RESUMO
BACKGROUND: Numerous studies have explored the association between social anxiety and bullying victimization. However, inconsistency are found regarding the strength and the direction of this relationship. Moreover, it remains unclear how different subtypes of bullying victimization associate with social anxiety. OBJECTIVE: The purpose of this study was to conduct a meta-analysis to systematically investigate the cross-sectional and longitudinal relationships between social anxiety and bullying victimization. PARTICIPANTS AND SETTING: Individuals experiencing social anxiety and bullying victimization. METHODS: The present study employed three-level random effects model to combine the correlation coefficients r to indicate the strength of the cross-sectional association between social anxiety and bullying victimization. Cross-lagged regressions were utilized to examine the prospective relationship between both variables. RESULTS: A total of 133 cross-sectional studies reporting 220 effect sizes were included in the meta-analysis, and the results showed a significant moderate association between social anxiety and bullying victimization (r = 0.268, 95 % CI [0.244, 0.292]). Nineteen longitudinal studies were also identified, revealing that social anxiety at Time 1 significantly predicted bullying victimization at Time 2 (ß = 0.067, 95 % CI [0.038, 0.096]). However, bullying victimization did not significantly predict subsequent social anxiety (ß = 0.012, 95 % CI [-0.026, 0.049]). Subgroup analyses revealed that social anxiety had the strongest association with relational victimization (r = 0.382, 95 % CI [0.335, 0.430]), followed by reputational victimization (r = 0.254, 95 % CI [-0.171, 0.337]), physical victimization (r = 0.226, 95 % CI [0.144, 0.308]) and overt victimization (r = 0.202, 95 % CI [0.146, 0.257]). Social anxiety was significantly more associated with traditional bullying victimization (r = 0.281, 95 % CI [0.233, 0.328]) than cyberbullying victimization (r = 0.177, 95 % CI [0.137, 0.218]; p < 0.001). CONCLUSIONS: Social anxiety was found to be moderately associated with and prospectively predict bullying victimization. Future research and interventions could focus on reducing social anxiety to prevent bullying victimization.
RESUMO
Background: We sought to determine whether circulating inflammatory biomarkers were associated with the frequent exacerbator phenotype in stable COPD patients ie, those with two or more exacerbations in the previous year. Methods: Eighty-eight stable, severe, COPD patients (4 females) were assessed for exacerbation frequency, pulmonary function, fraction of expired nitric oxide (FENO); inflammatory variables were measured in venous blood. Logistic regression assessed associations between the frequent exacerbator phenotype and systemic inflammation. Results: Compared with infrequent exacerbators, frequent exacerbators (n=10; 11.4%) had greater serum concentration (median (25th-75th quartile)) of serum amyloid A (SAA; 134 (84-178) vs 71 (38-116) ng/mL; P=0.024), surfactant protein D (SP-D; 15.6 (9.0-19.3) vs 8.5 (3.6-14.9) ng/mL; P=0.049) and interleukin-4 (IL-4; 0.12 (0.08-1.44) vs 0.03 (0.01-0.10) pg/mL; P=0.001). SAA, SP-D and IL-4 were not significantly correlated with FEV1%predicted or FVC %predicted. After adjusting for sex, age, BMI, FEV1/FVC and smoking pack-years, only SAA remained independently associated with the frequent exacerbator phenotype (OR 1.49[1.09-2.04]; P=0.012). The odds of being a frequent exacerbator was 18-times greater in the highest SAA quartile (≥124.1 ng/mL) than the lowest SAA quartile (≤44.1 ng/mL) (OR 18.34[1.30-258.81]; P=0.031), and there was a significant positive trend of increasing OR with increasing SAA quartile (P=0.008). For SAA, the area under the receiver operating characteristic curve was 0.721 for identification of frequent exacerbators; an SAA cut-off of 87.0 ng/mL yielded an 80% sensitivity and 61.5% specificity. Conclusion: In stable COPD patients, SAA was independently associated with the frequent exacerbator phenotype, suggesting that SAA may be a useful serum biomarker to inform progression or management in COPD.