Patients with Covid-19 exhibit different immunological profiles according to their clinical presentation.

OBJECTIVES: A novel beta coronavirus has been identified as responsible for the 2019 coronavirus infection (Covid-19). Clinical presentations range from asymptomatic cases to acute respiratory distress syndrome with fatal outcome. Such a broad spectrum of disease expression calls for an investigation of immune response characteristics. METHODS: We identified subjects admitted for Covid-19 in whom a large panel of immunological markers were measured, including B- and T- and NK-lymphocyte phenotypes, T-lymphocyte subpopulation cells and plasma cytokines. Patients were divided according to symptom severity during hospitalisation, in those with uncomplicated and complicated infection. Differences between groups were analyzed. RESULTS: Seventeen patients were included (mean age: 83 years; 9 women; mean delay of symptoms onset: 4 days). Six had uncomplicated infection, while 11 developed complicated forms during hospitalization. CD10 + B lymphocyte levels were inversely correlated with clinical severity (5.8% vs 2.0%, p = 0.04) and CD10+ levels above 3% were independently associated with uncomplicated forms [Odds Ratio 0.04 (CI 0.002-0.795, p = 0.034)]. TNF-alpha, IL-1, Il-6 and Il-8 measurements upon admission differed between patients who died and those who survived (p < 0.01 for all comparisons). CONCLUSIONS: In a population of elderly patients recently infected with Covid-19, CD10 + B cell levels were inversely correlated with clinical severity. Cytokine values upon admission were highly predictive of fatal outcome during hospitalisation. These findings could explain differences in the clinical presentation and allow rapid identification of patients at risk for complications.

[Influence of alcohol on plasma lipids and atherogenesis. Epidemiological and biochemical aspects]. / Influence de l'alcool sur les lipides plasmatiques et l'athérogenèse. Aspects épidémiologique et biochimique.

The results of epidemiological and clinical studies published since 1980 concerning the effects of alcohol intake on coronary artery disease are rather contradictory. Although some protective action of alcohol, notably of wine against atherosclerosis, has been described by some authors, the methodological limitations of these studies make it impossible to establish a cause-effect relationship in this matter. Biochemical studies have provided a more precise approach of the effect of alcohol on the mechanism of atherosclerosis. An increase of HDL has been shown in patients who regularly consume alcoholic drinks. However, a detailed analysis of HDL subfractions (and notably HDL2 regarded as an antiatherogenic lipoprotein) has given equally contradictory results. When the antiatherogenic lipoprotein particles present in HDL are accurately identified, the physiopathological consequences of regular alcohol consumption will be more clearly determined. Biochemical and epidemiological information is still insufficient for us to attribute an antiatherogenic effect to alcohol.