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Int J Clin Pract ; 75(11): e14624, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1398444

ABSTRACT

AIMS: The relationship between the innate immune system that creates the polysaccharide antibody response and COVID-19 is not fully understood. In this study, it was aimed to determine the predictive values of isohaemagglutinins in COVID-19 severity/mortality. METHODS: Approximately 15 440 patients diagnosed with COVID-19 were examined, and a total of 286 patients with anti-B and anti-A1 IgM isohaemagglutinins test results were randomly enrolled in the study. These patients were stratified into two groups according to anti-A1 (n: 138 blood type B or O) and anti-B (n: 148 blood type A) IgM isohaemagglutinins. Anti-A1 or/and anti-B IgM, biochemical parameters, symptoms, chronic diseases, hospitalisation status, intubation status, admission to intensive care unit (ICU) and exitus status were recorded and evaluated for all patients. RESULTS: Anti-A1 IgM and anti-B IgM were significantly lower in ICU patients (7.5 ± 9.9 vs 18.0 ± 20.4 and 5.5 ± 6.3 vs 19.3 ± 33.6 titres, respectively; P < .01) and in exitus patients (3.8 ± 3.6 vs 16.7 ± 18.7 and 3.5 ± 4.7 vs 16.9 ± 29.6 titres respectively; P < .01). In the ROC analysis performed to differentiate between exitus and discharge within groups, the sensitivity of anti-B IgM and anti-A1 IgM at cut-off ≤4 was 88.9% and 79.6%, specificity 66.0% and 73.4%, and AUC 0.831 and 0.861, respectively (P < .01). Anti-A1 IgM decreased the mortality risk 0.811 times per unit while anti-B IgM decreased 0.717 times (P < .01). CONCLUSION: Anti-B and anti-A1 isohaemagglutinins, which are an expression of the innate immune system, can be used to predict the severity and mortality of COVID-19 disease.


Subject(s)
COVID-19 , Hemagglutinins , Humans , Immunity, Innate , Immunoglobulin M , Intensive Care Units , SARS-CoV-2
2.
Clin Exp Hypertens ; 42(8): 738-742, 2020 Nov 16.
Article in English | MEDLINE | ID: covidwho-610458

ABSTRACT

INTRODUCTION: The present research aimed to determine the relation between the use of angiotensin-converting enzyme inhibitors (ACE inh) and angiotensinogen receptor blockers (ARBs) and in-hospital mortality of hypertensive patients diagnosed with Covid-19 pneumonia. MATERIAL AND METHOD: In this retrospective study, we included 113 consecutive hypertensive patients admitted due to Covid-19 infection. In all patients, Covid-19 infection was confirmed with using reverse-transcription polymerase chain reaction. All patients were on ACE inh/ARBs or other antihypertensive therapy unless no contraindication was present. The primary outcome of the study was the in-hospital all-cause mortality. RESULTS: In total, 113 hypertensive Covid-19 patients were included, of them 74 patients were using ACE inh/ARBs. During in-hospital follow up, 30.9% [n = 35 patients] of patients died. The frequency of admission to the ICU and endotracheal intubation were significantly higher in patients using ACE inh/ARBs. In a multivariable analysis, the use of ACE inh/ARBs was an independent predictor of in-hospital mortality (OR: 3.66; 95%CI: 1.11-18.18; p= .032). Kaplan-Meir curve analysis displayed that patients on ACE inh/ARBs therapy had higher incidence of in-hospital death than those who were not. CONCLUSION: The present study has found that the use of ACE inh/ARBs therapy might be associated with an increased in-hospital mortality in patients who were diagnosed with Covid-19 pneumonia. It is likely that ACE inh/ARBs therapy might not be beneficial in the subgroup of hypertensive Covid-19 patients despite the fact that there might be the possibility of some unmeasured residual confounders to affect the results of the study.


Subject(s)
Angiotensin Receptor Antagonists/adverse effects , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Betacoronavirus , Coronavirus Infections/mortality , Hypertension/drug therapy , Pneumonia, Viral/mortality , Aged , COVID-19 , Female , Hospital Mortality , Hospitalization , Humans , Male , Middle Aged , Pandemics , Retrospective Studies , SARS-CoV-2
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