Aims To identify the metabolic pattern and prognostic predictors in anti‐gamma‐aminobutyric‐acid B (GABAB) receptor encephalitis using 18F‐fluorodeoxy‐glucose positron emission tomography (18F‐FDG‐PET). Methods Twenty‐one patients diagnosed anti‐GABAB receptor encephalitis who underwent 18F‐FDG‐PET at first hospitalization were retrospectively reviewed. 18F‐FDG‐PET images were analyzed in comparison with controls. Further group comparisons of 18F‐FDG‐PET data were carried out between prognostic subgroups. Results 18F‐FDG‐PET was abnormal in 81% patients with anti‐GABAB receptor encephalitis and was more sensitive than MRI (81% vs. 42.9%, p = 0.025). Alter limbic lobe glucose metabolism (mostly hypermetabolism) was observed in 14 patients (66.7%), of whom 10 (10/14, 71.4%) demonstrated hypermetabolism in the medial temporal lobe (MTL). Group analysis also confirmed MTL hypermetabolism in association with relative frontal and parietal hypometabolism was a general metabolic pattern. After a median follow‐up of 33 months, the group comparisons revealed that patients with poor outcome demonstrated increased metabolism in the MTL compared to those with good outcome. Conclusion 18F‐FDG‐PET may be more sensitive than MRI in the early diagnosis of anti‐GABAB receptor encephalitis. MTL hypermetabolism was associated with relative frontal or parietal hypometabolism and may serve as a prognostic biomarker in anti‐GABAB receptor encephalitis.
Purpose Smoking, alcohol consumption, allergic rhinitis (AR), asthma, and obesity are associated with chronic rhinosinusitis (CRS), albeit the causal relationships between them remain elusive. Therefore, we conducted a bidirectional two-sample Mendelian randomization (MR) study to investigate the bidirectional causal effects between these potential risk factors and CRS. Methods The data for daily cigarette consumption, age of smoking initiation, weekly alcohol consumption, AR, asthma, body mass index (BMI), and CRS were drawn from large sample size genome-wide association studies. Single-nucleotide polymorphisms associated with each exposure were considered instrumental variables in this study. We investigated causal effects by using the inverse-variance weighted (IVW) method with random effects, and weighted median and MR–Egger methods were used for sensitivity analyses. Pleiotropic effects were detected and corrected by the MR pleiotropy residual sum and outlier test and MR–Egger model. Results We found the causal effects of daily cigarette consumption (IVW, OR = 1.15, 95% CI 1.00−1.32, p = 0.046), AR (IVW, OR = 4.77, 95% CI 1.61−14.13, p = 0.005), asthma (IVW, OR = 1.45, 95% CI 1.31 − 1.60, p < 0.001), and BMI (IVW, OR = 1.05, 95% CI 1.00−1.09, p = 0.028) on CRS. Furthermore, we found a causal effect of CRS on asthma (IVW OR = 1.08, 95% CI 1.05−1.12, p < 0.001). Conclusions We confirmed the causal effects of daily cigarette consumption, AR, asthma, and BMI on CRS, and the causal effect of CRS on asthma, while no causal relationship between age of smoking initiation, weekly alcohol consumption, and CRS was found. These findings are expected to provide high-quality causal evidence for clinical practice and the pathogenesis of CRS and asthma. Supplementary Information The online version contains supplementary material available at 10.1007/s00405-022-07798-6.
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