Using part of the initial analgesic dose as the epidural test dose did not delay the onset of labor analgesia: a randomized controlled clinical trial.

BACKGROUND: Epidural test dose for labor analgesia is controversial and varies widely in clinical practice. It is currently unclear whether using a portion of the initial dose for analgesia as the test dose delays the onset time of analgesia, compared to the traditional test dose. METHODS: One hundred and twenty-six parturients who chose epidural analgesia during labor were randomly assigned to two groups. The first dose in group L was 3 ml 1.5% lidocaine, and in the RF group was 10 ml 0.1% ropivacaine combined with 2 µg/ml fentanyl. After 3 min of observation, both groups received 8 ml 0.1% ropivacaine combined with 2 µg/ml fentanyl. The onset time of analgesia, motor and sensory blockade level, numerical pain rating scale, patient satisfaction score, and side effects were recorded. RESULTS: The onset time of analgesia in group RF was similar to that in group L (group RF vs group L, 7.0 [5.0-9.0] minutes vs 8.0 [5.0-11.0] minutes, p = 0.197). The incidence of foot numbness (group RF vs group L, 34.9% vs 57.1%, p = 0.020) and foot warming (group RF vs group L, 15.9% vs 47.6%, p < 0.001) in group RF was significantly lower than that in group L. There was no difference between the two groups on other outcomes. CONCLUSIONS: Compared with 1.5% lidocaine 3 ml, 0.1% ropivacaine 10 ml combined with 2 µg/ml fentanyl as an epidural test dose did not delay the onset of labor analgesia, and the side effects were slightly reduced. CLINICAL TRIAL REGISTRATION: http://www.chictr.org.cn (ChiCTR2100043071).

Serum levels of CXCL5 are decreased and correlate with circulating platelet counts in systemic lupus erythematosus.

OBJECTIVE: To identify disease-specific serum chemokine profiles and potential anti-inflammatory chemokines in three rheumatic diseases. METHODS: The discovery cohort included 18 patients with rheumatoid arthritis (RA), 20 patients with primary Sjögren's syndrome (pSS), 24 patients with systemic lupus erythematosus (SLE) and 28 healthy subjects. Findings from the discovery cohort were validated in two replication cohorts, consisting of 23 patients with SLE matched with 23 healthy subjects and 62 patients with SLE, 16 patients with ANCA-associated vasculitis (AAV), and 32 healthy controls, respectively. Serum levels of chemokines were determined using multiplex assay or ELISA. RESULTS: In the discovery cohort, serum levels of multiple chemokines were increased in one or more diseases in comparison to healthy subjects, including CCL2, CCL20, CXCL9, CXCL10, and CXCL11 in SLE, CCL2, CCL4, and CXCL11 in pSS, and CCL2, CCL4, and CXCL9 in RA. Notably, serum levels of CCL3 (p = .0003) and CXCL5 (p = .0003) were decreased in SLE. The SLE-specific decrease in CXCL5 serum levels was confirmed in the two replication cohorts, with p = .0034 and p = .0006, respectively. Moreover, a positive correlation between serum levels of CXCL5 and circulating platelet counts (R = .71, p = .00018) in SLE observed in the discovery cohort was confirmed in both replication cohorts (R = .52, p = .011 and R = .49, p = .00005, respectively). CONCLUSION: In the present study, we demonstrate that serum levels of CXCL5 are decreased in patients with SLE and positively correlated with circulating platelet count. These findings suggest that platelet-associated CXCL5 is presumably involved in the development of SLE.

Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy Is Associated with HLA-A*3303 and HLA-DPB1*0501.

We determined the genetic association between specific human leucocyte antigen (HLA) loci and autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy. Our results showed that autoimmune GFAP astrocytopathy was associated with HLA-A*3303 (odds ratio [OR] = 2.02, 95% confidence interval [CI] = 1.32-3.06, p = 0.00072, padj. = 0.046) and HLA-DBP1*0501 (OR = 0.51, 95% CI = 0.36-0.71, p = 0.000048, padj. = 0.0062). Moreover, HLA-A*3303 carriers with the disease had a longer hospital stay (p = 0.0005) than non-carriers. This study for the first time provides evidence for a role of genetic factor in the development of autoimmune GFAP astrocytopathy. ANN NEUROL 2024;95:901-906.

Burden of Chronic and Heavy Opioid Use Among Elderly Community Dwellers in the U.S.

Introduction: Opioid overprescribing may fuel the opioid epidemic and increase the risk of complications of opioid misuse. This study examined trends and determinants of chronic and heavy opioid use among elderly community dwellers in the U.S. Methods: Medicare Current Beneficiary Surveys data from 2006 to 2019 were used. Common opioid medications were identified in the prescription medication files (n=47,264). Patients with Chronic users were defined as those receiving 6 or more opioid prescriptions within a year or on medication for 3 or more months, and heavy users were those having an average daily dose of 90 or more morphine milligram equivalents or 3,780 morphine milligram equivalents or more per continuous treatment episode. Results: One in 6 elderly community dwellers ever used opioids during the study period. Chronic users were more likely to be women than men (68.9% vs 31.1%, p<0.001). Of all survey participants, 4.3% were chronic users, and 2.8% were heavy users. Among ever users, 27.7% were chronic users, and 18.1% were heavy users. The rate of opioid use rose from 12.1% in 2006, peaked at 22.8% in 2013, and decreased to 11.7% in 2019. Chronic use was 5.1%, 10.7%, and 7.6%, respectively. Heavy use was 5.5%, 10.7%, and 7.6%, respectively. However, for chronic and heavy users, there was no significant difference in the median opioid dosage and opioid duration between males and females. Conclusions: Among elderly Medicare beneficiaries, opioid prescriptions have been decreasing since 2013. However, a substantial number of elderly people were chronic and heavy users, calling for better opioid management among them.

Bidirectional associations between alcohol drinking and depressive symptom scores among US older adults.

BACKGROUND: This study examines the bidirectional associations between alcohol drinking and depression in which low to moderate alcohol drinking may reduce the risk of depression, while the occurrence of depression may increase the amount of alcohol drinking as a coping strategy. METHOD: Data for the community-dwelling older adults from the Medicare Current Beneficiary Survey (MCBS) 2016 to 2019 were analyzed using random intercept cross-lagged panel models to explore the within-individual causal associations for males and females separately. Socioeconomic status (SES), smoking and comorbidities were adjusted in the models. RESULTS: Among 3388 older adults with three measures for the number of alcohol drinks and Patient Health Questionnaire (PHQ) depression scores, a prior increase in the number of drinks was related to a moderate non-significant decrease in PHQ scores in the follow-up, but a previous increase in the PHQ scores was significantly associated with a decrease in the number of drinks at the follow-up visit in the adjusted models (regression coefficient = -0.144, p = 0.017 for males; and coefficient = -0.11, p < 0.001 for females). CONCLUSION: Prior depression may lead to reduced drinking in the follow up visits, but no bidirectional association was found among US older adults.