gracelive

AUTHOR: SEOK WOO YANG, MD & PhD

CONTACT: E.mail: soplab@outlook.kr

DATE: 2020.03.22.

CONTENT:

 Besides the acute respiratory distress syndrome in the patients affected by COVID-19, the possibility of subclinical adrenal insufficiency should be considered. When patients are lethargic and dehydrated, intravenous glucose infusion can be considered. But if patients have adrenal insufficiency, intravenous glucose infusion can cause lethal damage, as the following reasons:

 Based on the genetic and clinical similarity of COVID-19 to SARS coronaviruses, the autopsy findings in SARS affected patients are helpful to expect the things to come during the disease progression. 

 In the autopsy of SARS cases, the adrenal glands in patients revealed necrosis, infiltration of monocytes and lymphocytes loaded with SARS coronaviruses within vessels, and thrombosis in small veins.[1][2]

 With this finding, we can infer the possibility of adrenal insufficiency.

 In patients with adrenal insufficiency who have not received glucocorticoids, glucose infusion may cause high fever ("glucose fever") followed by collapse and death. Presumably, the glucose is metabolized, and the water dilutes the plasma, and the resultant osmotic gradient between the plasma and the cells causes the cells of the thermoregulatory centers in the hypothalamus to swell to such an extent that their function is disrupted.[3]

 The author infers that the neuropathologic change of glucose fever may be similar to that of central pontine myelinolysis after too rapid medical correction of sodium deficiency (hyponatremia). Hyponatremia is often accompanied by adrenal insufficiency. Central pontine myelinolysis causes damage to myelin and neuron in the brainstem, especially pons and even extrapontine brain tissue.

 On this point, intravenous fluid therapy in COVID-19 patients, subclinical hyponatremia conditions should be also considered.  

 The brain tissues infected with SARS coronaviruses are supposed to be susceptible to this hypothetical neural damage. 

 Gu J et al summarized many reports about observations of the central nervous system affected with SARS-coronaviruses, as follows: 

 RT-PCR has detected SARS-CoV genomic sequences in cerebral spinal fluid and in brain tissue specimens. The virus has been successfully isolated from brain tissue. Edema and focal degeneration of neurons have been observed in the brains of SARS autopsies. IHC(immunohistochemical stain), in situ hybridization, and EM(electron microscopy) have confirmed viral infection of neurons. Gliocytes have also been found infected by SARS-coronaviruses.[4]

 With the above reasons, the possibility of adrenal insufficiency and related neurologic damage can be applied to the cases with COVID-19.

 For this reason, when patients with COVID-19 are lethargic and dehydrated, intravenous fluid therapy should be done without glucose except for overt hypoglycemic conditions and without rapid correction of hyponatremia. 

 To correct the adrenal insufficiency, the physiologic dose of steroids should be prescribed in the early phase of COVID-19. This may be also beneficial to prevent acute respiratory distress syndrome in COVID-19, for alveolar macrophages induce cytokine-related inflammatory responses that can be lessened by steroids. 

P.S.

 The physiologic dose of steroids the author recommends is methylprednisolone 1mg #2 (0.5mg intake two times) per day at a 60kg weighted person.

REFERENCE:

[1] Ding YQ, Wang HJ, Shen H, Li ZG, Geng J, Han HX, Cai JJ, Li X, Kang W, Weng DS, Lu YD, Wu DH, He L, Yao KT. The clinical pathology of severe acute respiratory syndrome (SARS): a report from China. J Pathol. 2003;200:282–289.

[2] Gu J, Gong EC, Zhang B, Zheng J, Gao ZF, Zhong YF, Zou WZ, Zhan J, Wang SL, Xie ZG, Zhuang H, Wu BQ, Zhong HH, Shao HQ, Fang WG, Gao DX, Pei F, Li XW, He ZP, Xu DZ, Shi XY, Anderson VM, Leong ASY. Multiple organ infection and the pathogenesis of SARS. J Exp Med. 2005;202:415–424.

[4] Gu J, Korteweg C. Pathology and Pathogenesis of Severe Acute Respiratory Syndrome. Am J Pathol. 2007 Apr; 170(4): 1136–1147.

[3] Ganong WF. Chapter 20. The Adrenal Medulla & Adrenal Cortex, In Review of Medical Physiology, 22nd ed. Appleton & Lange, 2005, p 370.

AUTHOR:SEOK WOO YANG, M.D. & Ph.D. (E.mail: soplab@outlook.kr)

DATE: 2020.03.09

CONTENT:

 Human coronaviruses have a property to haemagglutinate with sheep erythrocytes(red blood cells).[1] In contrast, human coronaviruses do not haemagglutinate with chick erythrocytes.[2] 

 These findings are reminiscent of the interpretaton by Yang(2013) about 'Passover and Blood of Sheep or Goat'.[3] 

 The story about 'Passover and Blood of Sheep or Goat' is below: 

 In chapter 12: verse 5th ~ 7th of Exodus, Bible says, "5 The animals you choose must be year-old males without defect, and you may take them from the sheep or the goats. 6; Take care of them until the fourteenth day of the month, when all the people of the community of Israel must slaughter them at twilight. 7 Then they are to take some of the blood and put it on the sides and tops of the doorframes of the houses where they eat the lambs".

 There is a question, "why did God designate the blood of lamb or goat for doorframe painting?”.

 In that time of Exodus, there should be poultry and animals besides sheep and goat.

 If the stickiness of blood is enough for removing infectious microbial pathogens, why did God designate specifically the blood of lamb or goat?

 Concerning this question, I think the blood painted on doorframe even at night can be dry in some degree. In the partial dry state, the microbial organisms attached within blood can be detached and easily floated into the air. The microbial-contaminated air can be inhaled into the lung of the Israelite and cause an infectious state.

 To overcome this problem, the blood of lamb or goat should have a certain specific attribute to seize microbial organism, even in the dry state of the blood.

 Regarding this problem, there is an interesting report by Medeiros et al (2001. Virology 289:74-85).[4] Medeiros et al found influenza virus particles stick to the RBCs (Red Blood Cell) in the blood of lamb or goat and aggregates RBCs (termed 'agglutination'). In contrast, the RBCs in the blood of chicken does not cause this reaction. As inferred from this fact, there must be specificity in each species of animal or poultry, in RBC agglutination to particular microbial pathogens.

 So I think God may order the blood of lamb or goat to remove the particular microbial pathogens at the Passover day night.

Through the stickiness and the RBC agglutination of the blood of lamb or goat, it is more likely that the amount of filtered microbial pathogens may work as a vaccine effect.

 In the chapter 12 of Exodus in the old testament, verse 12th and 13th, the Bible says, "12 on that same night I will pass through Egypt and strike down every firstborn - both men and animals - and I will bring judgment on all the gods of Egypt. I am the LORD. 13 The blood will be a sign for you on the houses where you are; and when I see the blood, I will pass over you.

 Although there can be other pathogens and view points to be considered, the plausible facts of haemagglutination with sheep erythrocytes and the rapid occurrence of death overnight seem to be similar to those of COVID-19 infection.

REFERENCE:

1. Hierholzer JC, Tannock GA. Quantitation of antibody to non-hemagglutinating 

viruses by single radial hemolysis: serological test for human coronaviruses. J Clin Microbiol. 1977 Jun;5(6):613-20.

2. Gerdes JC, Klein I, DeVald BL, Burks JS. Coronavirus isolates SK and SD from multiple sclerosis patients are serologically related to murine coronaviruses A59 and JHM and human coronavirus OC43, but not to human coronavirus 229E. J 
Virol. 1981 Apr;38(1):231-8.

3. Yang SW. Episode 2. Passover and Blood of Sheep or Goat. PASSOVER DAY – Medical Interpretation by a Pathologist (English). Copyright (C-2013-017025) 

4. Medeiros R, Escriou N, Naffakh N, Manuguerra JC, van der Werf S. Hemagglutinin residues of recent human A(H3N2) influenza viruses that contribute to the inability to agglutinate chicken erythrocytes. Virology. 2001 Oct 
10;289(1):74-85.