tetano
Editor, Senior Moderator
Clin Exp Med
. 2022 May 24.
doi: 10.1007/s10238-022-00836-x. Online ahead of print.
Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties
Hayder M Al-Kuraishy[SUP] 1 [/SUP], Ali I Al-Gareeb[SUP] 1 [/SUP], Maisra M El-Bouseary[SUP] 2 [/SUP], Fatma I Sonbol[SUP] 3 [/SUP], Gaber El-Saber Batiha[SUP] 4 [/SUP]
Affiliations
Abstract
Hyperviscosity syndrome (HVS) recently emerged as a complication of coronavirus disease 2019 (COVID-19) and COVID-19 vaccines. Therefore, the objectives of this critical review are to establish the association between COVID-19 and COVID-19 vaccines with the development of HVS. HVS may develop in various viral infections due to impairment of humoral and cellular immunity with elevation of immunoglobulins. COVID-19 can increase blood viscosity (BV) through modulation of fibrinogen, albumin, lipoproteins, and red blood cell (RBC) indices. HVS can cause cardiovascular and neurological complications in COVID-19 like myocardial infarction (MI) and stroke. HVS with or without abnormal RBCs function in COVID-19 participates in the reduction of tissue oxygenation with the development of cardio-metabolic complications and long COVID-19. Besides, HVS may develop in vaccine recipients with previous COVID-19 due to higher underlying Ig concentrations and rarely without previous COVID-19. Similarly, patients with metabolic syndrome are at the highest risk for propagation of HVS after COVID-19 vaccination. In conclusion, COVID-19 and related vaccines are linked with the development of HVS, mainly in patients with previous COVID-19 and underlying metabolic derangements. The possible mechanism of HVS in COVID-19 and related vaccines is increasing levels of fibrinogen and immunoglobulins. However, dehydration, oxidative stress, and inflammatory reactions are regarded as additional contributing factors in the pathogenesis of HVS in COVID-19. However, this critical review cannot determine the final causal relationship between COVID-19 and related vaccines and the development of HVS. Prospective and retrospective studies are warranted in this field.
Keywords: COVID-19; COVID-19 vaccination; Hyperviscosity syndrome.
. 2022 May 24.
doi: 10.1007/s10238-022-00836-x. Online ahead of print.
Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties
Hayder M Al-Kuraishy[SUP] 1 [/SUP], Ali I Al-Gareeb[SUP] 1 [/SUP], Maisra M El-Bouseary[SUP] 2 [/SUP], Fatma I Sonbol[SUP] 3 [/SUP], Gaber El-Saber Batiha[SUP] 4 [/SUP]
Affiliations
- PMID: 35608715
- DOI: 10.1007/s10238-022-00836-x
Abstract
Hyperviscosity syndrome (HVS) recently emerged as a complication of coronavirus disease 2019 (COVID-19) and COVID-19 vaccines. Therefore, the objectives of this critical review are to establish the association between COVID-19 and COVID-19 vaccines with the development of HVS. HVS may develop in various viral infections due to impairment of humoral and cellular immunity with elevation of immunoglobulins. COVID-19 can increase blood viscosity (BV) through modulation of fibrinogen, albumin, lipoproteins, and red blood cell (RBC) indices. HVS can cause cardiovascular and neurological complications in COVID-19 like myocardial infarction (MI) and stroke. HVS with or without abnormal RBCs function in COVID-19 participates in the reduction of tissue oxygenation with the development of cardio-metabolic complications and long COVID-19. Besides, HVS may develop in vaccine recipients with previous COVID-19 due to higher underlying Ig concentrations and rarely without previous COVID-19. Similarly, patients with metabolic syndrome are at the highest risk for propagation of HVS after COVID-19 vaccination. In conclusion, COVID-19 and related vaccines are linked with the development of HVS, mainly in patients with previous COVID-19 and underlying metabolic derangements. The possible mechanism of HVS in COVID-19 and related vaccines is increasing levels of fibrinogen and immunoglobulins. However, dehydration, oxidative stress, and inflammatory reactions are regarded as additional contributing factors in the pathogenesis of HVS in COVID-19. However, this critical review cannot determine the final causal relationship between COVID-19 and related vaccines and the development of HVS. Prospective and retrospective studies are warranted in this field.
Keywords: COVID-19; COVID-19 vaccination; Hyperviscosity syndrome.