Kwai Chung Hospital is a psychiatric hospital in Kwai Chung, Hong Kong, located near Princess Margaret Hospital. Officially opened on 15 October 1981, the hospital currently provides 920 psychiatric beds, serving the population of Kwai Chung, Tsing Yi, Tsuen Wan, Tung Chung, North Lantau and part of Kowloon.Apart from in-patient psychiatric services for adult psychiatric patients, it also develops psychiatric specialty services which include Child and Adolescent Psychiatric Services, Psychogeriatric Services, Community Psychiatry, Consultation Liaison Services, Substance Abuse Assessment Unit and Psychiatric Unit for Learning Disabilities.The hospital also provides out-patient department and day hospital services for psychiatric patients at West Kowloon Psychiatric Centre and East Kowloon Psychiatric Centre.The hospital is reachable by Lai King Hill Road.
Objective Clinical insight and cognitive insight are two different dimensions. The theoretical model of insight growth posits that cognitive insight and social cognition are central for gaining clinical insight in schizophrenia patients, but empirical evidence remains limited. We aimed to examine the mediating role of two social cognitive constructs (theory-of-mind and empathy) in linking cognitive insight and clinical insight, and to clarify their role in bringing confluence of the two insight dimensions in schizophrenia patients. Method Our sample comprised 139 schizophrenia patients. The Schedule for the Assessment of Insight (SAIE) and the Beck Cognitive Insight Scale (BCIS) measured the two dimensions of insight. The Faux Pas Task and the self-report Questionnaire of Cognitive and Affective Empathy (QCAE) were used to measure theory-of-mind and empathy respectively. Correlational analyses and mediation modelling were used to clarify the relationships and mediating roles of social cognition with clinical insight and cognitive insight. Explorative cluster analysis was used to categorize patients into different groups with different insight patterns. Results Theory-of-mind statistically mediated the relationship between clinical insight and cognitive insight. The three groups/clusters with varied insight patterns differed in theory-of-mind, empathy, social functioning, negative and disorganized symptoms. The group with non-confluent insight pattern showed poorer theory-of-mind and empathy than the group with high clinical insight and cognitive insight. Discussion Theory-of-mind links cognitive insight with clinical insight. Schizophrenia patients may have a “non-confluent” insight pattern. Social cognition may bring confluence of insight dimensions. Together, our findings lend support to the insight-growth model of schizophrenia.
BACKGROUND:Clozapine is the gold standard for treatment-resistant schizophrenia, but its use is constrained by the risk of severe neutropenia, thus requiring mandatory lifelong hematological monitoring in many jurisdictions. However, a significant evidence gap persists regarding the long-term comparative risk profiles of clozapine versus other second-generation antipsychotics (SGAs), complicating shared decision-making. AIMS:To compare the risk of neutropenia associated with clozapine versus non-clozapine SGAs, assess temporal risk evolution and identify high-risk subgroups to optimise monitoring. METHOD:This retrospective cohort study used Hong Kong's electronic health records to identify patients initiating clozapine or non-clozapine SGAs (2003-2019), with follow-up until 2023. Outcomes included minor (absolute neutrophil count (ANC) 1.0-1.5 × 109/litre) and serious neutropenia (ANC <1.0 × 109/litre). Serious neutropenia leading to clozapine discontinuation within 6 weeks was considered clozapine-associated. RESULTS:Among 4868 clozapine and 38 277 non-clozapine SGA users, clozapine users showed higher unadjusted incidences of minor (7.05 v. 3.74%) and serious neutropenia (2.53 v. 1.45%). However, adjusted rates of serious neutropenia were similar between groups (0.37 v. 0.36 per 100 person-years). Clozapine was associated with higher risks of minor (incidence rate ratio (IRR) 5.91; 95% CI 3.96-8.70) and serious neutropenia (IRR 3.48; 1.70-6.84) in the first 18 weeks. Bayesian change-point analysis showed sharply declining clozapine-associated risk after 26-29 weeks, converging with non-clozapine SGAs by 82-135 weeks (around 2 years). No significant early excess risk was found in patients younger than 45, while males experienced a transient risk of minor neutropenia. CONCLUSIONS:The risk of clozapine-associated neutropenia is highest in the initial 18 weeks, declining to levels seen with non-clozapine SGAs by 2 years. Weekly monitoring for 18 weeks and monthly for up to 2 years is advisable, with potential for personalised schedules based on age and sex.
This systematic review and meta-analysis examined the effects of probiotics on major depressive disorder (MDD). MEDLINE, EMBASE, PsycINFO, Web of Science, Cochrane Library, ProQuest Dissertations and Theses A&I, and Google Scholar were searched for randomised controlled trials published from inception to 1 March 2025 that compared changes in validated depression rating scale scores among patients diagnosed with MDD who received either probiotics or placebo. Standardised mean differences (SMDs) were calculated using random-effects models; subgroup analyses and meta-regression were performed to identify potential moderators of heterogeneity. In total, 13 studies involving 710 patients with MDD were included in the analysis. The pooled SMD was 0.38, favouring probiotics use. Between-study heterogeneity was moderate, with an I2 of 42.8%. Subgroup analyses and meta-regression identified no significant moderators of the SMD. Probiotics appear to reduce depressive symptoms, but factors contributing to heterogeneity remain uncertain.
OBJECTIVE:Anorexia nervosa (AN) has one of the highest mortality rates among psychiatric disorders. This systematic review and meta-analysis examined the all-cause mortality of AN patients compared to the general population using the standardized mortality ratio (SMR). METHOD:MEDLINE, PsycINFO, EMBASE, WOS, Dissertations and Theses A&I, and Google Scholar were searched from inception to May 2025 for longitudinal studies reporting all-cause SMR for AN patients. Risk of bias was assessed using the Newcastle-Ottawa Scale. Random-effects meta-analysis was conducted and presented as a forest plot. Subgroup and meta-regression analyses were done. SMRs for male- and female-specific samples were compared. RESULTS:Thirty studies involving 33,176 patients were identified. The pooled SMR from 22 studies was 5.06 (95% CI [3.47-7.38]). Suicide and cardiac deaths accounted for 21% and 19% of deaths, respectively. Studies with lower mean BMI were associated with higher SMRs before correction for multiple testing (p = 0.018, adjusted p = 0.252). The pooled SMR of male-specific samples was 3.47, 95% CI (1.60-7.52), similar to female-specific samples (3.86, 95% CI [1.82-8.20]). DISCUSSIONS:Our findings confirm that AN remains a severe psychiatric disorder, underscoring the clinical importance of suicide prevention and monitoring cardiac complications. A low BMI is a crucial clinical indicator for high-risk groups and allocating resources. Limitations include excluding studies with zero deaths, substantial heterogeneity among included studies, the underrepresentation of male and non-Western populations, and most studies originating from specialist clinics.
Attention-deficit hyperactivity disorder (ADHD) is a common neuropsychiatric disorder with a significant genetic component. The latest genome-wide association study (GWAS) meta-analysis of ADHD identified 27 whole-genome significant risk loci in the European population. However, genetic risk factors for ADHD are less well-characterized in the Asian population, especially for low-frequency / rare variants. In this study, we aimed to investigate the contributions of both common and low-frequency / rare variants to ADHD in a Hong Kong sample. Our sample comprised 279 cases and 432 controls who underwent genotyping using the Illumina Infinium Global Screening Array. We employed various analytical methods at different levels, while also leveraging multi-omics data and large-scale summary statistics to comprehensively analyze the genetic basis of ADHD. We identified 41 potential genomic risk loci with a suggestive association (p < 1e−4), pointing to 111 candidate risk genes, which were enriched for genes differentially expressed during late infancy brain development. Furthermore, tissue enrichment analysis implicated the involvement of the cerebellum. At the polygenic level, we also discovered a strong genetic correlation with resting-state functional MRI connectivity of the cerebellum involved in the attention/central executive and subcortical-cerebellum networks. In addition, an accumulation of ADHD common-variant risks found in European ancestry samples was found to be significantly associated with ADHD in the current study. In low-frequency / rare variant analyses, we discovered the correlations between ADHD and collapsing effects of rare damaging variants in TEP1, MTMR10, DBH, TBCC, and ANO1. Based on biological and functional profiles of the potential risk genes and gene sets, both common and low-frequency / rare variant analyses demonstrated that ADHD genetic risk was associated with immune processes. These findings re-validate the abnormal development of the neural system in ADHD and extend the existing neuro-dysfunction hypothesis to a multi-system perspective. The current study identified convergent risk factors from common and low-frequency / rare variants, which implicates vulnerability in late-infancy brain development, affecting especially the cerebellum, and the involvement of immune processes.
