AUTHOR: SEOK WOO YANG, MD & PhD

CONTACT: E mail: soplab@outlook.kr

DATE: 2020.03.17

CONTENT:

 

 In the pulmonary cases of COVID-19, Xu et al found the cytotoxic T cells with cytolytic activity which is associated with Th17 CD4 T cells polarized by IL-6 and TGF-β. This immunopathology led to diffuse alveolar and interstitial damage with pulmonary edema, pathologically and subsequent acute respiratory distress syndrome(ARDS) and secondary pneumonia, clinically.[1]   

 

 As a nutritional candidate to modulate both IL-6 and TGF-β, vitamin D can be considered. 

 

 Dalvi et al reported that the serum level of IL-6 was significantly increased and vitamin D3 decreased in tuberculosis multidrug-resistant group. Conversely, we can expect that the elevated serum level of vitamin D may reduce that of IL-6.[2]

 

 Hu et al mentioned the protecting role of vitamin D in diabetic nephropathy. One of the mechanisms to suppress pro-inflammatory responses was to inhibit production of TGF-β.[3]


 In conclusion, because the problematic immunopathology in the lung injury by COVID-19 is the elevated serum levels of IL-6 and TGF-β, we can infer that vitamin D to counteract these inflammatory responses may play a role somewhat in ameliorating the lung injury by COVID-19. About this, further studies will be necessary. 

 

 

REFERENCE:

[1] Xu Z, Shi L, Wang Y, Zhang J, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020;S2213-2600(20)30076-X.

[2] Dalvi SM, Ramraje NN, Patil VW, Hegde R, Yeram N. Study of IL-6 and vitamin D3 in patients of pulmonary tuberculosis. Indian J Tuberc. 2019 Jul;66(3):337-345.

[3] Hu X, Liu W, Yan Y, Liu H, Huang Q, Xiao Y, Gong Z, Du J. Vitamin D protects against diabetic nephropathy: Evidence-based effectiveness and mechanism. Eur J Pharmacol. 2019 Feb 15;845:91-98. 

'Vitamin' 카테고리의 다른 글

Vitamin C in Common Colds & Virus; about Its Effectiveness  (0) 2020.03.17

AUTHOR: SEOK WOO YANG, MD & PhD (E mail: soplab@outlook.kr)

DATE:2020.03.09

CONTENT:

 

ORGAN ANATOMIC PATHOLOGIC FINDINGS CLINICAL IMPLICATION
Lung

Diffuse alveolar damage.

Desquamation of pneumocytes.

Hyaline membrane disease.

Intra-alveolar fibromyxoid exudate.

Pulmonary edema.

Interstitial mononuclear cell infiltration, predominantly lymphocytes.

Multinucleated syncytial cells with atypical enlarged pneumocytes characterised by large nuclei, amphophilic granular cytoplasm, and prominent nucleoli.[1]

 

Acute respiratory distress syndrome.

Acute lung injury.

Heart Interstitial mononuclear inflammatory infiltrates  
Liver

Moderate microvesicular steatosis.

Mild lobular and portal activity.[1]

 
Kidney in COVID-19

No datum.

 
Kidney in MERS-CoV

Acute kidney injury.

Tubular epithelial cell degnerative/regenerative change.[2]

Kidney failure.
Central nervous system in COVID-19 No datum.  
Central nervous system in SARS-CoV Viral particles rich in brain neurons.[3] A potential neuroinvasion

 

REFERENCE:

[1] Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, Liu S, Zhao P, Liu H, Zhu L, Tai Y, Bai C, Gao T, Song J, Xia P, Dong J, Zhao J, Wang FS. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020 Feb 18:S2213-2600(20)30076-X

[2] Alsaad KO, Hajeer AH, Al Balwi M, Al Moaiqel M, Al Oudah N, Al Ajlan A, AlJohani S, Alsolamy S, Gmati GE, Balkhy H, Al-Jahdali HH, Baharoon SA, Arabi YM. Histopathology of Middle East respiratory syndrome coronovirus (MERS-CoV)
infection - clinicopathological and ultrastructural study. Histopathology. 2018 Feb;72(3):516-524.

[3] Li YC, Bai WZ, Hashikawa T. The neuroinvasive potential of SARS-CoV2 may be at least partially responsible for the respiratory failure of COVID-19 patients. J Med Virol. 2020 Feb 27.

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