Q: Once infected, are recovered patients immune?

Answer:

So far, no cases of secondary infection have been reported. COVID-19 specific IgG antibody can be detected in most patients 14 days after symptom onset. (Clin Infect Dis. 2020 Mar 21. pii: ciaa310.).  The probability of reinfection is very low, but the duration of antibody still needs longer observation. However, a few rehabilitation patients did not detect antibodies, these patients need more attention.

Q: What was your criteria for doing echocardiograms in COVID patients?

Answer:

The following COVID19 patients should be considered for echocardiography:


1.  Patients who have basic cardiovascular disease before admission. 

2.  Patients with high risk factors for cardiovascular disease. 

3.  Patients with manifestations of heart failure. 

4.  Patients who have chest pain, palpitation and other symptoms. 

5.  Other tests, such as an electrocardiogram, which suggest heart damage. 

6.  Lab tests suggest cTnI or BNP are significant increased.


Q: Are there any people that are COVID19 positive but have no symptoms?

Answer:

Yes, we did find some of these patients. These patients have no clinical manifestations such as fever, cough, fatigue, diarrhea, poor appetite and so on. There is no typical focus on lung CT. Some patients were detected by nucleic acid test as close contacts, and some patients were diagnosed by IgG positive antibody test when they were treated for other diseases.

Q: When you started caring for the patients, what impressed you most? What is the most unusual or different about starting care for COVID19 patients? How did you know that these cases are more than just the usual bad seaso

Answer:

When I was starting care of the patients, the cruel fact impressed me most, that no special effective drugs could prevent the progress of those severe cases of COVID-19, and the patients were packed into overcrowded hospitals. Any real physician if he sees one severe case of COVID-19, he will know, it is not season flu at all! The imaging of chest CT scan, the rapid progress, the severe ARDS and the super contagious feature all tell us, it is not flu!

Q: Are you recommending that people have....routinely? Or testing positively, when the screening occured? You gave an example of people with chestpain, so naturally we would be thinking about the heart. But your Ch

Answer:

Our routine detection of cTnI and BNP changes in patients did find that these indicators were increased in many patients. But heart events are not common. Autopsy results also do not support direct myocardial damage caused by the COVID-19.At present, the mechanism of myocardial damage (elevated NT-Pro-BNP and cTnI) caused by COVID-19 infection is not much clear. The possible reasons are as follows: 1) direct damage: viral infection can directly cause damage to myocardial cells; 2) immune damage: the excessive activation of the immune system results in an extremely immune response, releasing a large number of cytokines, and the conversion into a triggered cytokine storm may be one of the mechanisms of myocardial damage; 3) Hypoxemia: severe COVID-19 patients affected blood gas due to diffuse alveolar injury and pulmonary clear film formation, leading to severe hypoxemia, sustained hypoxia will increase anaerobic fermentation, cause acidosis, increase intracellular oxygen free radicals, intracellular calcium overload, and cause damage to myocardial cells; 4) Angiotensin converting enzyme 2 (ACE2): currently known as ACE2, an important target for COVID-19 infection, and ACE2 receptors are widely expressed in the cardiovascular system. Therefore, ACE2-related signaling pathways may also cause myocardial damage.

Q: Why the need to do CRP if lymphopenia is sign of poor prognosis? CRP is non-specific for inflammation.

Answer:

In general, COVID-19 patients always had concomitant bacterial infection and sometimes systemic inflammatory storm. CRP could be a measurement for the evaluation of treatment.


Q: The cases in China is very low now. Are you relaxing and what is happening in society now in China?

Answer:

Although the numbers are low, but still more than 4000 cases in Wuhan, and most of the cases are severe or critically ill patients. We are still fighting against the virus. 

During the past two months, the COVID-19 has imposed an enormous impact on our daily life and healthcare. We suspended all elective procedures, ordinary clinics, except for the fever clinic and emergency department. We used the telephonic or telehealth visits substitute for in-person routine visits for chronic diseases patients to avoid nosocomial infection. With the stringent containing measures, now the epidemic has been well contained in China. In Wuhan, there is no new confirmed, suspected cases reported for one week now. In other areas outside of Hubei province, most of things has returned to prior status. For example, in 26 provinces, all the social and life order has restored to normal. All the hospitals and factories re-opened. Most of the schools will re-open one week later.

We really hope the epidemic in the U.S. will be effectively contained soon.


Q: Are you testing stool in all patients? We have not even heard about stool testing here, but I wonder if we are seeing more diarrhea in our patients than in China? It seems to be common, even if respiratory symptoms are

Answer:

Although the common symptoms is fever, fatigue, and dry cough, some patients have diarrhea. For the suspected patients, if the routine nasopharyngeal or throat swab of the NAT test is negative, we’ll perform the anal swab. But we believe that anal swab could get the exactitude results, and then nasopharyngeal, the throat is the lowest.

Q: Are you checking procalcitonin levels in these patients? We wonder if that will help differentiate those with bacterial co-infection

Answer:

Actually, we have tested PCT and found that some patients with uncontrollable body temperature are coinfected with bacterial. After adjusting antibiotics, we achieved better results

Q: The doctor pointed out that the lymphopenia was indicative of a poor prognosis. Did they see further decrease in the lymphocyte count as the disease progressed?

Answer:

Yes, severe or critically ill COVID-19 patients showed that Lymphopenia is positively related with poor prognosis. If the treatment is not working for the patients.  The lymphocyte count will not increase and sometimes decrease when the condition of patients goes rapid deterioration and even death.

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet, undefined(undefined), undefined. doi:10.1016/S0140-6736(20)30566-3


Q: How about crp (c-reactive protein) levels? Are you checking that? And are your patients with high crp levels having worse clinical outcomes?

Answer:

We routinely test CRP. CRP levels were elevated in most patients. CRP level in severe patients can be higher than 100mg / L. CRP level is positively related to the course of disease. CRP monitoring is conducive to disease monitoring and prognosis evaluation

Q: Will recovered patients be immune or they can be infected again?

Answer:

Thus far, there are no evidence showed that recovered patients re-infected with COVID-19. Most physicians believe that the recovered patients are immune because of the antibody (IgG) levels. But we do find a case of a 50-year-old woman with COVID-19 who were treated for one month. Prior to discharge, she received more than 5 times nucleic acid testing, all are negative. But she wants to accompany with her husband (admitted to the same ward), she still isolated in the hospital, 20 days later, her NAT got positive again. We think there are a lot of research need to do to get the answer. 

Q: Are you finding that the degree of CT findings on admission is prognostic of patient outcome? In other words, does the severity of infiltrates on CT correlate to bad clinical outcome and more severe illness?

Answer:

1. CT plays an important role in the diagnosis and evaluation of the severity and extent of the COVID-19 disease

2. There are significant correlations between the degree of pulmonary inflammation and the main clinical

     symptoms and laboratory results.

3. In comparison with other types of pneumonia, COVID-19 seemed to cause milder symptoms and severer pulmonary changes on CT

4. At present, it is not clear whether it has clinical value in evaluating the prognosis of patients.


Q: One thing I find interesting is that I have not heard of any meningitis or encephalitis. Have any physicians in China detected any COVID-19 in the cerebral spinal fluid?

Answer:

I have not heard of this either. All of my patients are conscious, and no symptoms caused us to suspect meningitis or encephalitis, so there was no indication for performing a spinal tap. 

Q: How was the diastolic function? In this case, could the patient with hypoxia be experiencing diastolic dysfunction causing evidence of acute HF? Could this be explained by diastolic heart failure? High ProBNP with norma

Answer:

It is a good question. Yes, diastolic dysfunction is presented in some patients with severe hypoxia. However, not only diastolic dysfunction, but also directly damage of heart by virus, cytokine storm or the patient was associated with cardiovascular disease could cause acute heart failure. COVID-19 currently has a crude mortality rate of 4% in China but a mortality rate of more than 10% in patients combined with cardiovascular disease. Though BNP is not fit for evaluation of diastolic dysfunction, it is still useful for explaining the abnormal systolic function and pulmonary edema in patients with acute heart failure.

Q: Shouldn’t we correlate the heart rate with the patient’s ejection fraction?

Answer:

Yes, heart rate increased significantly with the aggravation of heart failure in patients. Heart rate was easily affected by a variety of factors such as fever, anoxia, or shock. It could not be regarded as an independent evaluation standard for cardiac insufficiency in COVID-19 patients. LVEF is an assessment of the systolic function of the whole body of the heart.  Generally, it is no time limit. However, the decline of the function is not inversely proportional to the increase of the heart rate, though there is inverse trend. Undoubtedly, correlate the heart rate with the patient’s ejection fraction can reflect the changing trend of corresponding index more sensitively, but we didn’t do that according to the routine.

Q: There appears to be apical/periapical dysfunction in a Takostubo’s pattern, but distal segments are not well-visualized.

Answer:

Takotsuko may be caused by catalamine surge, which can lead the contraction of cardiac microvascular. What’s more, the lack of cholinergic nerve in the apex of the heart leads to more severe injury.


COVID pneumonia can causes myocardial injury in many ways: 

1.  Directly infect hear cells, causing myocardial injury

2.  Combined with ACE2 to cause myocardial injury. 

3. Hypoxemia

4. Immune disorder


Now, some COVID19 patients’ heart show apical/periapical dysfunction in a Takostubo’s pattern.  We hypothesize that the causes of similar symptoms of cardiomyopathy in the heart may be as follows: 

1. The diagnosis as COVID pneumonia can be a stress event for patients ,which leads to Takotsuko cardiomyopathy. 

2.  It may be related to the myocardial injury because of the combination of the virus and ACE2, but it still needs to be confirmed by relevant studies.


Q: How about the survival rate of ECMO? What is the indication of the patient who received C-A ECMO? Thank you!

Answer:

Extremely low. Experience were exchanged among difference centers, and the survival rate is about 10-20% in all patients with ECMO. I don’t quite catch what you refer to C-A ECMO. I suppose it V-A ECMO. V-A ECMO is used for patients combined with respiratory failure and cardiac shock. But most ECMO cases received V-V mode.

Q: Which biomarker is the most predictive of patient’s prognosis?

Answer:

Most severe patients with pneumonia had increased D-dimer, IL-6 level and decreased lymphocyte count level which is associated with fatal outcome of COVID-19. 

Reference: Henry Brandon Michael. (2020). COVID-19, ECMO, and lymphopenia: a word of caution. Lancet Respir Med, undefined(undefined), undefined. doi:10.1016/S2213-2600(20)30119-3

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet, undefined(undefined), undefined. doi:10.1016/S0140-6736(20)30566-3


Q: Is there any data on the incidence of death in patients with HTN on ACE/ARB versus those not on ACE/ARB? That is, is the cause of increased mortality in HTN patients due not to the disease but the medications we are usin

Answer:

A retrospective analysis in our hospital found that there was no statistical difference in ACEI / ARB utilization rate (18 / 95 vs 4 / 17) between the cured group and the dead group. But this is only a cross-sectional study, which is not enough to answer this question

Q: Should cardiac troponin measurements be obtained routinely for risk stratification in these patients?

Answer:

TnI or TnT has been routinely tested after admission to monitor myocardial ischemia. Elevation of cardiac troponin has also been found in many COVID-19 patients. We have done a retrospective study about the relationship between fatal outcomes and elevation of TnT for COVID-19 patients. The results imply that elevation of TnT plays a crucial role in the fatal outcome of COVID-19. Elevation of TnT results in the impairment of cardiac function and malignant arrhythmia. Furthermore, the mortality of COVID-19 patients with elevation of TnT is high. So we think that cardiac troponin can be used as a stratified management test for COVID-19 patients.

Q: We have heard reports of delayed arrhythmia and cardiovascular collapse as patients begin to recover from respiratory symptoms. Have you seen this and do you have special recommendations for rhythm management?

Answer:

In our hospital, about 20% of patients will have cardiovascular damage,  It is caused by hypoxia, or by the direct damage of virus. In particular, we need to be alert to the occurrence of fulminant myocarditis. Even among the recovered  patients, we have also observed that some patients have heart function decline. This is worthy of further study. Therefore, we should pay attention to the treatment of myocardial protection while we treated the novel coronavirus pneumonia.

Q: Is there a resource with a protocol for directing care from suspected COVID-19 patients, so that they are triaged into appropriate care? (eg. Not infected, infected outpatient quarantine, inpatient observation, critical

Answer:

People suspected of being infected by COVID-19 should accept virus test ASAP. If the test result is positive, they should be immediately quarantined or admitted to the hospital for treatment. If the test result is negative (at least twice repeatedly), they will can go home for isolation. If the virus tests of the patient are negative (at least twice repeatedly) after the treatment, they will be discharged from the hospital to the isolation point for medical observation for another two weeks, then go back home if there are no recurrence of symptoms.

Q: I noticed that there is high elevated of D-dimer in all patients, especially in severe cases and in patients who have died. What is the mechanism of thrombrosis and that it impacts the whole body with the onseet of COVID

Answer:

Pathological anatomy has confirmed the existence of thrombosis.  We also found that some patients have deep vein thrombosis in the lower extremity. In some COVID-19 patients, the disease worsened suddenly, D-dimer increased significantly, and patients even died suddenly. In this regard, we should pay attention to whether there is pulmonary thromboembolism (PTE) after the fall off of deep vein thrombosis (DVT). It is suggested that in the process of prevention and treatment of COVID-19, the risk of venous thromboembolism (VTE) should be assessed, and effective prevention should be carried out for high-risk patients. Patients with sudden deterioration of oxygenation, respiratory distress, blood pressure drop and other clinical manifestations should be alert to the occurrence of PTE and be treated in time.

Q: You gave an example of people with chest pain, so naturally we would be thinking about the heart. But your Chinese colleagues are reporting to us a very high rate of cardiac involvement. I think most cardiologists in th

Answer:

Our routine detection of cTnI and BNP changes in patients did find that these indicators were increased in many patients. But heart events are not common. Autopsy results also do not support direct myocardial damage caused by  COVID-19.  At present, the mechanism of myocardial damage (elevated NT-Pro-BNP and cTnI) caused by COVID-19 infection is not much clear. The possible reasons are as follows: 


1) Direct damage: viral infection can directly cause damage to myocardial cells

2)  Immune damage: the excessive activation of the immune system results in an extreme immune response, releasing a large number of cytokines, and the conversion into a triggered cytokine storm may be one of the mechanisms of myocardial damage

3) Hypoxemia: severe COVID-19 patients affected blood gas due to diffuse alveolar injury and pulmonary clear film formation, leading to severe hypoxemia, sustained hypoxia will increase anaerobic fermentation, cause acidosis, increase intracellular oxygen free radicals, intracellular calcium overload, and cause damage to myocardial cells

4) Angiotensin converting enzyme 2 (ACE2): currently known as ACE2, an important target for COVID-19 infection, and ACE2 receptors are widely expressed in the cardiovascular system. Therefore, ACE2-related signaling pathways may also cause myocardial damage.


Q: Among patients who are positive in respiratory tract sample, are those patients also having positive stool tests?

Answer:

Yes, we have detected the new coronavirus nucleic acid from the stool of some patients, but not every one.  


1.  Prior to respiratory symptoms--many patients reported diarrhea and abdominal discomfort. 

2.  COVID-19 has been isolated from feces of multiple patients in China.

3. Of 73 patients, 39 tested positive in the stool (10-78 years of age)

4. Duration of positive stool was 1-12 days. 

5. 17 patients remained positive in the stool even after negative respiratory samples


Q: Another colleague is wondering about patients' fever curve in your experience. Our first patient had very high fever up to 42 in the last day before he quickly decompensated and died. Do you typically see this?

Answer:

The most common symptoms were fever (98%). Among 52 critically ill patients, six (11%) did not experienced fever until  2–8 days after the onset of symptoms related to SARS-CoV-2 infection.(You Shang,Lancet Respir Med 2020)

Fever was present in 43.8% of the patients on admission but developed in 88.7% during hospitalization.  (Nanshan Zhong N Engl J Med. 2020 Feb 28.) 

The most common symptoms at onset of illness were fever (40 [98%] of 41 patients) ( Bin Cao, Lancet 2020; 395: 497–506)


Q: We also are seeing in our first patients who are in intensive care on ventilators that they are staying clinically at the same place for days- no improvement like we would see with bacterial pneumonia. In your experience

Answer:

Yes, I share your concerns. I had a patient with a prolonged clinical course. He was on a non-invasive mechanical ventilator for about 30 days. At that time he had severe respiratory failure so that he couldn’t eat without the ventilator. Afterwards, we gave him enteral nutrition to reduce the weaning time as much as possible. After 10 days, we stopped the anti-virus medicine arbidol, prescribed only steroid and intravenous immunoglobulin, gradually he had no fever, and was weaned from respiratory support. Because he was 57 years old and strong, he was able to expectorate and clear his own secretions. As a side note, sputum of COVID-19 patients is very sticky and can’t be expectorated easily. We were thankful to be able to avoid intubation, which would increase the risk of ventilator-related injuries. So in summary, this virus infection is a self-limited process.  During the process, mechanical ventilation is a tool to help the patients get through the acute danger of respiratory failure. With time, respiratory function should begin to improve, and the ventilator can be weaned gradually. So in my opinion, anti-virus medications are not the most important treatment. And up to this point, the results of remdesevir research haven’t been convincing. 

Q: It is interesting because we have seen a couple of patients already develop a new cardiomyopathy. I wonder if the elevated troponins you are seeing are more from demand ischemia? Are you doing echocardiograms and seeing

Answer:

Among my patients, the elevated troponin is one of the most important negative prognostic indicators. However, the patients who have elevated troponins don’t show hypokinesis related to myocardial infarction and ECG changes from demand ischemia. I think the myocardial injury is another manifestation of multiple organ dysfunction caused by coronavirus. On the other hand, I do suspect that the coronavirus may have a predilection for attacking the myocardium over the liver and kidney. Additionally, the general duration of the virus is about 30-40 days, while the elevation of troponin always begin at the 10th day. Greater elevation in troponins is also clearly correlated with a worsening prognosis, so the protection of heart is necessary. 

Q: Are you doing echocardiograms and seeing new hypokinesis and reduced ejection fraction on COVID19 patients? We are finding this I think in a couple of the initial patients.

Answer:

We did do echocardiograms for almost every patient, but most patients have normal echocardiograms with no evidence of new hypokinesis or reduced ejection fraction at all. Only individual patients had reduced ejection fraction. There were isolated patients with reduced ejection fraction, but these recovered rapidly as troponins decreased. So most ECG are normal, with isolated cases showing sinus tachycardia, or T wave inversion in precordial leads, but no dynamic evolution. 

Q: I have several questions to ask you. My colleague may also add additional questions. We work in a community hospital. Now we have > 70 patients and 12 death. Our CT scan is limited. This is because we do not have a ci

Answer:

Thank you for your questions. For question one, CT scan may be required in the following situations:

(1) To determine the confirmed cases:The nucleic acid detection for COVID-19 is important but not sensitive. It might be negative repeatedly even in those severe COVID-19 patients required for ventilator support,and CT scan could help in the situation. The antibody test for COVID-19 also helps if it is available. In the guideline of China, the suspected cases can be exclude if the IgM is still negative after 7 days.

(2) To determine discharge home for admitted patients: We did not use the CT scan to determine admission or discharge home for mild patients (which mainly depends on the symptom and whether they suffer from hypoxia). We use symptom, nucleic acid detection and CT scan to codetermine which admitted patient could be discharged, when nucleic acid detection is not sensitive. Besides, I believe the antibody test could help if CT scan is not available. CT scan contributes to following progression, but it is not necessary. The change of arterial blood gas analysis is more important. The lymphocyte is also important. Progressive lymphocyte decrease is very common in those severe patients, which means severe secondary bacterial infection is highly likely.


Q: What’s the role D-dimer?

Answer:

Because of the damage of alveoli and capillaries in the COVID-19 patients, we can see the formation of pulmonary microthrombus of the autopsy results of the patients. At the same time, microthrombus formation has also been observed in the blood vessels of critically ill patients, so the d-dimer is generally high in all patients. The results of our retrospective study showed that elevation of the D-dimer level was more significant in the non-survivors, and was an independent risk factor of death. If these patients have no contraindications for anticoagulants, we would recommend the routine use of low molecular weight heparin as an anticoagulant for critically ill patients. For critical COVID-19 patients who need to be bedridden for a long time or who are on a non-invasive/invasive mechanical ventilation ventilator, anticoagulants should be routinely used to prevent thrombosis in the lower extremities and pulmonary thrombosis.

Q: Are there any recommendations like scoring to predicts the critical conditions? Before the shock and all happen?

Answer:

We should pay more attention to the moderate cases with persistent high fever, old age, serious basic diseases, persistent lymphocytopenia and rapid progress of lung CT before and after contrast, and pay more attention to prevent them from developing into severe patients.  Most severe patients with pneumonia had increased D-dimer, IL-6 level and decreased lymphocyte count level which is associated with fatal outcome of COVID-19.

Q: The doctor pointed out that the lymphopenia was indicative of a poor prognosis. Did they see further decrease in the lymphocyte count as the disease progressed?

Answer:

Yes, severe or critically ill COVID-19 patients showed that Lymphopenia is positively related with poor prognosis. If the treatment is not working for the patients.  The lymphocyte count will not increase and sometimes decrease when the condition of patients goes rapid deterioration and even death.

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet, undefined(undefined), undefined. doi:10.1016/S0140-6736(20)30566-3


Q: Why the need to do CRP if lymphopenia is sign of poor prognosis? CRP is non-specific for inflammation.

Answer:

In general, COVID-19 patients always had concomitant bacterial infection and sometimes systemic inflammatory storm. CRP could be a measurement for the evaluation of treatment.

Q: The reason of increased D-dimmer?

Answer:

The coagulation function in patients with SARS-CoV-2 is significantly deranged compared with healthy people, but monitoring D-dimer and FDP values may be helpful for the early identification of severe cases.

Q: Liver dysfunction?

Answer:

Answer:There are four major reasons for liver injury associated with COVID-19: 1) immune damage; 2) drug use; 3) systemic inflammation; 4) ischemic hypoxia-reperfusion injury.

Q: When you do echo, the heart function is still ok. The COVID-19 patient changes too fast. In this situation, when you have the laptest, the elevated pro-BMP, the echo examine are at the same period. Could it explain?

Answer:

In severe COVID-19 patients, although cTnI is often elevated, while the heart function is not severely impaired. Such as severe COVID-19 patients received ecmo, we usually apply VV-ECMO, but not VA-ECMO, because the blood pressure could be maintained.

Q: Do you have any dynamic risk scores for COVID-19 patients?

Answer:

We don’t have detailed dynamic risk scores for COVID-19 patients. A confirmed case is based on epidemiological history (including cluster transmission), clinical manifestations (fever and respiratory symptoms), lung imaging, and results of COVID-19 nucleic acid detection and serum-specific antibodies. We use clinical classifications to determine the degree of risk for patients. Confirmed cases include mild cases, moderate cases, severe cases and critical cases, critical cases are further divided into early, middle and late stages according to the oxygenation index and compliance of respiratory system.

Q: Is that just elder people go to hospital? Any strong relationship bwtween age and outcome?

Answer:

The age of inpatient ranged from 20s to 90s in our hospital. In our department, we have received 80 patients, 26 cases for≥65 years old (32.5%) and 17 for ≥70 (21.25%). The age of all fatality patients were ≥65 years old in our hospital, the duration for the COVID-19 RNA negative and pulmonary inflammation absorption was much longer for old patients then young patients. Recent online report also showed similar result (https://www.cdc.gov/mmwr/volumes/69/wr/mm6912e2.htm). Therefore, we agree that there is strong relationship between age and outcome.

Q: We have heard in the news that Wuhan has reinstated travel restrictions due to concerns over new asymptomatic cases. Can you tell us about this situation regarding asymptomatic cases?

Answer:

So far we have found more than 100 asymptomatic cases in Wuhan, especially in my hospital.  Even if there were no symptoms, they have some signs and were at high risk of getting infected.  For example, the cleaning people in Wuhan's hospitals.  We are doing testing for every high risk close contact person to avoid a second wave of the epidemic.

Q: Is serology antibody testing important for IgG?

Answer:

IgM can be detected 5-7 days after symptom onset and lasts for about 1 month. IgM positive patients are infected within 1 month, so it is necessary to eliminate its infectivity according to nucleic acid detection. IgG can be detected 7-14 days after onset and last for months or longer. IgM negative and IgG positive people who have been infected with COVID-19 will not be re-infected.

Q: What’s your experience with chloroquine and z-pack?

Answer:

I didn't combine the two drugs. However, several patients with persistent positive nucleic acids turned negative after 7 days (200mg / D) administration of hydroxychloroquine(200mg / d). Preliminary results from a multicenter clinical study showed the efficacy and safety of hydroxychloroquine.

Q: Do you have experience with gen1 rapid COVID19 IgG/IgM serum tests vs gen2 tests?

Answer:

I don't know about antibody test reagents. However, some of my NCP cured colleagues' IgM were weak positive continuously, and I think this may be a non-specific result caused by interfering substances in serum.