METHODS: This is a retrospective cohort study. All records for admissions to paediatric wards in Sabah for acute rheumatic fever from January 2016 to December 2018 were collected. The patient records were then traced and required information were collected.
RESULTS: A total of 52 cases of acute rheumatic fever were admitted. It was observed that the incidence of acute rheumatic fever was 74.4 per 100,000 paediatric admissions. Patients from the West Coast Division made up most of the admissions (n = 24, 46.2%). Male patients (n = 35, 67.3%) of the indigenous Kadazan-Dusun ethnicity (n = 21, 40.4%) were most commonly encountered. The mean age at time of presentation was 9.58 years. Most cases admitted (n = 38, 73.1%) were categorised as Priority 1 (severe rheumatic heart disease).
CONCLUSION: Most patients who were admitted had symptoms of heart failure and were diagnosed with severe rheumatic heart disease. Although this disease is preventable, the incidence in Sabah remains high. This study was limited as we only looked at patients who were admitted and we foresee the real incidence to be higher. Hence, there is an urgent need for a rheumatic heart disease registry in Malaysia to gather more data for prevention and early intervention.
METHOD: A cross-sectional survey was conducted at a tertiary care center in Malaysia from February 2019 to June 2019. Parents of children with epilepsy who were on AED for at least 3 months and aged ≤18 years old were recruited. Medication self-management was assessed using a validated Pediatric Epilepsy Medication Self-Management Questionnaire (PEMSQ). A higher total score reflects better medication self-management.
RESULTS: A total of 166 patients were recruited. The mean ± standard deviation (SD) age of patients was 8.20 ± 5.21 years, and 51.8% and 36.7% of patients have generalized seizure and focal seizure, respectively. The mean ± SD PEMSQ score was 116.2 ± 11.28 from a total score of 135. Among the four domains of PEMSQ, the barriers to treatment contributed to the lowest mean scores. Univariate analysis showed that the following were significantly associated with poorer medication self-management: differences in ethnicity, religion; higher number of medications; presence of comorbidities; inability to swallow tablets; and a more complex AED regimen. Other variables were not significant. Multivariate analysis showed that only ethnicity and presence of comorbidity remained independently significant (R2 = 0.14; F [4, 161] = 6.28; p
OBJECTIVE: To investigate the effect of zerumbone on HDM extract-induced airway epithelial barrier dysfunction.
MATERIALS AND METHODS: Human bronchial epithelial cells 16HBE14o- were incubated with 100 μg/mL HDM extract and treated with non-cytotoxic concentrations of zerumbone (6.25 μM, 12.5 μM, and 25 μM) for 24 h. The epithelial junctional integrity and permeability were evaluated through transepithelial electrical resistance (TEER) and fluorescein isothiocynate (FITC)-Dextran permeability assays, respectively. The localization of junctional proteins, occludin and zona occludens (ZO)-1, was studied using immunofluorescence (IF) while the protein expression was measured by western blot.
RESULTS: Zerumbone inhibited changes in junctional integrity (6.25 μM, p ≤ .05; 12.5 μM, p ≤ .001; 25 μM, p ≤ .001) and permeability (6.25 μM, p ≤ .05; 12.5 μM, p ≤ .01; 25 μM, p ≤ .001) triggered by HDM extract in a concentration-dependent manner. This protective effect could be explained by the preservation of occludin (12.5 μM, p ≤ .01 and 25 μM, p ≤ .001) and ZO-1 (12.5 μM, p ≤ .05 and 25 μM, p ≤ .001) localization, rather than the prevention of their cleavage.
DISCUSSION AND CONCLUSION: Zerumbone attenuates HDM extract-induced epithelial barrier dysfunction which supports its potential application for the treatment of inflammation-driven airway diseases such as asthma.
AIM OF THE STUDY: As allergy could be mediated by both IgE and IgG, we further evaluated the anti-allergy potential of CNAE in both in vitro model of IgG-induced macrophage activation and in vivo anaphylaxis models to further dissect the mechanism of action underlying the anti-allergic properties of CNAE.
MATERIAL & METHODS: The anti-allergy potential of CNAE was evaluated in in vivo anaphylaxis models of ovalbumin-challenged active systemic anaphylaxis (OVA-ASA) and IgE-challenged passive systemic anaphylaxis (PSA) using Sprague Dawley rats as well as IgG-challenged passive systemic anaphylaxis (IgG-PSA) using C57BL/6 mice. Meanwhile, in vitro model of IgG-induced macrophage activation model was performed using IC-21 macrophages. The release of soluble mediators from both IgE and IgG-mediated pathways were measured using enzyme-linked immunosorbent assay (ELISA). The signaling molecules targeted by CNAE were identified by performing Western blot.
RESULTS: IgG, platelet-activating factor (PAF) and IL-6 was suppressed by CNAE in OVA-ASA, but not IgE. In addition, CNAE significantly suppressed PAF and IL-6 in IgG-PSA but did not suppress histamine, IL-4 and leukotrienes C4 (LTC4) in IgE-PSA. CNAE also inhibited IL-6 and TNF-α by inhibiting the phosphorylation of ERK1/2 in the IgG-induced macrophage activation model.
CONCLUSION: Overall, our findings supported that CNAE exerts its anti-allergic properties by suppressing the IgG pathway and its mediators by inhibiting ERK1/2 phosphorylation, thus providing scientific evidence supporting its traditional use in managing allergy.