In addition to rather well studied hematologic, biochemical, inflammatory and coagulative markers of a new koronavirusny infection, there are some more markers which can be perspective in definition of severe forms of this disease. We will consider them in this article.
The first applicant for a role of a new biomarker of COVID-19 — gomotsistein. From the moment of opening in 1932, concerning this substance was suggested much. This amino acid is formed due to methionine amino acid heating with sulphuric acid.
High level of a gomotsistein in a blood plasma considerably increases risk of damage of both small, and large vessels; concentration over 90% is connected with the increased risk of degenerative and atherosclerotic processes in the systems of coronary, cerebral and peripheric circulation. In spite of the fact that gomotsistein is an effective marker of a condition of a cardiovascular system, and cardiovascular complications play a critical role at the hospitalized patients with COVID-19, this marker is not accepted and not studied for use in clinical practice, and in one of the perspective published researches attention was not paid to laboratory markers which can help to estimate clinical picture COVID-19.
Definition of a gipergomotsisteinemiya differs in different researches. Understand the medical state which is characterized by abnormally high level (more than 15 µmol/l) of a gomotsistein in blood as a gipergomotsisteinemiya. The general concentration of a gomotsistein in plasma of healthy people (on an empty stomach) low (from 5.0 to 15.0 µmol/l at assessment by the highly effective liquid chromatograph or from 5.0 to 12.0 µmol/l when using the immunoenzymatic analyzer). Easy degree of a gipergomotsisteinemiya from 16 to 30 µmol/l, average degree — from 31 to 100 µmol/l, and heavy — more than 100 µmol/l are considered. Recent researches connect a gipertsisteinemiya with cardiovascular diseases, diabetes, a chronic renal failure and a steatosis of a liver.
According to the latest data, concentration of a gomotsistein (together such factors as age, the level of lymphocytes and time from the moment of emergence of symptoms before hospitalization) allows to predict heavy pneumonia when carrying out KT of lungs on the first week at patients with COVID-19, but about involvement other bodies of data were not. In the same research authors reported that the level of lymphocytes was much higher at patients with progressing according to the visualizing researches in comparison with patients without that. Thus, this question demands further studying.
The following applicants for a role of new biomarkers are Angiotensin II, angiotensin - (1-7), angiotensin - (1-9) and alamandin. During the researches on animals it was revealed that drop intravenous injection of APF2 and angiotensin - (1-7) had protective action at the expense of inhibition of a way of RhoA/Rho of a kinase (ROCK). This way actively participates in changes of a tone and structure of vessels that leads to hypertensia, and damage of kidneys, and a cardiovascular system, and plays a significant role in induction of a pneumosclerosis.
APF2 will transform angiotensin II to angiotensin - (1-7), and angiotensin I in angiotensin - (1-9). Angiotensin - (1-7) and angiotensin - (1-9) have a biological impact at the expense of receptors of Mas (MasR) and AT2 (AT2R), respectively. Angiotensin - (1-7) induces regional and system vasodilatation, a diuresis and a natriuresis. Angiotensin - (1-9) increases bioavailability of nitrogen oxide (NO) due to stimulation of emission of bradykinin (BK). Activation of these ways provides antiinflammatory and antifibrous action, performing function of protection of a cardiovascular system, kidneys and lungs.
Alamandin is developed as a result of a catalysis of APF2 of angiotensin A or by means of angiotensin decarboxylation reaction - (1-7) in N-trailer residue of amino acid of aspartate. Alamandin has the same effect, as angiotensin - (1-7): vasodilatation and antifibrous action. It modulates regulation of peripheral and central pressure and also mechanisms of cardiovascular correction. According to mechanistic researches can suppress APF2, leading to excess accumulation of toxic angiotensin II that leads to development of ORDS and lightning myocarditis. Angiotensin level in plasma of the patients infected with the SARS-CoV-2 virus was considerably raised and linearly connected with virus loading and injury of lungs.
Currently data on angiotensin level - (1-7), angiotensin - (1-9) and an alamandina in plasma of patients with COVID-19 are absent. After the termination of performance of APF2 of the function because of performance of APF2 of a role of the center of linking with the SARS-CoV-2 virus, increase in level angiotensin II and lowerings of the level of angiotensin - (1-7), angiotensin - (1-9) and an alamandina at patients with a severe form of a disease in comparison with patients with an easy form is expected.