Highlights
A report of a young patient with COVID-19 presenting with an encephalitis syndrome mimicking acute demyelinating encephalomyelitis.
The patient was successfully treated with immunoglobulins and cytokine blockade.
Acute encephalitis amenable to immunomodulation could be a feature of COVID-19.
NutriCoviD30 is a longitudinal multicenter cohort study that aimed to provide nutritional objective data of inpatients during COVID-19 infection. Food intake and weight trajectories, as well as clinical signs of the disease, pre-existing chronic diseases, and nutritional strategies were collected and analyzed during the course of the disease. Their association was estimated using mixed-effect regression modeling. Patients were recruited from French university hospitals from May until July 2020. For the 403 included patients (mean age 62.2 ± 14.2 years; 63% males), median [interquartile] hospitalization duration was 13 days [8; 20], and 30% of patients were admitted in intensive care unit. Patients declared a median 70% food intake decrease in the acute phase, and the disease resulted in an average loss of 8% of the pre-disease weight (corresponding to -6.5 kg). While most patients recovered their usual food intake one month after hospital discharge, they only regained half of their weight loss, such that malnutrition, which affected 67% of patients during their hospitalization, persisted in 41% of them. Patients with overweight, obesity and diabetes reported an additional weight loss of over 1.5% of their initial bodyweight during the hospitalization and recovery phase.
In order to prevent malnutrition and its long-term effect, mainly combined with a rapid weight loss predominantly affecting lean body mass, implementation of nutritional support is needed for COVID-19 inpatients. It should start early in the course of the infection, and be extended up to the recovery phase.
Allergic inflammation is thought to play a role in atherogenesis and atherosclerotic disease progression. IgE may activate mast cells and macrophages located within atheromatous lesions, which may contribute to local inflammation and disease progression. On the other hand, increased IgE levels in individuals with acute myocardial infarction might also be the consequence of immunological reactions to damaged coronary arteries or myocardium. In this study, total IgE and mast cell tryptase were measured in a series of forensic autopsy cases showing various degrees of coronary artery disease, in order to correlate laboratory results with morphological findings and compare them to conclusions reported in the clinical setting. A total of 84 subjects were selected and two study groups were retrospectively formed, a non-allergic, cardiac death group (42 cases) and a non-allergic, non-cardiac control group (42 cases). Our findings indicated that a portion of acute coronary syndromes and coronary deaths characterized by coronary atherosclerotic lesions of various severities are also characterized by increased total IgE and mast cell tryptase levels, thus corroborating the data previously reported in both clinical and forensic literature on this topic as well as the necessity of combining morphological investigations focusing on the heart and coronary arteries with biochemical analyses.
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