METHOD: The Cochrane Central Register of Controlled Trials (1996 to Feb 2019) and MEDLINE (1966 to Feb 2019) were searched, including the related randomised control trials and reviewed articles to find unpublished trials or trials not obtained via electronic searches. Inclusion criteria for the studies included comparing recovery time, recording clinician satisfaction, and assessing the adverse effects of ketofol.
RESULTS: Eleven trials consisting of a total of 1274 patients met our criteria and were included in this meta-analysis. Five trials compared ketofol with a single agent, while six trials compared ketofol with combined agents. While comparing between ketofol and a single agent (either ketamine or propofol), ketofol showed significant effect on recovery time (MD: -9.88, 95% CI: - 14.30 to - 5.46; P = 0.0003; I2 = 92%). However, no significant difference was observed while comparing ketofol with combined agents (RR: 0.75, 95% CI: - 6.24 to 7.74; P < 0.001; I2 = 98%). During single-agent comparison, ketofol showed no significant differences in terms of clinician satisfaction (RR: 2.86, 95% CI: 0.64 to 12.69; P = 0.001; I2 = 90%), airway obstruction (RR: 0.72, 95% CI: 0.35 to 11.48; P = 0.81; I2 = 0%), apnoea (RR: 0.9, 95% CI: 0.33 to 2.44; P = 0.88; I2 = 0%), desaturation (RR: 1.11, 95% CI: 0.64 to 1.94; P = 0.28; I2 = 21%), nausea (RR: 0.52, 95% CI: 0.91 to 1.41; P = 0.2; I2 = 38%), and vomiting (RR: 0.63, 95% CI: 0.25 to 1.61; P = 0.18; I2 = 42%). During comparison with combined agents, ketofol was more effective in reducing hypotension (RR: 4.2, 95% CI: 0.2 to 0.85; P = 0.76; I2 = 0%), but no differences were observed in terms of bradycardia (RR: 0.70, 95% CI: 0.14 to 03.63; P = 0.09; I2 = 53%), desaturation (RR: 1.9, 95% CI: 0.15 to 23.6; P = 0.11; I2 = 61%), and respiratory depression (RR: 1.98, 95% CI: 0.18 to 21.94; P = 0.12; I2 = 59%).
CONCLUSION: There is low certainty of evidence that ketofol improves recovery time and moderate certainty of evidence that it reduces the frequency of hypotension. There was no significant difference in terms of other adverse effects when compared to other either single or combined agents.
TRIAL REGISTRATION: PROSPERO CRD42019127278 .
Methods: This quasi-experimental study will assess community member and community health volunteer knowledge, attitudes, and practices on noncommunicable disease prevention, risk factors, and health-seeking behavior in three geographical areas of Kuala Lumpur, each representing a different ethnicity (Malay, Indian, and Chinese). Assessment will take place before and after a 9-month intervention period, comparing intervention areas with matched control geographies. We plan to engage 2880 community members and 45 community health volunteers across the six geographic areas. A digital health needs assessment will inform modification of digital health tools to support project aims. Intervention co-creation will use a discrete choice experiment to identify community preferences among evidence-based intervention options, building from data collected on community knowledge, attitudes, and practices. Community health volunteers will work with local businesses and other stakeholders to effect change in obesogenic environments and NCD risk. The study has been approved by the Malaysian Ministry of Health Medical Research Ethical Committee.
Discussion: The Better Health Programme Malaysia anticipates a bottom-up approach that relies on community health volunteers collaborating with local businesses to implement activities that address obesogenic environments and improve community knowledge, attitudes, and practices related to NCD risk. The planned co-creation process will determine which interventions will be most locally relevant, feasible, and needed. The effort aims to empower community members and community health volunteers to drive change that improves their own health and wellbeing. The learnings can be useful nationally and sub-nationally in Malaysia, as well as across similar settings that are working with community stakeholders to reduce noncommunicable disease risk.
Trial registration: National Medical Research Register, Malaysia; NMRR-20-1004-54787 (IIR); July 7, 2020.
METHODS: The methodological and cross-sectional study design was used to translate, culturally adapt it, and validate PSPSQ 2.0 in Nepalese. The Nepalese version of PSPSQ 2.0 went through the full linguistic validation process and was evaluated in 300 patients visiting different community pharmacies in Kathmandu district, Nepal. Exploratory factor analysis was carried out using principal component analysis with varimax rotation, and Cronbach's alpha was used to evaluate the reliability.
RESULTS: Three-hundred patients were recruited in this study. Participants ranged in age from 21 to 83 years; mean age was 53.93 years (SD: 15.21). 62% were females, and 34% educational level was above 12 and university level. Only 7% of the participants were illiterate. Kaiser-Meyer-Olkinwas found to be 0.696, and Bartlett's test of sphericity was significant with a chi-square test value of 3695.415. A principal axis factor analysis conducted on the 20 items with orthogonal rotation (varimax). PSPSQ 2.0 Nepalese version (20 items) had a good internal consistency (Cronbach's alpha = 0.758). Item-total correlations were reviewed for the items in each of the three domains of PSPSQ 2.0.
CONCLUSION: The PSPSQ 2.0 Nepalese version demonstrated acceptable validity and reliability, which can be used in the Nepalese population for evaluating the satisfaction of patients with pharmacist services in both community pharmacy and research.
MATERIAL AND METHODS: This was a five-year retrospective open cohort study using secondary data from the National Diabetes Registry. The study setting was all public health clinics (n = 47) in the state of Negeri Sembilan, Malaysia. Time to treatment intensification was defined as the number of years from the index year until the addition of another oral antidiabetic drug or initiation of insulin. Life table survival analysis based on best-worst case scenarios was used to determine the time to treatment intensification. Discrete-time proportional hazards model was fitted for the factors associated with treatment intensification.
RESULTS: The mean follow-up duration was 2.6 (SD 1.1) years. Of 7,646 patients, the median time to treatment intensification was 1.29 years (15.5 months), 1.58 years (19.0 months) and 2.32 years (27.8 months) under the best-, average- and worst-case scenarios respectively. The proportion of patients with treatment intensification was 45.4% (95% CI: 44.2-46.5), of which 34.6% occurred only after one year. Younger adults, overweight, obesity, use of antiplatelet medications and poorer HbA1c were positively associated with treatment intensification. Patients treated with more oral antidiabetics were less likely to have treatment intensification.
CONCLUSION: Clinical inertia is present in the management of T2D patients in Malaysian public health clinics. We recommend further studies in lower- and middle-income countries to explore its causes so that targeted strategies can be developed to address this issue.
METHODS: We utilized data from genome-wide association studies within the Pancreatic Cancer Cohort Consortium and Pancreatic Cancer Case-Control Consortium, involving approximately 9,269 cases and 12,530 controls of European descent, to evaluate associations between pancreatic cancer risk and genetically predicted plasma n-6 PUFA levels. Conventional MR analyses were performed using individual-level and summary-level data.
RESULTS: Using genetic instruments, we did not find evidence of associations between genetically predicted plasma n-6 PUFA levels and pancreatic cancer risk [estimates per one SD increase in each PUFA-specific weighted genetic score using summary statistics: linoleic acid odds ratio (OR) = 1.00, 95% confidence interval (CI) = 0.98-1.02; arachidonic acid OR = 1.00, 95% CI = 0.99-1.01; and dihomo-gamma-linolenic acid OR = 0.95, 95% CI = 0.87-1.02]. The OR estimates remained virtually unchanged after adjustment for covariates, using individual-level data or summary statistics, or stratification by age and sex.
CONCLUSIONS: Our results suggest that variations of genetically determined plasma n-6 PUFA levels are not associated with pancreatic cancer risk.
IMPACT: These results suggest that modifying n-6 PUFA levels through food sources or supplementation may not influence risk of pancreatic cancer.