RESUMEN
Casirivimab/Imdevimab therapy reportedly retains neutralization potency against circulating SARS-CoV-2 variants, including Delta (B.1.617.2), but there are sparse data on its clinical benefit against the Delta variant among vaccinated and unvaccinated patients. We explored its therapeutic effect on COVID-19 severity outcome in terms of room air saturation <93% within 14 days of initial presentation and 45-day all-cause mortality among high-risk patients with SARS-CoV-2 Delta variant infection and compared its effect between vaccinated and unvaccinated patients. We conducted a retrospective cohort study at a tertiary care medical center between 6/2021 and 9/2021 and included patients who presented with a positive PCR for SARS-CoV-2 and fulfilled the criteria for Casirivimab/Imdevimab treatment. Of the 359 suitable patients (52% female, median age 63 years), 116 were treated with Casirivimab/Imdevimab and 243 were not. Two-hundred and one (56%) patients had received at least 2 SARS-CoV-2 vaccinations. Casirivimab/Imdevimab treatment was not an independent protective factor of COVID-19 severity outcome (multivariable analysis). Chronic kidney disease (aOR=3.51 [95%CI: 1.34-9.20], P=0.01), lower saturation levels (aOR=0.7 [95%CI: 0.58-0.85], P<0.01), abnormal chest x-ray findings (aOR=2.92, [95%CI: 1.24-6.87, P=0.01), and higher C-reactive protein levels (aOR=1.01 [95%CI: 1.00-1.01], P=0.008) were independent risk factors of COVID-19 severity. Positive immunization status was an independent protective factor (aOR=0.33 [95%CI: 0.14-0.77], P=0.01). A sub analysis of patients treated with Casirivimab/Imdevimab revealed no significant difference in COVID-19 severity between vaccinated and unvaccinated patients. These findings demonstrate no added benefit of Casrivimab/Imdevinab treatment for high-risk patients with the SARS-CoV-2 Delta variant infection, regardless of their vaccination status.
RESUMEN
BACKGROUND: Micro-inflammation is involved in the pathogenesis of irritable bowel syndrome (IBS). The parasympathetic nervous system, via acetylcholine (ACh), and its hydrolytic enzymes, plays a role in regulating inflammation. Increased serum cholinesterase activity, named cholinergic Status (CS), is associated with decreased inflammatory inhibition (ie, pro-inflammation). We assessed the association between IBS diarrhea-predominant (IBS-D) symptoms, CS, and inflammatory biomarkers. METHODS: Women with IBS-D were prospectively recruited. Serum acetylcholinesterase (AChE), CS, and high-sensitivity C-reactive protein (hs-CRP) levels were analyzed and fecal calprotectin (FC) in a subgroup of patients. The control group included women attending routine health checkups (matched by age and BMI). KEY RESULTS: Ninety-four women with IBS-D were compared to matched controls (1:1). Serum CS, AChE, and the AChE/butyrylcholinesterase (BChE) ratios were significantly increased in the IBS-D group compared to matched controls (P = 0.018, P = 0.001, and P = 0.004, respectively). Using a multiple logistic regression model, IBS-D was almost twice as likely in women with high CS compared to women with low CS (adjusted OR=1.84 (95% CI: 1.01-3.33), P = 0.045). Furthermore, IBS-D patients with higher hs-CRP levels demonstrated lower CS and BChE activity and elevated AChE and AChE/BChE ratios compared to patients with lower hs-CRP levels (P = 0.026, P = 0.036, P = 0.002; and P = 0.0007, respectively). CS was not correlated with the IBS symptoms score. CONCLUSIONS AND INFERENCES: This is the first study to explore the potential role of serum CS in IBS-D. The findings emphasize the possible role of the autonomic nervous system and its anti-inflammatory properties in IBS.
