gracelive

AUTHOR: SEOK WOO YANG, MD & PhD.

CONTACT: Email: soplab@outlook.kr

DATE: 2020.07.22

CONTENT:

  About the facial mask-wearing, there have been many debates about the efficacy to block the viral particle spread. 

  The author has also fully recognized the incompleteness of the facial mask to prevent the viral particle spread perfectly.

  Nonetheless, the author emphasizes the facial mask-wearing, as the following reasons:

  1. The known key factors to facilitate the spread of respiratory droplets including viral particles are humidity and temperature in the environmental air. The environmental air humidity and temperature vulnerable to COVID-19 is not affected by the seasonal weather, for even in summer, many people live in the air-conditioned situation. With the reasons posted in [ https://gracelive.tistory.com/39?category=838022 ], the facial mask is helpful to keep our air-way mucosa from being infected by COVID-19 and other viral disorders.

 https://gracelive.tistory.com/39?category=838022

2. In 2008, MacIntyre et al reported that the masks as a group had protective efficacy in excess of 80% against clinical influenza-like illness. They concluded that in compliant mask users, masks were highly efficacious to prevent the respiratory viral transmission [ www.ijidonline.com/article/S1201-9712(08)01008-4/fulltext ]. 

 This finding can be checked in the case of Taiwan and Iceland during COVID-19 pandemic, where the early facial mask and social distance were adopted and applied in two nations [ https://theconversation.com/what-coronavirus-success-of-taiwan-and-iceland-has-in-common-140455 ].

 Similarly, Singapore and HongKong showed remarkable success in the early prevention of COVID-19. South Korea (ROK), where even opened to China, became to suppress the further spread of COVID-19 as time went on. [ https://www.weforum.org/agenda/2020/04/should-we-be-promoting-the-widespread-use-of-masks/ ]

3. About above 1. & 2., the author speculates the background medical mechanism why these events happened as the mechanism of live attenuated vaccine effect. Although the facial mask is not perfect to block the viral particle spread via respiratory droplets, the amount of spread viral particles must be reduced down, to some extent. The reduced amount of viral particles can be presumed to act as the live attenuated vaccine effect rather than pathogenic(causing to provoke disease condition) effect. 

 Passover in the Old Testament may be a suitable historic case for live attenuated vaccine effects. The air containing certain microorganisms was penetrable to all houses of Israelites and Egyptians. The only different point is that the houses of Israelites were painted with sheep blood on the doorframes. The author infers the sheep blood on the doorframe might be functioned as a filter like a facial mask for air-borne viral or bacterial particles. The reduced amount of microorganisms might act as live attenuated vaccines rather than pathogens.

[ https://gracelive.tistory.com/53?category=838022 ]

Cautiously, the author predicts that the herd immunity to COVID-19 can be achieved as time goes on, like Rabies, Influenza, and other viral diseases, without an increase in mortality rate when with the above reasons.

AUTHOR: SEOK WOO YANG, MD & PhD.

CONTACT: Email: soplab@outlook.kr

DATE: 2020.07.30

CONTENT:

 During the early phase of the pandemic COVID-19, I published many therapeutic and preventive suggestions for COVID-19. The predictability of my suggestions are as the followings:

 Above 7 suggestions have been proved. 

 In addition to these, the significance of inherent herpes neuritins in association with COVID-19 will be unraveld in my opinion.

 There are several reports about the skin rash and Kawasaki disease-like symptoms in COVID-19 patients. A majority of these cases may be confirmed as the secondary clinical expression to inherent herpes neuritis.

 In this perspective, inherent herpes neuritis as the side effect of Hydroxychloroquine should be monitered and prepared for its treatment to use Hydroxychloroquine safely.

AUTHOR: SEOK WOO YANG, MD & PhD.

CONTACT: Email: soplab@outlook.kr

DATE: 2020.04.07

CONTENT:

 As of 7th April, in a small city with approximately 160,000 citizens, the confirmed COVID-19 + cases are 50. The mortality rate is 0.

 The patients in my clinic were mainly those with respiratory diseases. There have been no confirmed COVID-19 cases.

 Some patients had fevers. With the therapeutic strategy in line with several previous posts, there have been no confirmed cases of COVID-19 yet. Even several patients with fevers and bronchitis who dropped out of screening hospitals concerning COVID-19 without testing recovered without the aggravation of respiratory diseases. About the reason why they were dropped out of COVID-19 test even with fevers, has not it known.

 The therapeutic drugs administered did NOT include hydroxychloroquine and azithromycin.

 The taken home message is that primary care in the early phase of respiratory diseases amid COVID-19 contagion is a key factor to a key factor to prevent the patients from being vulnerable to COVID-19.

 Early diagnosis, Early treatment!

P.S.

 In some patients with neurologic signs, including headache, alteration of smell and taste and oral mucosa, acyclovir was prescribed simultaneously as I posted.

AUTHOR: SEOK WOO YANG, MD & PhD

CONTACT: soplab@outlook.kr

DATE: 2020.04.03

CONTENT:

 There are many reports about the potential neural damage by COVID-19 coronaviruses in light of SARS coronaviruses. 

 As a cause of the sudden death by COVID-19, the neural injury at the brainstem and brain spread through the olfactory nerve is presumed to play a role in respiratory failure. [1] 

 One interesting fact in the patients with COVID-19 is the loss of smell and taste, about which the author suggested the possibility of provocation of inherent herpes neuritis in the trigeminal ganglion within the brain.[2]

In the endemic area of COVID-19, the author has treated many patients with bronchitis. 

 Among them, some patients had fevers. Interestingly they all had concurrent herpetic mucosal change in their oral pharynx. The herpes mucosal change was various from the overt herpes aphthous minute ulcer to discoloration of the pharynx, the latter of which may be equivocal among physicians. After being treated with acyclovir and antibiotics, acetaminophen, mucolytics, a physiologic dose steroid for bronchitis, the fevers were subsided after 1-day treatment.

 Concerning another cause of sudden death by COVID-19, we need to focus on the possibility of the brainstem injury by inherent herpes neuritis in the brainstem or hypothalamus.[1] 

 But there is no statistical study about the presence of herpes viral infection in the brainstem or hypothalamus as yet. 

  The author experienced some cases with unknown fever, which at last proved to be herpes neuritis probably at the brainstem or/and hypothalamus involved in temperature control. The proof of herpes neuritis was measured by clinical improvement in response to acyclovir, valaciclovir, or famciclovir.  

 Like these cases, if patients have inherent herpes neuritis in the brainstem or hypothalamus and are newly affected with COVID-19, the antiviral immunity may be weakened, the condition of which provokes latent inherent herpes infection and aggravates COVID-19 coronaviral infection in the brainstem or hypothalamus. As a result of this event, the brainstem or hypothalamic injury may be induced and leading to the death of patients.    

 Unfortunately, this hypothesis can not be proved with MRI or blood tests. As the author's clinical experiences for several years, many patients with no abnormality in MRI or blood tests complained of their herpetic symptoms and eventually they were treated and clinically improved by taking in anti-herpetic drugs. 

 With the above facts on the concurrent and inherent herpes neuritis in the brainstem, the author thinks that the early prescription of acyclovir during treating bronchitis in the cases suspicious of COVID-19 may play a role in decreasing the mortality rate in the cases affected with the underlying herpes neuritis in the brainstem. 

P.S.

 About which to choose in antiherpetic drugs like acyclovir or famciclovir in the suspicious herpes neuritis in the patients with COVID-19, the author prefers to prescribing acyclovir as a first-line treatment. Famciclovir can be considered when there is no remarkable clinical improvement, even after using acyclovir.

REFERENCE:

[1]  Li YC, Bai WZ, Hashikawa T. The neuroinvasive potential of SARS-CoV2 may play
a role in the respiratory failure of COVID-19 patients. J Med Virol. 2020 Feb 27.

[2] Yang SW. Herpes Neuritis Should Be Checked After Treating With Hydroxychloroquine or Chloroquine: Medical Inference.
https://gracelive.tistory.com/64?category=838022.

AUTHOR: SEOK WOO YANG, MD & PhD.

CONTACT: soplab@outlook.kr

DATE: 2020.03.30

CONTENT:

 On March 30th, FDA approves hydroxychloroquine or chloroquine to be used in treating COVID-19.

 As of today, the main purpose of using hydroxychloroquine and chloroquine is to modulate the cytokine storm and to decrease viral load. 

 There are several reports to favor the use of hydroxychloroquine and chloroquine in COVID-19. But some are skeptical about this theme.

 For example, Guastalegname & Vallone quoted the experimental case of Chikungunya viral infection which is treated with chloroquine. In this experiment, there was a paradoxical effect to show no effect on the acute phase of the disease but the chronic complications of Chikungunya, more frequently in the treated group compared with the control group.

 For this reason, they recommended that clinicians should use hydroxychloroquine and chloroquine cautiously.[1] 

  Coronaviruses and SARS coronaviruses can cause neurologic diseases including loss of smell and taste during a respiratory infection.[2] 

 Among the viruses inherent in human DNA, herpesvirus including simplex and zoster form should be kept in mind after respiratory viral infection.

 Herpesviruses normally reside in the DNA of our cell nucleus and acquire virulent infectivity when our immunity is weakened. 

 Herpesviruses in the trigeminal ganglion of the brain can cause loss of smell and taste like the cases with COVID-19.

 There are several reports that hydroxychloroquine was associated with an increased herpes zoster risk in patients.[3]

 For the above reasons, in the cases of COVID-19 with the administration of hydroxychloroquine and chloroquine, clinicians should check the neurologic diseases by herpes zoster or simplex, such as neural hearing loss, neurogenic dyspnea, etc.  

REFERENCE:

[1] Guastalegname M, Vallone A. Could chloroquine /hydroxychloroquine be harmful
in Coronavirus Disease 2019 (COVID-19) treatment? Clin Infect Dis. 2020 Mar
24:ciaa321.

[2] Bohmwald K, Gálvez NMS, Ríos M, Kalergis AM. Neurologic Alterations Due to
Respiratory Virus Infections. Front Cell Neurosci. 2018 Oct 26;12:386.

[3] Liao TL, Chen YM, Liu HJ, Chen DY. Risk and severity of herpes zoster in
patients with rheumatoid arthritis receiving different immunosuppressive
medications: a case-control study in Asia. BMJ Open. 2017 Jan 5;7(1):e014032.

Living rules to prevent COVID-19

For detailed explanation, refer to category "2019-nCoV, COVID-19" within this blog.

REVIEWER & COMMENTER: SEOK WOO YANG, MD & PhD

CONTACT: E.mail: soplab@outlook.kr

DATE: 2020.03.25

CONTENT:

 Casanova et al demonstrated fecally contaminated liquid droplets of SARS cases are a potential vehicle for contagion besides respiratory droplets. This study reported that SARS coronaviruses remained infectious in water and sewage for days to weeks.[1]

 For this reason, waterborne infection of COVID-19 coronaviruses should be checked meticulously to prevent further spread of COVID-19. 

 In addition to facial masks for blocking respiratory droplets, drinking water should be sterilized. At home, we must boil water or mix bitter herbs or lemons with water before drinking.

 The government should pay attention to sterilize water supply source.

REFERENCE:

Casanova L, Rutala WA, Weber DJ, Sobsey MD. Survival of surrogate
coronaviruses in water. Water Res. 2009 Apr;43(7):1893-8.

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.