clinical observations of low molecular weight heparin in relieving inflammation in CORD-Papers-2021-10-25 (Version 1)

Title: Clinical observations of low molecular weight heparin in relieving inflammation in COVID-19 patients: A retrospective cohort study
Abstract: Abstract: Background On March 11, 2020, the World Health Organization declared its assessment of COVID-19 as a global pandemic. Effective therapeutic drugs are urgently needed to improve the overall prognosis of patients, but currently no such drugs are available. Methods Patients in the study were divided into a heparin and a control group based on whether low molecular weight heparin (LMWH) was used. D-dimer, C-reactive protein (CRP), peripheral blood lymphocyte percentage, interleukin-6, and other indices in 42 patients with novel coronavirus pneumonia were retrospectively analyzed to compare and evaluate the progress of patients before and after LMWH treatment. Results Compared to the control group, D-dimer levels in the heparin group significantly increased before treatment, and there was no significant difference after treatment. There was no significant difference in the change of CRP levels between the two groups of patients before and after LMWH treatment, and levels for both groups were significantly lower after, compared to before, treatment. Compared to the control group, patients in the heparin group had a higher percentage of lymphocytes after treatment and lower levels of interleukin-6; these differences were statistically significant. Conclusions Under conventional antiviral treatment regimens, LMWH can improve hypercoagulability, inhibit IL-6 release, and counteract IL-6 biological activity in patients. LMWH has potential antiviral effects and can help delay or block inflammatory cytokine storms. It can also increase the lymphocytes (LYM%)of patients and has the potential for treatment of COVID-19.
Published: 4/1/2020
DOI: 10.1101/2020.03.28.20046144
DOI_URL: http://doi.org/10.1101/2020.03.28.20046144
Author Name: SHI, C
Author link: https://covid19-data.nist.gov/pid/rest/local/author/shi_c
Author Name: WANG, C
Author link: https://covid19-data.nist.gov/pid/rest/local/author/wang_c
Author Name: WANG, H
Author link: https://covid19-data.nist.gov/pid/rest/local/author/wang_h
Author Name: YANG, C
Author link: https://covid19-data.nist.gov/pid/rest/local/author/yang_c
Author Name: CAI, F
Author link: https://covid19-data.nist.gov/pid/rest/local/author/cai_f
Author Name: ZENG, F
Author link: https://covid19-data.nist.gov/pid/rest/local/author/zeng_f
Author Name: CHENG, F
Author link: https://covid19-data.nist.gov/pid/rest/local/author/cheng_f
Author Name: LIU, Y
Author link: https://covid19-data.nist.gov/pid/rest/local/author/liu_y
Author Name: ZHOU, T
Author link: https://covid19-data.nist.gov/pid/rest/local/author/zhou_t
Author Name: DENG, B
Author link: https://covid19-data.nist.gov/pid/rest/local/author/deng_b
Author Name: LI, J
Author link: https://covid19-data.nist.gov/pid/rest/local/author/li_j
Author Name: ZHANG, Y
Author link: https://covid19-data.nist.gov/pid/rest/local/author/zhang_y
sha: d8a3c1fcef5f6368eb1d55864373bb44c19b7db8
license: medrxiv
source_x: MedRxiv; WHO
source_x_url: https://www.who.int/
url: https://doi.org/10.1101/2020.03.28.20046144 http://medrxiv.org/cgi/content/short/2020.03.28.20046144v1?rss=1
has_full_text: TRUE
Keywords Extracted from Text Content: D-dimer heparin Patients COVID-19 patients CRP lymphocytes IL-6 peripheral blood lymphocyte interleukin-6 coronavirus LMWH b p SARS-CoV-2 surface protein electrolytes sputum IFN-γ C-reactive HSR1 Derhaschnig INR fibrinogen lymphocytes (LYM%)as IL-4 patient COVID-19 kidney lymphocytes organ NF-κB lymphocyte Hubei . Mycroft-West Figure 2G monocyte% SIL-6R FC IL-10 plasma AT 46 patients chest cardiovascular https://doi.org/10.1101/2020.03.28.20046144 Figure 2O CRP bbb p IL-2 Wuhan CY FZ medRxiv preprint women D-dimer TNFα WBC coronavirus ccc p heparin lactate dehydrogenase platelets C3 glycosaminoglycan non-anticoagulant FIB IL- 6 medRxiv preprint APTT IL-6 heart sodium d-dimer Coronavirus platelet H3 TNF-α serum blood ATIII Registry,number c p human body LMWH PT BD kidneys nuclear factor κB SARS-CoV-2 RBC TT APC FDP medRxiv sgp130 enoxaparin carcinomas anorexia liver
Extracted Text Content in Record: First 5000 Characters:Background On March 11, 2020, the World Health Organization declared its assessment of COVID-19 as a global pandemic. Effective therapeutic drugs are urgently needed to improve the overall prognosis of patients, but currently no such drugs are available. Methods Patients in the study were divided into a heparin and a control group based on whether low molecular weight heparin (LMWH) was used. D-dimer, C-reactive protein (CRP), peripheral blood lymphocyte percentage, interleukin-6, and other indices in 42 patients with novel coronavirus pneumonia were retrospectively analyzed to compare and evaluate the progress of patients before and after LMWH treatment. Compared to the control group, D-dimer levels in the heparin group significantly increased before treatment, and there was no significant difference after treatment. There was no significant difference in the change of CRP levels between the two groups of patients before and after LMWH treatment, and levels for both groups were significantly lower after, compared to before, treatment. Compared to the control group, patients in the heparin group had a higher percentage of lymphocytes after treatment and lower levels of interleukin-6; these differences were statistically significant. Conclusions Under conventional antiviral treatment regimens, LMWH can improve hypercoagulability, inhibit IL-6 release, and counteract IL-6 biological activity in patients. LMWH has potential antiviral effects and can help delay or block inflammatory cytokine storms. It can also increase the lymphocytes (LYM%)of patients and has the potential for treatment of COVID-19. Coronavirus is an enveloped, non-segmented, positive-sense, single-stranded RNA virus that causes common colds and severe respiratory diseases, 1 such as Middle East respiratory syndrome (MERS) 2 and severe acute respiratory syndrome (SARS) 2 . In December 2019, a series of unexplained pneumonia cases appeared in Wuhan, Hubei . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. The copyright holder for this preprint this version posted April 1, 2020. . https://doi.org/10.1101/2020.03.28.20046144 doi: medRxiv preprint Province, China, and their clinical manifestations suggested viral pneumonia. 4 Deep sequencing of lower respiratory tract samples identified a novel coronavirus named SARS-CoV-2 and the disease it caused was named COVID-19. 5 Its clinical manifestations include fever, cough, sputum, chest distress or asthma, fatigue, myalgia, diarrhea, nausea, and vomiting. 6, 7, 8 Severe cases may progress rapidly to acute respiratory distress syndrome, metabolic acidosis, septic shock, coagulopathy, and organ failure (e.g., liver, kidneys, and heart), which all pose a serious threat to human health. On March 11, 2020 , the World Health Organization (WHO) declared its assessment of COVID-19 as a global pandemic. SARS-CoV-2 is characterized by a long incubation period, high infectivity, and multiple routes of transmission. 9, 10 According to real-time WHO statistics, the total number of confirmed cases of COVID-19 worldwide as of March 28, 2020 has exceeded 600,000, with more than 28,000 deaths. However, no effective medicines are currently available, and it can only be treated symptomatically. As the worldwide patient base continues to expand and the number of severely and critically ill patients increases rapidly, determining the mechanism through which patients progress from mild to severe and from severe to critical is the main avenue for discovering effective treatment strategies. Lymphopenia and inflammatory cytokine storms are typical abnormalities observed in highly pathogenic coronavirus infections (such as SARS and MERS), 12 and are believed to be associated with disease severity. 12, 13, 14 Multiple studies have shown that cytokine storms are important mechanisms of disease exacerbation and death in patients with COVID-19. 12, 13, 14 IL-6 levels are significantly higher in severely ill patients with COVID-19 compared to those with mild cases. 15 A cytokine storm may occur when cytokines reach a certain threshold in the body. 16 Reducing the release or activity of IL-6 can prevent or even reverse the cytokine storm syndrome caused by the virus, thereby improving the condition of patients with COVID-19. In recent years, a large number of studies have revealed that low molecular weight heparin (LMWH) has various non-anticoagulant properties that play an anti-inflammatory role by reducing the release and biological activity of IL- 6. 17,18,19 . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. The copyright holder for this preprint this version posted April 1, 2020. . https://doi.org/10.1101/2020.03.28.20046144 doi: medRxiv preprint However, the anti-inflammatory effects of LMWH in COVID-19
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