Cold agglutinin syndrome as a complication of Covid-19 in two cases

Jensen, Christopher E.; Wilson, Samuel; Thombare, Aparna; Weiss, Susan R.; Ma, Alice

doi:10.1016/j.clinpr.2020.100041

Cited by 30 publications

(22 citation statements)

References 4 publications

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“…Several reports of acute hemolysis after SARS-CoV-2 infection were published, but not from direct viral action on Hb. Twelve patients presented with autoimmune hemolytic anemia (AIHA), among them 4 had B lymphoid malignancy, one had monoclonal gammapathy (Jensen et al, 2020;Lazarian et al, 2020;Lopez et al, 2020) and 2 had Evans syndrome (Li et al, 2020;Wahlster et al, 2020). Later, it was stated that AIHA could concern 12% of the subgroup of anemic COVID-19 patients (Algassim et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

The Affinity of Hemoglobin for Oxygen Is Not Altered During COVID-19

et al. 2021

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Background: A computational proteomic analysis suggested that SARS-CoV-2 might bind to hemoglobin (Hb). The authors hypothesized that this phenomenon could result in a decreased oxygen (O2) binding and lead to hemolytic anemia as well. The aim of this work was to investigate whether the affinity of Hb for O2 was altered during COVID-19.Methods: In this retrospective, observational, single-center study, the blood gas analyses of 100 COVID-19 patients were compared to those of 100 non-COVID-19 patients. Fifty-five patients with carboxyhemoglobin (HbCO) ≥8% and 30 with sickle cell disease (SCD) were also included (“positive controls” with abnormal Hb affinity). P50 was corrected for body temperature, pH, and PCO2.Results: Patients did not differ statistically for age or sex ratio in COVID-19 and non-COVID-19 groups. Median P50 at baseline was 26 mmHg [25.2–26.8] vs. 25.9 mmHg [24–27.3], respectively (p = 0.42). As expected, P50 was 22.5 mmHg [21.6–23.8] in the high HbCO group and 29.3 mmHg [27–31.5] in the SCD group (p < 0.0001). Whatever the disease severity, samples from COVID-19 to non-COVID-19 groups were distributed on the standard O2-Hb dissociation curve. When considering the time-course of P50 between days 1 and 18 in both groups, no significant difference was observed. Median Hb concentration at baseline was 14 g.dl–1 [12.6–15.2] in the COVID-19 group vs. 13.2 g.dl–1 [11.4–14.7] in the non-COVID-19 group (p = 0.006). Among the 24 COVID-19 patients displaying anemia, none of them exhibited obvious biological hemolysis.Conclusion: There was no biological argument to support the hypothesis that SARS-CoV-2 could alter O2 binding to Hb.

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Section: Discussionmentioning

confidence: 99%

The Affinity of Hemoglobin for Oxygen Is Not Altered During COVID-19

et al. 2021

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“…There are also other autoantibodies were found in COVID-19, such as autoantibodies against red blood cell [ 17 ], anti-neutrophil cytoplasmic antibodies (ANCA) [ 5 ], anti-cyclic peptide containing citrulline (CCP) antibody [ 18 ]. Taken together, various autoantibodies were found in COVID-19, the existing autoantibodies might be associated with the severity of illness and autoimmune symptoms.…”

mentioning

confidence: 99%

Autoantibodies in COVID-19: frequency and function

Gao

Zhang

Liu

et al. 2021

Autoimmunity Reviews

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“…Both autoimmune haemolytic anaemia (AIHA), a rare blood condition characterised by the presence of autoantibodies to red blood cells, and cold agglutinin syndrome, a form of AIHA characterised by anti-red blood cell agglutination at low temperatures, have been reported in COVID-19 patients [64][65][66][67]. Across these reports, consisting of a total of 11 cases, 54.5% were positive for cold agglutinin antibodies [64][65][66][67], 46.4% of patients with anti-erythrocyte antibodies diagnosed with warm AIHA [66] and 9.1% were positive for both cold agglutinin antibodies and anti-globulin antibodies [67]. The onset of AIHA (either warm or cold) is reported to range from 4-13 days following the onset of COVID-19 symptoms [64,66].…”

Section: Autoimmune Haemolytic Anaemia and Cold Agglutinin Syndromementioning

confidence: 99%

Adaptive Immunity and the Risk of Autoreactivity in COVID-19

Moody

Wilson

Flanagan

et al. 2021

IJMS

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While first and foremost considered a respiratory infection, COVID-19 can result in complications affecting multiple organs. Immune responses in COVID-19 can both protect against the disease as well as drive it. Insights into these responses, and specifically the targets being recognised by the immune system, are of vital importance in understanding the side effects of COVID-19 and associated pathologies. The body’s adaptive immunity recognises and responds against specific targets (antigens) expressed by foreign pathogens, but not usually to target self-antigens. However, if the immune system becomes dysfunctional, adaptive immune cells can react to self-antigens, which can result in autoimmune disease. Viral infections are well reported to be associated with, or exacerbate, autoimmune diseases such as multiple sclerosis (MS) and systemic lupus erythematosus (SLE). In COVID-19 patients, both new onset MS and SLE, as well as the occurrence of other autoimmune-like pathologies, have been reported. Additionally, the presence of autoantibodies, both with and without known associations to autoimmune diseases, have been found. Herein we describe the mechanisms of virally induced autoimmunity and summarise some of the emerging reports on the autoimmune-like diseases and autoreactivity that is reported to be associated with SARS-CoV-2 infection.

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Cold agglutinin syndrome as a complication of Covid-19 in two cases

Cited by 30 publications

References 4 publications

The Affinity of Hemoglobin for Oxygen Is Not Altered During COVID-19

The Affinity of Hemoglobin for Oxygen Is Not Altered During COVID-19

Autoantibodies in COVID-19: frequency and function

Adaptive Immunity and the Risk of Autoreactivity in COVID-19

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