ABSTRACT
AIMS: Endotoxemia commonly occurs in severe and fatal COVID-19, suggesting that concomitant bacterial stimuli may amplify the innate immune response induced by SARS-CoV-2. We previously demonstrated that the endogenous glucagon like peptide 1 (GLP-1) system in conjunction with increased procalcitonin (PCT) is hyperactivated in patients with severe Gram-negative sepsis and modulated by type 2 diabetes (T2D). We aimed to determine the association of COVID-19 severity with endogenous GLP-1 activation upregulated by increased specific pro-inflammatory innate immune response in patients with and without T2D. MATERIALS AND METHODS: Plasma levels of total GLP-1, IL-6, and PCT were estimated on admission and during hospitalisation in 61 patients (17 with T2D) with non-severe and severe COVID-19. RESULTS: COVID-19 patients demonstrated ten-fold increase of IL-6 levels regardless of disease severity. Increased admission GLP-1 levels (p = 0.03) accompanied by two-fold increased PCT were found in severe as compared with non-severe patients. Moreover, GLP-1 and PCT levels were significantly increased in non-survived as compared with survived patients at admission (p = 0.01 and p = 0.001, respectively) and at 5 to 6 days of hospitalisation (p = 0.05). Both non-diabetic and T2D patients demonstrated a positive correlation between GLP-1 and PCT response (r = 0.33, p = 0.03, and r = 0.54, p = 0.03, respectively), but the intensity of this joint pro-inflammatory/GLP-1 response was modulated by T2D. In addition, hypoxaemia down-regulated GLP-1 response only in T2D patients with bilateral lung damage. CONCLUSIONS: The persistent joint increase of endogenous GLP-1 and PCT in severe and fatal COVID-19 suggests a role of concomitant bacterial infection in disease exacerbation. Early elevation of endogenous GLP-1 may serve as a new biomarker of COVID-19 severity and fatal outcome.
ABSTRACT
BACKGROUND: Many people recovering from COVID-19 suffer from long-term sequelae. The objective of this study was to assess health-related quality of life (HRQoL) in COVID-19 patients several months after discharge. METHODS: We conducted a retrospective cross-sectional case-control study on COVID-19 and non-COVID-19 pneumonia patients admitted to Shamir Medical Center, Israel (03-07/2020). In the months following discharge, patients were invited to participate in a survey and fill the RAND-36 questionnaire. Patients' characteristics and comorbidities were extracted from electronic charts. RESULTS: Among 66 COVID-19 participants, the median age was 58.5 (IQR 49.8-68.3), 56.1% were female, and 36.4% were obese. The median length of stay was 7 days (IQR 4-10). Patient-reported outcome measures were reported at a median follow-up of 9-months (IQR 6-9). Pain, general health, vitality, and health change had the lowest scores (67.5, 60, 57.5, and 25, respectively). Matching to patients hospitalized with pneumonia due to other pathogens was performed on 42 of the COVID-19 patients. Non-COVID-19 patients were more frequently current or past smokers (50% vs 11.9%, p < 0.01) and suffered more often from chronic lung disease (38.1% vs 9.5%, p = 0.01). The score for health change was significantly lower in the COVID-19 group (25 vs 50, p < 0.01). CONCLUSION: Post COVID-19 patients continue to suffer from an assortment of symptoms and perceive a deterioration in their health many months after hospitalization. This emphasizes the importance of prolonged medical follow-up in this population, and the need for additional research to better understand this novel disease's long-term effects.