on what would be the fourth floor, gives both staff and patients the opportunity to enjoy fresh air, sunshine and a scenic view of the local area.
Alzheimer's disease (AD) is the most common aetiology of cognitive impairment worldwide and in Hong Kong. There have been rapid advances in the use of biomarkers for the diagnosis of AD and in the availability of anti-amyloid therapies (AAT) to slow cognitive and functional decline. At present, there is no consensus in Hong Kong regarding the application of AD biomarkers or the use of AAT. A multidisciplinary group of 20 medical specialists from five professional societies discussed issues related to the application of biomarkers for the diagnosis of AD pathology and the use of AAT, and reviewed the evidence in the context of local experience to inform recommendations. A modified Delphi approach was adopted to finalise the recommendations. Consensus was defined as ≥75% agreement on a 9-point Likert scale among panellists. The panel finalised 26 consensus statements addressing the use of AD biomarkers, including neuroimaging and fluid biomarkers, as well as the use of AAT, including inclusion criteria, serial neuroimaging monitoring during treatment, and management of infusion reactions. These recommendations are relevant to the Hong Kong healthcare setting and may serve as guidance for doctors across specialties to facilitate appropriate management of AD.
Abstract Introduction Glycemic variability (GV) independently predicts diabetic complications, with fluctuations promoting oxidative stress, inflammation, and endothelial dystunction. Insomnia and obstructive sleep apnea (OSA) are highly prevalent in Type 2 Diabetes (T2D) and may exacerbate metabolic dysregulation, but their impact on nocturnal GV in treated patients with apparently stable glycemic control remains unclear. This study evaluated whether insomnia, OSA, and their co-occurrence (COMISA) have distinct nocturnal GV profiles in a real-world cohort of well-controlled T2D. Methods Fifty-nine patients with T2D (median age 62.0 years) underwent up to 15 consecutive nights of continuous glucose monitoring (CGM; Abbott Libre 2) paired with objective sleep assessment via Belun Ring (BR). Participants were classified as OSA (BR-AHI3% ≥15; N=19), insomnia (BR sleep efficiency < 80% with intake interview; N=11), or COMISA (meeting criteria for both disorders; N=29). Nocturnal GV was quantified using sleep-time coefficient of variation (SLP-CV) and sleep-time continuous overall net glycemic action (SLP-CONGA). Groups differences in median GV were tested, followed by generalized linear mixed-effects models (GLMMs) adjusted for age, sex, BMI, and HbA1c, incorporating participant-level random intercepts to account for night-to-night variability. Results COMISA and insomnia exhibited higher SLP-CV (12.3% and 13.3%) than OSA (8.9%, both p< 0.05), despite comparable glycemic control across groups (median HbA1c 7.3 vs 7.2% vs 7.1% for COMISA, insomnia, and OSA; p=0.81; 83% on metformin; 19% on insulin). Males exhibited higher nocturnal GV than females for both SLP-CV (p=0.07) and SLP-CONGA (p< 0.05). In adjusted GLMMs, COMISA was associated with a 39% increase in nocturnal SLP-CV (β=0.33, p< 0.05) and insomnia with a 43% increase (β=0.36, p< 0.05) compared with OSA. Moreover, male sex (β=-0.24, p< 0.05) and a higher REM% (β< 0.01, p< 0.05) were independently associated with higher SLP-CV. Conclusion This pioneering study identifies Insomnia and COMISA as independent drivers of elevated nocturnal GV in pharmacologically treated T2D, a metabolic risk factor linked to microvascular and macrovascular complications that is not reflected by HbA1c. Multi-night CGM integrated with sleep monitoring reveals hidden nocturnal metabolic instability, suggesting T2D patients with insomnia-related phenotypes and male sex, represent a high-risk subgroup who may benefit from personalized sleep and metabolic interventions. Support (if any)
PURPOSE:To evaluate the corneal biomechanical and biometric properties in immunoglobulin G4-related ophthalmic disease (IgG4-ROD) patients. SETTING:Ethnic Han Chinese biopsy-proven IgG4-ROD patients from a territory wide cohort and sex-, age-, smoking- and lens status-matched healthy controls. DESIGN:A case-controlled (1:1) study. METHODS:Corvis ST analyzer and IOL Master 700 biometry assessment. RESULTS:Sixty-seven eyes from 67 patients with IgG4-ROD (41 = males), aged 63.9 ± 13.1 years and 67 right eyes from 67 healthy ethnically Han Chinese controls were recruited. IgG4-ROD eyes were associated with a more negative applanation 2 velocity (-0.30 versus -0.27 m/s, P = 0.0143), and reduced radius of curvature (7.48 versus 7.98 mm, P = 0.0136). There was no difference in intraocular pressure, applanation 1 length, applanation 1 velocity, applanation 2 length, deformation amplitude and peak distance. Corneal astigmatism was greater in IgG4-ROD eyes (-1.2 versus -0.9 D, P = 0.0132), and the deep axis is along 90.2 degree. There is no difference in the steep and flat keratometry, deep axis, lens thickness, cornea thickness, and anterior chamber depth. CONCLUSIONS:We found multiple corneal changes in biomechanics and fine structures in a cohort of biopsy-proven IgG4-ROD with potential long-term implications in ocular surface functions. A longitudinal follow-up would be useful to identify the clinical implications and observe if these changes improve with treatments.
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss in the aging population. Although frailty has been recognized as a potential risk factor, previous studies relying on static assessments cannot capture its dynamic nature. This study aims to prospectively evaluate the association between dynamic frailty trajectories and incident AMD. The baseline cohort included 462,573 UK Biobank participants who were free of AMD and had frailty phenotype (FP) data at enrollment. Among them, 53,059 with at least one follow-up FP assessment comprised the trajectory cohort. Participants were categorized as nonfrail, prefrail, or frail based on their FP scores. Annualized frailty progression (ΔFP/year) was estimated via linear regression. Cox models assessed hazard ratios (HRs) and 95
