Previous meta-analyses that found an inverse association between coffee consumption and metabolic syndrome pooled data from cross-sectional and longitudinal studies, which could lead to potentially misleading conclusions. Hence, this work aimed to reassess this association by analyzing data from the 2 types of studies separately and including recent studies. Online databases including PubMed, Scopus, Embase, The Cumulative Index to Nursing and Allied Health Literature (CINAHL) Plus, and Science Direct were searched for relevant studies published up to July 2020. Both cross-sectional and longitudinal studies were included if published after 1999, reported both effect estimates and CIs, and presented results adjusted for confounding variables. Data of the highest coffee consumption level in each study, as well as those of medium consumption levels in studies with ≥3 consumption categories, were pooled using random-effect models, with sex-stratified and sex-adjusted results being analyzed separately. Results were obtained based on data from 13 cross-sectional studies involving 280,803 participants and 2 longitudinal studies involving 17,014 participants. The overall sex-adjusted association of the highest consumption level was not significant (n = 9 studies; OR: 0.88; 95% CI: 0.70, 1.10; I2: 91.5%) and the 2 longitudinal studies both yielded no association. Subgroup analysis revealed inverse associations in both males and females, as well as in Caucasians with medium coffee consumption (n = 4 studies, OR: 0.88; 95% CI: 0.84, 0.93; I2: 0%). Although residual confounding could affect the results of this meta-analysis, our findings suggested with a low certainty that coffee consumption may not be associated with metabolic syndrome, a finding that is different from those of previous meta-analyses and could be due to variation in characteristics of study participants. More longitudinal studies are also needed to further assess the temporal association between coffee consumption and metabolic syndrome. This meta-analysis was registered at https://www.crd.york.ac.uk/prospero as CRD42018110650.
In an attempt to assess the level of quinolone resistance and its association with other antimicrobial resistance in faecal Escherichia coli isolated from routine outpatient specimens in Hong Kong, ciprofloxacin-supplemented MacConkey agar was used to screen for resistant isolates. Antimicrobial susceptibility testing of the isolates was done by VITEK 2 and previous amplification-based methods were employed to characterize the genetic determinants behind some of the resistance phenotypes. One hundred and seventy-six (43%) of 409 specimens had quinolone-resistant E. coli isolated (199 isolates). Quinolone resistance was found to be associated with resistances to penicillins (>80%) and co-trimoxazole (69%). Nonsusceptibility to combinations of penicillins and clavulanic acid was above 20% and up to 50% for the aminoglycosides gentamicin and tobramycin. CTX-M-type extended-spectrum β-lactamases were found responsible for most cephalosporin resistances but the transferable quinolone resistance determinant qnrA was not detected. Our data suggested that a high percentage of E. coli isolates as part of the alleged normal intestinal microflora in humans appeared to be resistant to quinolones. Co-resistance to various other frequently used antimicrobials was also observed. Transferable genetic determinants were found to be involved in some cases.
Authors' reply to 'Controversial data on the association of Aeromonas with diarrhoea in a recent Hong Kong study'In the correspondence article that we published (Chu et al., 2006), no attempt was made to demonstrate whether Aeromonas spp. are capable of causing diarrhoea or not, in contrast to the interpretation of our data by Figueras et al. (2007). We take a neutral stance on the issue. What our data have shown is that our current method for detection of the organism, i.e. culture, in our clinical setting whereby specimens are coming into our laboratory from outpatient clinics around Hong Kong, is not providing clinically useful information. Our faecal specimens are characterized by (1) an origin from patients with relatively mild clinical presentations which do not merit hospitalization, (2) limited clinical information provided on the laboratory request form, and (3) the possibility of delayed processing during transport from diverse outpatient settings to the laboratory. The limitations of our study have already been discussed in the original correspondence article, and our conclusion merely stated the lack of a statistically significant association between diarrhoeal symptoms and the isolation of aeromonads in faeces.As front-line workers providing public health services, we would very much welcome the association of definitive pathogenic traits with Aeromonas that could at the same time be applied for laboratory diagnosis (e.g. Shiga toxin production in enterohaemorrhagic Escherichia coli), instead of detection of an array of putative virulence factors. We await reports of such characteristics in Aeromonas, which will no doubt help us to provide a better and more cost-effective clinical laboratory service.
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