Background A high proportion of COVID‐19 patients have cardiac involvement, even those without known cardiac disease. Downregulation of angiotensin converting enzyme 2 (ACE2), a receptor for SARS‐CoV‐2 and the renin‐angiotensin system, as well as inflammatory mechanisms have been suggested to play a role. ACE2 is abundant in the gut and associated with gut microbiota composition. We hypothesized that gut leakage of microbial products, and subsequent inflammasome activation could contribute to cardiac involvement in COVID‐19 patients. Methods Plasma levels of a gut leakage marker (LPS‐binding protein, LBP), a marker of enterocyte damage (intestinal fatty acid binding protein, IFABP), a gut homing marker (CCL25, ligand for chemokine receptor CCR9) and markers of inflammasome activation (IL‐1β, IL‐18 and their regulatory proteins) were measured at three time points (day 1, 3‐5 and 7‐10) in 39 hospitalized COVID‐19 patients and related to cardiac involvement. Results Compared to controls, COVID‐19 patients had elevated plasma levels of LBP and CCL25 but not IFABP, suggesting impaired gut barrier function and accentuated gut homing of T cells without excessive enterocyte damage. Levels of LBP were twice as high at baseline in patients with elevated cardiac markers compared with those without and remained elevated during hospitalization. Also, markers of inflammasome activation were moderately elevated in patients with cardiac involvement. LBP was associated with higher NT‐pro‐BNP levels, whereas IL‐18, IL‐18BP and IL‐1Ra were associated with higher troponin levels. Conclusion Patients with cardiac involvement had elevated markers of gut leakage and inflammasome activation, suggestive of a potential gut‐heart axis in COVID‐19.
Probiotic intervention seemed to reduce markers of coagulation and inflammation without overt changes in microbial translocation. These findings warrant further studies in larger cohorts with long-term follow-up.
Objective To test the hypotheses that blood biomarkers for nervous system injury, serum concentrations of neurofilament light chain protein (NfL) and glial fibrillary acidic protein (GFAp) can serve as biomarkers for disease severity in COVID-19 patients. Methods Forty-seven inpatients with confirmed COVID-19 had blood samples drawn on admission for assessing serum biomarkers of CNS injury by Single molecule array (Simoa), NfL and GFAp. Concentrations of NfL and GFAp were analyzed in relation to symptoms, clinical signs, inflammatory biomarkers and clinical outcomes. We used multivariate linear models to test for differences in biomarker concentrations in the subgroups, accounting for confounding effects. Results In total, 21% (n = 10) of the patients were admitted to an intensive care unit, and the overall mortality rate was 13% (n = 6). Non-survivors had higher serum concentrations of NfL (p < 0.001) upon admission than patients who were discharged alive both in adjusted analyses (p = 2.6 × 10–7) and unadjusted analyses (p = 0.001). The concentrations of NfL in non-survivors increased over repeated measurements; whereas, the concentrations in survivors were stable. The GFAp concentration was also significantly higher in non-survivors than survivors (p = 0.02). Conclusion Increased concentrations of NfL and GFAp in COVID-19 patients on admission may indicate increased mortality risk. Measurement of blood biomarkers for nervous system injury can be useful to detect and monitor CNS injury in COVID-19.
BackgroundUp to date information on poisoning trends is important. This study reports the epidemiology of all hospitalized acute poisonings in Oslo, including mortality, follow-up referrals, and whether the introduction of over-the-counter sales of paracetamol outside pharmacies had an impact on the frequency of poisonings.MethodsAll acute poisonings of adults (≥16 years) treated at the five hospitals in Oslo from April 2008 to April 2009 were included consecutively in an observational cross-sectional multicentre study. A standardized form was completed by the treating physician, which covered the study aims. All deaths by poisoning in and outside hospitals were registered at the Institute of Forensic Medicine.ResultsThere were 1065 hospital admissions of 912 individuals; 460 (50%) were male, and the median age was 36 years. The annual incidence was 2.0 per 1000. The most frequent toxic agents were ethanol (18%), benzodiazepines (15%), paracetamol (11%), and opioids (11%). Physicians classified 46% as possible or definite suicide attempts, 37% as accidental overdoses with substances of abuse (AOSA), and 16% as other accidents. Twenty-four per cent were discharged without any follow-up and the no follow-up odds were highest for AOSA. There were 117 deaths (eight in hospital), of which 75% were males, and the median age was 41 years. Thus, the annual mortality rate was 25 per 100 000 and the in-hospital mortality was 0.8%. Opioids were the most frequent cause of death.ConclusionsThe incidence of hospitalized acute poisonings in Oslo was similar to that in 2003 and there was an equal sex distribution. Compared with a study performed in Oslo in 2003, there has been an increase in poisonings with a suicidal intention. The in-hospital mortality was low and nine out of ten deaths occurred outside hospitals. Opioids were the leading cause of death, so preventive measures should be encouraged among substance abusers. The number of poisonings caused by paracetamol remained unchanged after the introduction of over-the-counter sales outside pharmacies and there were no deaths, so over-the-counter sales may be considered safe.
The incidence of child poisonings in Oslo has significantly reduced since 1980. Only half of the poisonings needed treatment, most of the poisonings were mild and the clinical outcome was good.
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