A marker for viral pneumonia and its application

Abstract

The present invention relates to the field of pharmaceutical applications, and in particular to a marker for viral pneumonia and its application, wherein the marker for viral pneumonia is prostaglandin E2 and / or prostaglandin M. The present invention uses prostaglandin E2 and / or prostaglandin M as markers for viral pneumonia, and the use of cyclooxygenase II inhibitors can effectively and quickly reduce prostaglandins, reverse the progression of common and severe cases, block the occurrence of critical illness, promote viral conversion to negative, pneumonia absorption and health recovery. The drug will expand its clinical use scope upon further confirmation of its efficacy, incorporate the treatment method into clinical diagnosis and treatment plans, and provide new strategies and diagnosis and treatment methods for the comprehensive treatment of new coronary pneumonia.

Description

Technical Field

[0001] The present invention relates to the field of drug application, and in particular to a viral pneumonia marker and application thereof. Background Art

[0002] Coronaviruses are a large family of viruses known to cause colds as well as more serious illnesses such as Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS). Common symptoms of coronavirus infection include respiratory symptoms, fever, cough, shortness of breath, and difficulty breathing. In more severe cases, infection can lead to pneumonia, severe acute respiratory syndrome, kidney failure, and even death. Currently, there is no specific treatment for illnesses caused by novel coronaviruses.

[0003] Celecoxib has a unique mechanism of action, specifically inhibiting COX-2. Its chemical name is 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1-hydro-1-pyrazol-1-yl]benzenesulfonamide, its molecular formula is C17H14F3N3O2S, and its molecular weight is 381.38. Celecoxib is the first specific cyclooxygenase II (COX-2) inhibitor, jointly developed by Searle and Pfizer. Celecoxib capsules were first approved for marketing in the United States in January 1999 for the relief of arthritis-related pain and are currently the most prescribed nonsteroidal anti-inflammatory analgesic drug worldwide. Inflammatory stimuli can induce COX-2 production, leading to the synthesis and accumulation of inflammatory prostaglandins, particularly prostaglandin E2, which in turn causes inflammation, edema, and pain. By inhibiting COX-2, celecoxib prevents the production of inflammatory prostaglandins, achieving anti-inflammatory, analgesic, and antipyretic effects. Celecoxib is clinically used to treat osteoarthritis, rheumatoid arthritis, acute pain, ankylosing spondylitis, etc.

[0004] However, there are no reports on the use of cyclooxygenase II inhibitors, especially celecoxib, in coronavirus pneumonia. Summary of the Invention

[0005] In view of the shortcomings of the existing technology and actual needs, the present invention provides a marker for viral pneumonia and its application. The present invention provides a new approach and option for the treatment of viral pneumonia, especially coronavirus pneumonia.

[0006] To achieve this object, the present invention adopts the following technical solutions:

[0007] In a first aspect, the present invention provides a marker for viral pneumonia, wherein the marker for viral pneumonia is prostaglandin E2 (PGE2) and / or prostaglandin M (PGEM).

[0008] In the present invention, the inventors analyzed clinical data and gene function studies of the new coronavirus, SARS-CoV and MERS-CoV and found that the three coronaviruses share a common protein: the nucleocapsid N protein. The nucleocapsid N protein directly binds to the COX-2 gene promoter, initiates COX-2 gene transcription, and causes increased COX-2 expression in the lungs. It can be seen that the concentrations of COX-2 and nucleocapsid N protein are positively correlated. The catalytic products of COX-2 are increased production of prostaglandins (PGE, D, F, TBX), and reduced degradation in the lung parenchyma, causing excessive prostaglandin accumulation. It is speculated that cyclooxygenase II (COX-2) is a key target, and increased prostaglandins are the pathological basis of viral pneumonia. It can be seen that PGE2 and PGEM can be used as markers of viral pneumonia.

[0009] According to the present invention, the marker is abnormally elevated in the urine of patients with viral pneumonia.

[0010] In the present invention, the inventors tested the urine of patients with new coronary pneumonia and found that there was a high amount of prostaglandin E2 (PGE2), the concentration of which could reach 1000-6000 ng / ml, while the level of normal people (in our current test samples) is 0-30 ng / ml. The inventors further measured the concentration of prostaglandins and their metabolites PGEM (prostaglandin E metabolites) in the serum and / or urine of patients, and their concentrations were far higher than the normal concentration of 0-20 ng / ml, thereby verifying the correlation between prostaglandin concentration and coronavirus pneumonia, and that COX-2 inhibitors can reduce prostaglandin concentrations, thereby achieving the treatment of coronavirus pneumonia.

[0011] According to the present invention, prostaglandin E2 in the marker is abnormally elevated in the early and middle stages of viral pneumonia, and the concentration of prostaglandin E2 in the marker is positively correlated with the progression of viral pneumonia.

[0012] In the present invention, the increase rate of PGE2 in the urine of patients with viral pneumonia is 100%, the change of PGE2 is 1-3 days earlier than the CT imaging diagnosis, and the accuracy rate of predicting the course of the disease is more than 85%.

[0013] According to the present invention, the prostaglandin M in the marker is abnormally elevated in the middle and late stages of viral pneumonia, and the concentration of prostaglandin M in the marker is positively correlated with the severity of viral pneumonia. When PGEM increases, it warns that viral pneumonia has entered a severe or critical stage, and multiple organs in the body experience functional decline or failure.

[0014] In the present invention, the inventors found that PGE2 and PGEM levels would increase during the course of pneumonia. The increase in PGE2 concentration was positively correlated with the aggravation of pneumonia, and the increase in PGEM concentration was positively correlated with the severity of pneumonia.

[0015] According to the present invention, the viral pneumonia is coronavirus pneumonia, preferably any one or a combination of at least two of influenza, avian influenza, pneumonia infected by coronavirus 2019-nCoV, pneumonia infected by coronavirus SARS-CoV or pneumonia infected by coronavirus MERS-CoV, preferably pneumonia infected by coronavirus 2019-nCoV.

[0016] In a second aspect, the present invention provides the markers as described in the first aspect as markers for any one or a combination of at least two of viral pneumonia early warning, efficacy observation and prognosis judgment, and preferably prostaglandin E2 among the markers as a marker for any one or a combination of at least two of viral pneumonia early warning, efficacy observation and prognosis judgment.

[0017] According to the present invention, the viral pneumonia is coronavirus pneumonia, preferably any one or a combination of at least two of influenza, avian influenza, pneumonia infected by coronavirus 2019-nCoV, pneumonia infected by coronavirus SARS-CoV or pneumonia infected by coronavirus MERS-CoV, preferably pneumonia infected by coronavirus 2019-nCoV.

[0018] In a third aspect, the present invention provides the markers as described in the first aspect as markers for severe viral pneumonia and / or critical viral pneumonia, preferably prostaglandin M among the markers as markers for severe viral pneumonia and / or critical viral pneumonia.

[0019] According to the present invention, the viral pneumonia is coronavirus pneumonia, preferably any one or a combination of at least two of influenza, avian influenza, pneumonia infected by coronavirus 2019-nCoV, pneumonia infected by coronavirus SARS-CoV or pneumonia infected by coronavirus MERS-CoV, preferably pneumonia infected by coronavirus 2019-nCoV.

[0020] In the present invention, the main cause of death in patients infected with coronavirus is acute respiratory distress syndrome. Coronavirus infection causes increased expression of COX-2 in the lungs, catalyzing arachidonic acid into prostaglandins. At the same time, due to the decline in function of infected lung tissue cells, prostaglandins cannot be degraded. The combination of the two leads to excessive accumulation of prostaglandins in the lungs, which is also the key pathological basis of coronavirus pneumonia and respiratory distress syndrome. Excessive prostaglandins promote the pathological development of novel coronavirus pneumonia (COVID-19): (1) Increased inflammatory secretions, edema on the alveolar surface, and the formed water film covering the alveoli, hindering blood oxygen exchange and leading to a decrease in blood oxygen; (2) Causing high-intensity contraction of the smooth muscles of small bronchi and small blood vessels, leading to small bronchi spasm, increased airway resistance, and even incomplete expansion of the lung lobes; hemodynamic disorders, rapid and inefficient respiratory rate and heart rate, gradually developing into respiratory distress syndrome and multiple organ failure; (3) Inhibiting the function and number of lymphocytes, especially T cells, leading to a decrease in the total number and proportion of characteristic lymphocytes, which is conducive to the replication and amplification of the virus. This is the pathological evolution process of coronavirus pneumonia in the early and middle stages. Entering the critical stage can trigger an immune factor storm and endanger life.

[0021] In a fourth aspect, the present invention provides a drug for treating viral pneumonia, which inhibits the increase of prostaglandins.

[0022] According to the present invention, the active ingredient of the drug is a cyclooxygenase II inhibitor or a pharmaceutically acceptable salt, ester or solvate thereof.

[0023] According to the present invention, the cyclooxygenase II inhibitor is a non-steroidal compound, preferably a coxib compound, and more preferably celecoxib.

[0024] In the present invention, the inventors discovered that non-steroidal drugs, especially coxibs, as anti-inflammatory drugs, are a type of cyclooxygenase II antagonists that can reduce the production of prostaglandins, thereby achieving the treatment of viral pneumonia.

[0025] In a specific embodiment, the drug may be further added with one or more pharmaceutically acceptable carriers, which include any one or a combination of at least two of conventional excipients, diluents, carriers, flavorings, binders and fillers in the pharmaceutical field.

[0026] In a specific embodiment, the drug is introduced into the body alone by injection, spraying, penetration, absorption, physical or chemical mediation, and the body includes but is not limited to muscle, intradermal, subcutaneous, intravenous, and mucosal tissues; the drug can also be introduced into the body after being mixed or encapsulated with other substances.

[0027] In the present invention, the drug prepared with a cyclooxygenase II inhibitor or a pharmaceutically acceptable salt, ester, or solvate thereof as the active ingredient can be prepared in various forms such as injection, tablets, powder, granules, capsules, and oral liquids. The above-mentioned various dosage forms of the drug can be prepared according to conventional methods in the pharmaceutical field.

[0028] According to the present invention, the viral pneumonia is coronavirus pneumonia, preferably any one or a combination of at least two of influenza, avian influenza, pneumonia infected by coronavirus 2019-nCoV, pneumonia infected by coronavirus SARS-CoV or pneumonia infected by coronavirus MERS-CoV, preferably pneumonia infected by coronavirus 2019-nCoV.

[0029] In a fifth aspect, the present invention provides a pharmaceutical composition for treating viral pneumonia, which comprises a cyclooxygenase II inhibitor and an antiviral drug.

[0030] According to the present invention, the cyclooxygenase II inhibitor is a non-steroidal compound, preferably a coxib compound, and more preferably celecoxib.

[0031] According to the present invention, the viral pneumonia is coronavirus pneumonia, preferably any one or a combination of at least two of influenza, avian influenza, pneumonia infected by coronavirus 2019-nCoV, pneumonia infected by coronavirus SARS-CoV or pneumonia infected by coronavirus MERS-CoV, preferably pneumonia infected by coronavirus 2019-nCoV.

[0032] Compared with the prior art, the present invention has the following beneficial effects:

[0033] (1) The present invention found that the PGE2 increase rate during the course of COVID-19 patients was 100%, the increase in PGE2 concentration was positively correlated with the aggravation of pneumonia, the PGE2 change was 1-3 days earlier than the CT imaging diagnosis, and the accuracy rate of predicting the course of the disease was more than 85%. PGEM increased in the late stage of viral pneumonia and was closely related to the severity of viral pneumonia. It can be seen that changes in PGE2 and / or PGEM indicators can be used as markers of viral pneumonia;

[0034] (2) The present invention can warn of the progression of the disease 1-3 days in advance by monitoring the changes in the concentration of PGE2 in the patient's urine, so that corresponding treatment measures can be taken in advance. The use of a conventional dose of celecoxib to inhibit type II cyclooxygenase can effectively and quickly reduce prostaglandins, reverse the progression of common and severe diseases, block the occurrence of critical illness, promote viral conversion to negative, pneumonia absorption and health recovery. BRIEF DESCRIPTION OF THE DRAWINGS

[0035] Figure 1 The urine PEG2 level indicates changes in the condition, among which, Figure 1 (A) is the peak graph of PEG2 in urine exceeding 1000 ng / ml. Figure 1 (B) is the CT result of the patient in the case where PEG2 showed a peak value exceeding 1000 ng / ml. Figure 1 (C) is a graph showing the decrease of PEG2 in urine from a peak value exceeding 1000 ng / ml. Figure 1 (D) is the CT result of the patient's PEG2 falling from the peak value of more than 1000ng / ml. Figure 1 (E) is a small amplitude vibration diagram of PEG2 in urine below 100 ng / ml baseline. Figure 1 (F) is the CT result of the patient's PEG2 with a small amplitude fluctuation below the baseline of 100 ng / ml;

[0036] Figure 2 This is a result chart showing that celecoxib treatment can accelerate the improvement of the condition of common patients, among which, Figure 2 (A) is the change of PEG2 level in control case 1, Figure 2 (B) is the change of PEG2 level in case 31 of the experimental group. Figure 2 (C) is the CT result of control case 1. Figure 2 (D) CT findings of case 31 in the experimental group;

[0037] Figure 3 This is a graph showing that celecoxib treatment can accelerate the improvement of the condition of severe patients, among which, Figure 3 (A) is the change of PEG2 level in control case 2, Figure 3 (B) is the change of PEG2 level in case 22 of the experimental group. Figure 3 (C) is the CT result of control case 2. Figure 3 (D) CT findings of case 22 in the experimental group;

[0038] Figure 4 This is a chart showing the improvement of the condition of patients who were hospitalized for more than 10 days with exacerbated conditions after using celecoxib as an adjuvant treatment. Figure 4 (A) is the change of PEG2 level in case 1, Figure 4 (B) shows the changes in PEG2 levels in case 6. Figure 4 (C) is the CT result of case 1. Figure 4 (D) CT findings of case 6;

[0039] Figure 5 This is a graph showing the results of patients who stopped receiving celecoxib treatment, where: Figure 5 (A) shows the changes in PEG2 levels in case 5. Figure 5 (B) shows the changes in PEG2 levels in case 14. Figure 5 (C) is the CT result of case 5. Figure 5 (D) CT findings of case 14. DETAILED DESCRIPTION

[0040] To further illustrate the technical means and effects of the present invention, the technical solutions of the present invention are further described below with reference to the accompanying drawings and specific implementation methods, but the present invention is not limited to the scope of the embodiments.

[0041] Except for the contents specifically mentioned below, the processes, conditions, reagents, experimental methods, etc. for implementing the present invention are common knowledge and common common sense in the field and are not particularly limited by the present invention.

[0042] Unless otherwise specified, all technical and scientific terms used in this specification have the same meanings as those generally understood by those skilled in the art to which this invention belongs. However, in the event of any conflict, the present specification, including the definitions, shall prevail.

[0043] Example 1 Preliminary clinical trial of celecoxib

[0044] In this example, in collaboration with Guangzhou Eighth People's Hospital, we conducted a clinical study on the treatment of COVID-19 with the type II cyclooxygenase inhibitor celecoxib on the basis of conventional treatment according to the guidelines. The clinical study was conducted using celecoxib as an adjuvant, with oral administration for 10-14 days, twice a day, 200 mg each time. The specific cases are as follows:

[0045] The first cohort consisted of 8 patients in the experimental group (4 severe cases, 4 common cases) and 7 in the control group (7 common cases). Follow-up assessments on the 4th and 10th days of treatment revealed that all patients had improved, with no cases becoming more severe. In the control group, 42%, 14%, and 42% of patients had their condition improved, respectively. The efficacy of the experimental group was significantly superior to that of the control group. In accordance with the medical ethics and international standards of clinical trials, some patients with worsening conditions in the control group were removed from their control group status and transferred to the experimental group. The parallel grouping approach was abandoned, and the majority of new patients were enrolled in the experimental group.

[0046] Example 2 Celecoxib expanded clinical trial

[0047] In this example, in order to further verify the clinical study of the type II cyclooxygenase inhibitor celecoxib in the treatment of new coronary pneumonia, the enrolled population was further increased, and the specific cases are as follows:

[0048] As of February 23, 2020, 31 patients (6 severe cases and 25 common cases) were enrolled in the trial group. The specific medication conditions and results are shown in Table 1 below:

[0049] Table 1

[0050]

[0051] As can be seen from Table 1, among all 38 cases including the experimental group and the control group, 84.2% (32 / 38) of the patients had mild conditions (mild or ordinary CT imaging manifestations) when they were admitted to the hospital, and 15.7% (6 / 38) of the patients had severe conditions (severe) when they were admitted to the hospital. After treatment, (1) 31 / 31 cases improved (improvement rate 100%); (2) 31 / 31 cases turned negative for the virus (negative rate 100%); (3) 0 / 31 cases worsened (exacerbation rate 0%); (4) 0 / 31 cases remained unchanged (no change rate: 0%); (5) 15 cases have been discharged from the hospital, and 16 cases are still receiving treatment in the hospital; (6) Except for 1 case who stopped the drug due to suspected side effects such as excessive sweating, no side effects were observed in the rest. Observations from a limited number of clinical trial groups suggest that the use of regular doses of celecoxib (0.2 g / dose, bid) can effectively reduce prostaglandins, reverse the progression of common and severe cases, block the occurrence of critical illness, promote viral conversion to negative, pneumonia absorption and health recovery.

[0052] Example 3 Clinical Diagnosis of PGE2

[0053] In this example, in order to further verify the clinical study of the type II cyclooxygenase inhibitor celecoxib in the treatment of new coronary pneumonia, and further analyze the correlation between PGE2 and the changes in the condition of new coronary pneumonia, this example tracked and detected the level of PGE2 in the urine of patients with new coronary pneumonia every day, and compared the CT results. The results are as follows Figure 1 shown.

[0054] from Figure 1 It can be seen that there are three patterns of changes in PGE2 levels between two adjacent CT tests: 1) Figure 1 (A) showed a peak of more than 1000 ng / ml; 2) Figure 1 (C) dropped from a peak exceeding 1000 ng / ml; 3) Figure 1 (E) shows a small fluctuation below the baseline of 100 ng / ml. The corresponding analysis of two adjacent CT results also shows three types of disease regression, such as Figure 1 (B) Figure 1 (D) and Figure 1 (F), We defined three categories of PGE2 changes, which were completely consistent with the subsequent CT diagnosis results: pneumonia exacerbation, improvement, and no change.

[0055] After excluding interference factors such as other inflammatory diseases, a retrospective analysis was conducted on 58 events of dynamic changes in PGE2 concentrations, and the corresponding CT imaging results of patients before and after the PGE2 changes were analyzed. Among them, the early PGE2 change pattern of 47 events was completely consistent with the predicted disease progression shown by the subsequent CT diagnosis results. The accuracy rate of early prediction of the disease direction and progression reached 81%, and the advance time was 1-3 days, indicating that the change in urine PGE2 concentration is positively correlated with the progression of pneumonia, and has a predictive and early warning function.

[0056] Example 3 Clinical trial results of celecoxib in treating common patients

[0057] In this example, in order to further verify the clinical study of the type II cyclooxygenase inhibitor celecoxib in the treatment of new coronary pneumonia, this example analyzed and compared the PGE2 and lung CT imaging changes of two common cases with similar conditions and courses of disease (control group case 1 and experimental group case 31). The results are as follows Figure 2 shown.

[0058] from Figure 2 It can be seen that the PGE2 level of case 1 in the control group remained at a high level of 1000ng / ml from the 5th to the 9th day of admission ( Figure 2 (A)) However, the PGE2 level of case 31 in the experimental group dropped from over 1000 ng / ml on the second day of admission to around 100 ng / ml within two days ( Figure 2 (B)); The corresponding CT results showed that the absorption of pneumonia lesions in case 31 of the experimental group was faster than that in case 1 of the control group ( Figure 2 (C)- Figure 2 (D)).

[0059] Analysis of the efficacy of celecoxib for treating common COVID-19 revealed that none of the 25 common COVID-19 patients in the experimental group progressed to severe disease. Compared to the control group, celecoxib treatment effectively controlled PGE2 levels in the experimental group, leading to a relatively rapid resolution of pneumonia. This suggests that the use of celecoxib as an adjunct to conventional treatment may accelerate improvement in common COVID-19 patients.

[0060] Example 4 Clinical trial results of celecoxib in treating critically ill patients

[0061] In this example, in order to further verify the clinical study of the type II cyclooxygenase inhibitor celecoxib in the treatment of new coronary pneumonia, this example analyzed and compared the changes in PGE2 and lung CT images of 1 patient in each of the control group (control case 2) and the experimental group (experimental group case 22). The results are as follows: Figure 3 shown.

[0062] from Figure 3It can be seen that from the 5th to 12th day after admission, the PGE2 level of control case 2 fluctuated within the concentration range of 1000ng / ml ( Figure 3 (A)), while the PGE2 level of case 22 decreased steadily under the control of celecoxib and finally remained in the concentration range below 100 ng / ml ( Figure 3 (B)); CT imaging results showed that the pneumonia of the control group patients recurred, while the pneumonia of the experimental group case 22 was absorbed faster than that of the control case 2 ( Figure 3 (C)- Figure 3 (D)).

[0063] It can be seen that among the 6 severe patients in the experimental group, none of them progressed to critical illness after treatment with celecoxib. The use of celecoxib as an adjunct to conventional treatment may prevent the occurrence of critical illness.

[0064] Example 5 Clinical trial results of celecoxib in treating patients with severe illness who were hospitalized for more than 10 days and whose condition continued to worsen

[0065] In this example, in order to further verify the clinical study of the type II cyclooxygenase inhibitor celecoxib in the treatment of new coronary pneumonia, this example analyzed and compared two patients (Case 1 and Case 6). After admission, these two patients received conventional treatment for 12-15 days. Their condition worsened from common to severe. Celecoxib was used on the basis of the original conventional treatment. The changes in PGE2 and lung CT images of these two patients were compared. The results are as follows Figure 4 shown.

[0066] Case 1 stopped taking celecoxib on the 5th day of treatment due to excessive sweating. Even though the treatment course was only 5 days, the patient continued to improve until discharge ( Figure 4 (A)), Case 6's condition improved with continued medication ( Figure 4 (B)), CT imaging results showed that the condition gradually stabilized and improved ( Figure 4 (C)- Figure 4 (D)).

[0067] It can be seen that after the use of celecoxib, PGE2 was controlled, the condition gradually stabilized and improved, and the use of celecoxib treatment reversed the progression of severe illness and blocked the occurrence of critical illness.

[0068] Example 6 Clinical trial results of patients who stopped taking celecoxib

[0069] In this example, in order to further verify the clinical study of the type II cyclooxygenase inhibitor celecoxib in the treatment of new coronary pneumonia, this example analyzed and compared two patients (Case 5 and Case 14). These two patients stopped taking celecoxib after 11 days of treatment, and compared the changes in PGE2 and lung CT images of these two patients. The results are as follows Figure 5shown.

[0070] from Figure 5 It can be seen that the condition of case 5 worsened slightly on the third day after stopping the drug, and then recovered on its own ( Figure 5 (A)); while Case 14 experienced a slight worsening of the condition only on the 6th day after stopping the medication ( Figure 5 (B)), the CT results also showed that the disease recurred ( Figure 5 (C)- Figure 5 (D)).

[0071] It can be seen that the disease relapsed after stopping the use of celecoxib.

[0072] Example 7 Clinical Diagnosis of PGEM

[0073] In this example, in order to further verify the clinical study of the type II cyclooxygenase inhibitor celecoxib in the treatment of COVID-19 and further analyze the correlation between PEGM and the progression of COVID-19, the level of PEGM in the urine of COVID-19 patients was tracked and detected every day. The results are shown in Table 2.

[0074] Table 2 Daily urine PGEM (ng / mL) of patients

[0075]

[0076]

[0077]

[0078] As can be seen from Table 2, PGEM was abnormally elevated in all cases, PGEM increased in the middle and late stages of the disease, and the concentration of PGEM was related to the severity of pneumonia.

[0079] In summary, based on the observations of a limited number of clinical trial groups, the present invention suggests that changes in PGE2 indicators may have the functions of early warning, efficacy observation and prognosis judgment. At the same time, celecoxib can effectively reduce the PGE2 level in patients, promote the improvement of the condition of patients with common and severe COVID-19, and prevent the disease from progressing to severe or critical illness.

[0080] The applicant states that the present invention is intended to illustrate the detailed methods of the present invention through the above-described embodiments, but the present invention is not limited to the above-described detailed methods, that is, it does not mean that the present invention must rely on the above-described detailed methods in order to be implemented. Those skilled in the art should understand that any improvements to the present invention, equivalent substitutions for various raw materials in the products of the present invention, addition of auxiliary ingredients, and selection of specific methods, etc., are all within the scope of protection and disclosure of the present invention.

Claims

1. Use of a marker in the preparation of a viral pneumonia prognosis detection reagent, characterized in that: The marker is prostaglandin E2; the viral pneumonia is pneumonia caused by coronavirus 2019-nCoV infection; the concentration of prostaglandin E2 in urine is positively correlated with the progression of viral pneumonia.

2. The use according to claim 1, characterized in that The prostaglandin E2 is abnormally elevated in the early and middle stages of viral pneumonia.

3. The use of celecoxib in the preparation of a medicament for treating coronavirus 2019-nCoV infection pneumonia, characterized in that, The celecoxib inhibits the increase of prostaglandin E2 in urine; the concentration of prostaglandin E2 is positively correlated with the progression of pneumonia caused by coronavirus 2019-nCoV infection.

4. The use according to claim 3, characterized in that The drug also includes pharmaceutically acceptable excipients.

5. The use according to claim 4, characterized in that The auxiliary material is any one or a combination of at least two of an excipient, a diluent, a carrier, a flavoring agent, a binder and a filler.

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