scholarly journals COVID‐19 as a Blood Clotting Disorder Masquerading as a Respiratory Illness: A Cerebrovascular Perspective and Therapeutic Implications for Stroke Thrombectomy

2020 ◽  
Vol 30 (5) ◽  
pp. 555-561 ◽  
Author(s):  
Vallabh Janardhan ◽  
Vikram Janardhan ◽  
Vladimir Kalousek
2020 ◽  
Vol 24 (1) ◽  
pp. 59-63
Author(s):  
Nasser Ali Malik ◽  
Amjid Hammodi ◽  
Dayanidhi Ramachandra Jaiswara

Background: The outbreak caused by SARS CoV-2 of the recent coronavirus disease-2019 (COVID-19) has been marked as a public health concern with a significant mortality at the global level. Lignocaine a common anesthetic agent being used for pain free surgeries for over a long period of time has expressed extensive characteristic of being an anti-inflammatory, antibacterial, direct spasmolytic,  ion channel blocking and repolarization agent. We did a literature review Methodology: Currently compiled over-view has for the first time evaluated the probable curative and therapeutic role of nebulized lignocaine drug against SARS CoV-2 by utilization of PubMed, MEDLINE, NHS Evidence and Web of Science databases. Results: With evidence of nebulized lignocaine being used successfully in respiratory illness before and the established role of low concentration lignocaine as ion channel repolarization agent, we try to interpret and deduce the possible implication of nebulized lignocaine as possible therapeutic agent and a potential cure against SARS-CoV-2 caused respiratory illness by acting as an anti-inflammatory agent during SARS-CoV-2 caused acute lung injury and also possibly as an antiviral drug.  Conclusion: By the virtue of possessing anti-inflammatory effect and potential antiviral effects, nebulized lignocaine can be a breakthrough in the management of the current COVID-19 pandemic.     Citation: Malik NA, Lignocaine’s substantial role in COVID-19 management: potential remedial and therapeutic implications. Anaesth. pain & intensive care 2019;23(1):84-91 Received: 29 March 2020; Reviewed & Accepted: 5 April 2020;


JAMA ◽  
2019 ◽  
Vol 321 (11) ◽  
pp. 1042
Author(s):  
Feyza Sancar

Blood ◽  
1985 ◽  
Vol 65 (2) ◽  
pp. 441-443 ◽  
Author(s):  
HJ Hassan ◽  
M Orlando ◽  
A Leonardi ◽  
C Chelucci ◽  
R Guerriero ◽  
...  

Abstract This study includes 47 normal subjects and 25 hemophilia B patients without inhibitor(s), showing different factor IX coagulant activity and antigen levels. Genomic DNA, digested with various restriction endonucleases, was hybridized with two different factor IX probes, ie, the cDNA and the subgenomic probe for the intragenic TaqI polymorphic site. cDNA restriction patterns suggest absence of gross rearrangements and/or deletions in all hemophilic patients. The frequency of the X chromosome bearing the TaqI polymorphic site is 0.32 +/- 0.09 in hemophilic subjects v 0.36 +/- 0.06 in normal control subjects, the latter value being comparable to that reported for the normal British population. No association between this polymorphism and hemophilia B variants has been observed, thus indicating that a wide spectrum of mutations underlies this blood-clotting disorder and particularly each of its variants.


Blood ◽  
1985 ◽  
Vol 65 (2) ◽  
pp. 441-443
Author(s):  
HJ Hassan ◽  
M Orlando ◽  
A Leonardi ◽  
C Chelucci ◽  
R Guerriero ◽  
...  

This study includes 47 normal subjects and 25 hemophilia B patients without inhibitor(s), showing different factor IX coagulant activity and antigen levels. Genomic DNA, digested with various restriction endonucleases, was hybridized with two different factor IX probes, ie, the cDNA and the subgenomic probe for the intragenic TaqI polymorphic site. cDNA restriction patterns suggest absence of gross rearrangements and/or deletions in all hemophilic patients. The frequency of the X chromosome bearing the TaqI polymorphic site is 0.32 +/- 0.09 in hemophilic subjects v 0.36 +/- 0.06 in normal control subjects, the latter value being comparable to that reported for the normal British population. No association between this polymorphism and hemophilia B variants has been observed, thus indicating that a wide spectrum of mutations underlies this blood-clotting disorder and particularly each of its variants.


Microbiology ◽  
2011 ◽  
Vol 157 (3) ◽  
pp. 786-792 ◽  
Author(s):  
Takehisa Ohbayashi ◽  
Atsushi Irie ◽  
Yoji Murakami ◽  
Magdalena Nowak ◽  
Jan Potempa ◽  
...  

Staphylococcus aureus is the most frequently isolated pathogen in Gram-positive sepsis often complicated by a blood clotting disorder, and is the leading cause of infective endocarditis induced by bacterial destruction of endocardial tissues. The bacterium secretes cysteine proteases referred to as staphopain A (ScpA) and staphopain B (SspB). To investigate virulence activities of staphopains pertinent to clotting disorders and tissue destruction, we examined their effects on collagen, one of the major tissue components, and on plasma clotting. Both staphopains prolonged the partial thromboplastin time of plasma in a dose- and activity-dependent manner, with SspB being threefold more potent than ScpA. Staphopains also prolonged the thrombin time of both plasma and fibrinogen, indicating that these enzymes can cause impaired plasma clotting through fibrinogen degradation. Whereas SspB cleaved the fibrinogen Aα-chain at the C-terminal region very efficiently, ScpA degraded it rather slowly. This explains the superior ability of the former enzyme to impair fibrinogen clottability. Enzymically active staphopains, at concentrations as low as 10 nM, degraded collagen with comparable efficiency. These results show novel virulence activities of staphopains in degrading fibrinogen and collagen, and suggest an involvement of staphopains in the clotting impairment and tissue destruction caused by staphylococcal infection.


Sign in / Sign up

Export Citation Format

Share Document