Glaucoma is a progressive optic neuropathy characterised by visual field loss and structural damage to the optic nerve. The disease is a leading cause of irreversible blindness worldwide, affecting about 3.5% of individuals aged between 40 and 80 years1. While glaucoma-associated visual field loss may be asymptomatic until the late stages, the disease is commonly known as a silent thief of sight. Although early diagnosis of glaucoma remains a clinical challenge, recent advancements in therapeutics have significantly improved patient outcomes. In particular, laser treatment has been advocated to be safe and effective in managing glaucoma. In a recent sharing, Dr. Lai Sum Wai Isabel highlighted the pathophysiology of glaucoma and shared her insights into managing the disease.

Rheumatoid arthritis (RA) is a chronic, inflammatory, systemic autoimmune disease that initially affects small joints, and gradually involves larger joints with varying degree of severity. Apart from joint damage and bony erosion, pain is a common and often debilitating symptom reported by RA patients1. Essentially, RA-associated pain can be associated with psychological distress, and this may impair physical and social functioning, and increase healthcare utilisation. To counter RA-associated pain, a multimodal approach is taken that includes pharmaceutical agents, physical therapy, and patient education. Additionally, psychological interventions, such as cognitive behavioural therapy (CBT), has also shown to play an essential role in improving the well-being of RA patients in the setting of chronic or intermittent pain2. Thus, the aim of this article is to review the pathophysiology of RA-associated pain and to evaluate the clinical performance of current treatment against this phenomenon.

The field of rheumatology has undergone transformative changes in 2025, driven by innovations in biologic therapies, precision medicine, digital health, and neuroimmune modulation. This article explores the most significant advances in the diagnosis and treatment of rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and psoriatic arthritis (PsA). Key developments include the approval of novel biologics such as dapirolizumab pegol (DZP) and sonelokimab, the emergence of smart drug delivery systems, and the integration of artificial intelligence (AI) in clinical decision-making. These breakthroughs promise improved patient outcomes, reduced side effects, and more personalized care. The article concludes with a discussion on the implications of these advances for clinical practice and future research directions.

Coronary artery disease (CAD) is a significant health challenge, imposing substantial burdens on individuals and healthcare systems worldwide. Notably, in Hong Kong, 1.6% of those aged 15 or above are reported as doctor-diagnosed CAD, with a higher prevalence seen in males (2.1%) compared to females (1.2%). The prevalence increases with age, from 0.1% in those aged 15-24 to 7.7% for those aged 85 or above'. Thanks to the collaborative efforts by researchers, healthcare professionals, and government bodies, advancements in diagnostics, cutting-edge treatment including medications and surgical procedures for CAD are emerging. In addition, a better understanding on the risk factors associated with CAD facilitates more effective lifestyle modifications and cardiac rehabilitation leads to improved patients'outcomes and overall quality of life (QoL).

Precision oncology (PO), defined as molecular profiling of tumours to identify targetable alteration1. The approach has shifted away from non-specific cytotoxic treatment to a more individualised cancer treatment. The advancement in diagnostic technologies, such as next-generation sequencing (NGS), with decision support applications and the availability of patient databases has facilitated optimal cancer management. While PO has proven successful in improving patient outcomes and quality of life (QoL), challenges still persist due to hinderance its use for matching therapies to the patients. Fortunately, emerging techniques, including artificial intelligence (AI), have been implemented to enhance the clinical performance of PO. This review aimed to outline some of the practical issues related to PO and its recent development.

Non–small cell lung cancer (NSCLC) has entered a new era of precision oncology, where increasingly rare genomic targets—such as BRAF V600E, HER2 (ERBB2) activating mutations, ROS1 fusions, KRAS G12C/G12D, MET exon 14 skipping, and EGFR exon 20 insertions—are reshaping clinical outcomes for subsets of patients historically underserved by standard therapies.1 Drawing on 2025 updates from multi‑center trials and regulatory decisions, this article synthesizes the latest efficacy, safety, and translational insights across these targets, highlights milestones such as near 4‑year median overall survival (OS) in frontline BRAF inhibition, head‑to‑head phase III trajectories in HER2 tyrosine kinase inhibitor (TKI) development, robust intracranial control with lorlatinib after first‑line ROS1 TKI failure, and emerging central nervous system (CNS) activity with novel KRAS inhibitors. We further summarize progress for KRAS G12D, MET exon 14, and EGFR exon 20 insertions and articulate practical implications for diagnostic standardization, treatment sequencing, ctDNA‑guided response assessment, and equitable access. Finally, we outline future priorities—combination strategies, resistance profiling, trial designs for earlier disease stages, and biomarker refinement—to accelerate benefit across the NSCLC rare‑target landscape.

With the widespread implementation of vaccination programs and the development of potent antiviral therapies against chronic hepatitis B (CHB) virus infection in recent decades, the risk of horizontal and vertical transmission is decreasing. Accordingly, newly referred CHB patients are generally older and more often afflicted by various comorbidities1. Given that CHB patients may need long-term antiviral treatment to achieve optimal viral suppression, long-term safety would be a concern in the presence of comorbidities. In the symposium titled “Challenges and Strategies for Managing CHB Patients with Comorbidities”, organised by the Macao Society of Gastroenterology and Hepatology on 5th March 2024, Prof. Grace Lai-Hung Wong and Dr. Jimmy Che-To Lai highlighted the various impacts of comorbidities in CHB and discussed the essentials in the pharmacological management of CHB patients with comorbidities.

Lipid management for cardiovascular disease (CVD) prevention is entering a new phase defined by two converging trends: earlier intervention (“the earlier the better”) and broader targeting of residual risk beyond low-density lipoprotein cholesterol (LDL-C). Recent trial readouts and guideline updates (2025–2026) have reinforced the principle that sustained, deep lowering of atherogenic lipoproteins—especially LDL-C and apolipoprotein B (apoB)—reduces future events, while also elevating triglyceride-rich lipoproteins, lipoprotein(a) [Lp(a)], and metabolic comorbidities as major contributors to persistent risk.1,2 The field’s most visible breakthroughs include (1) expansion of proprotein convertase subtilisin/kexin type 9 (PCSK9) therapy into event reduction for high-risk patients without prior myocardial infarction (MI)/stroke (primary prevention), (2) the emergence of oral PCSK9 inhibition as a potentially adherence-transforming modality, (3) pivotal evidence that targeting apolipoprotein C-III (apoC-III) can meaningfully reduce severe hypertriglyceridemia and pancreatitis events, and (4) an accelerating race to develop Lp(a)-lowering agents with outcomes data anticipated in 2026.3,4,5,6 Meanwhile, guidelines in Europe and North America increasingly emphasize risk-based intensification, earlier combination therapy, and “lower for longer” LDL-C strategies.1 Taken together, these developments suggest a coming era of personalized lipid prevention that is earlier, more aggressive, and mechanistically broader than the statin-only paradigm of prior decades.

Type 2 diabetes mellitus (T2DM) is a persistent state of hyperglycaemia and glucose intolerance that occurs when the body cannot effectively respond to insulin. 14% of adults aged 18 or older were living with diabetes globally in 2022, whereas that was 7% in 19901. While T2DM reduces life expectancy by up to 10 years, the main cause of death for patients with T2DM is cardiovascular disease (CVD)2. In view of the burden of CVD on T2DM patients, clinical guidelines generally advocate glycaemic control as the cornerstone for managing T2DM and as a protective measure against cardiovascular complications3. In recent years, emerging studies on biomarkers and prediction models aiming to estimate the CVD risk among T2DM patients, which facilitate early treatment and optimise outcomes. The purpose of this article is to review the pathophysiology of T2DM complicated by CVD and highlight the clinical management, as well as recent advancements in combating the diseases.

Obesity is a global pandemic and a growing public health concern due to the burden exhibited on the psychosocial and economy. Furthermore, global incidence of obesity has doubled over the last three decades1. Needless to say, obesity has been widely reported to increase the risk of cardiovascular disease (CVD) and is recognised as a key driver of various metabolic syndromes, including type 2 diabetes (T2D) and hypertension. More recently, obesity and diet-induced metabolic dysfunction have been identified as the risk factors behind the development of a wide range of neurological disorders2. More importantly, the detrimental effects of obesity have recently been shown to affect the cognitive functioning3,4 despite there are contradicting clinical data suggesting the protective effect of excess adiposity5. Given that obesity may play a role in the development of cognitive decline, the potential of physical activities and weight control to minimise obesity-associated neurological complications has attracted the interest of researchers and clinicians. The aim of this article is to review the evidence correlating obesity with cognitive function decline, in addition to substantiate the clinical performance of weight control measures in reducing the risk of cognitive decline.

Anxiety disorders are one of the most prevalent psychiatric disorders, up to 30% of the population are reported to be affected by an anxiety disorder during their lifetime. While anxiety disorders are associated with a significant disease burden and economic costs, substantial underdiagnosis and undertreatment of the disorders have been demonstrated in clinical settings1. In the current Feature Story, Dr. Chong King Yee was invited to share her experiences in managing anxiety disorders and discuss specific clinical issues in psychiatric disorders, including the feasibility of anxiety screening and the role of artificial intelligence (AI).

Urticaria, also known as hives, is a common dermatologic condition characterised by pruritic, erythematous, and elevated plaques. Another manifestation associated with urticaria is angioedema, involving deeper blood vessels. These two conditions can sometimes coexist. The disease burden of urticaria substantially affects not only patients' physical wellbeing but overall quality of life (QoL)1, whereas the socioeconomic impact of the disease is significant as well. Thus, effective and timely management of urticaria is paramount to mitigate its adverse outcomes. The purpose of this article is to review the clinical issues related to urticaria and highlight recent pharmacological advancements against the disease.