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1.
Clin Appl Thromb Hemost ; 27: 10760296211051764, 2021.
Article in English | MEDLINE | ID: covidwho-1511654

ABSTRACT

The precise mechanisms of pathology in severe COVID-19 remains elusive. Current evidence suggests that inflammatory mediators are responsible for the manifestation of clinical symptoms that precedes a fatal response to infection. This review examines the nature of platelet activating factor and emphasizes the similarities between the physiological effects of platelet activating factor and the clinical complications of severe COVID-19.


Subject(s)
COVID-19/metabolism , Platelet Activating Factor/metabolism , Animals , COVID-19/complications , COVID-19/mortality , COVID-19/pathology , Humans , Inflammation/complications , Inflammation/metabolism , Inflammation/mortality , Inflammation/pathology , Multiple Organ Failure/complications , Multiple Organ Failure/metabolism , Multiple Organ Failure/mortality , Multiple Organ Failure/pathology , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/metabolism , Respiratory Distress Syndrome/mortality , Respiratory Distress Syndrome/pathology , SARS-CoV-2/physiology , Severity of Illness Index , Thrombosis/complications , Thrombosis/metabolism , Thrombosis/mortality , Thrombosis/pathology
3.
PLoS One ; 16(10): e0258684, 2021.
Article in English | MEDLINE | ID: covidwho-1480452

ABSTRACT

AIMS: Patients with cardiovascular comorbidities have a significantly increased risk for a critical course of COVID-19. As the SARS-CoV2 virus enters cells via the angiotensin-converting enzyme receptor II (ACE2), drugs which interact with the renin angiotensin aldosterone system (RAAS) were suspected to influence disease severity. METHODS AND RESULTS: We analyzed 1946 consecutive patients with cardiovascular comorbidities or hypertension enrolled in one of the largest European COVID-19 registries, the Lean European Open Survey on SARS-CoV-2 (LEOSS) registry. Here, we show that angiotensin II receptor blocker intake is associated with decreased mortality in patients with COVID-19 [OR 0.75 (95% CI 0,59-0.96; p = 0.013)]. This effect was mainly driven by patients, who presented in an early phase of COVID-19 at baseline [OR 0,64 (95% CI 0,43-0,96; p = 0.029)]. Kaplan-Meier analysis revealed a significantly lower incidence of death in patients on an angiotensin receptor blocker (ARB) (n = 33/318;10,4%) compared to patients using an angiotensin-converting enzyme inhibitor (ACEi) (n = 60/348;17,2%) or patients who received neither an ACE-inhibitor nor an ARB at baseline in the uncomplicated phase (n = 90/466; 19,3%; p<0.034). Patients taking an ARB were significantly less frequently reaching the mortality predicting threshold for leukocytes (p<0.001), neutrophils (p = 0.002) and the inflammatory markers CRP (p = 0.021), procalcitonin (p = 0.001) and IL-6 (p = 0.049). ACE2 expression levels in human lung samples were not altered in patients taking RAAS modulators. CONCLUSION: These data suggest a beneficial effect of ARBs on disease severity in patients with cardiovascular comorbidities and COVID-19, which is linked to dampened systemic inflammatory activity.


Subject(s)
Angiotensin Receptor Antagonists/administration & dosage , COVID-19 , Hypertension , Registries , SARS-CoV-2/metabolism , Adult , Aged , Aged, 80 and over , Angiotensin-Converting Enzyme Inhibitors/administration & dosage , Biomarkers/blood , COVID-19/blood , COVID-19/drug therapy , COVID-19/mortality , Comorbidity , Disease-Free Survival , Female , Humans , Hypertension/blood , Hypertension/drug therapy , Hypertension/mortality , Inflammation/blood , Inflammation/drug therapy , Inflammation/mortality , Male , Middle Aged , Severity of Illness Index , Survival Rate
4.
Jpn J Infect Dis ; 74(4): 307-315, 2021 Jul 21.
Article in English | MEDLINE | ID: covidwho-1323440

ABSTRACT

Steroids are expected to be effective in the treatment of cytokine release syndrome, which is considered to be associated with severe cases of coronavirus disease 2019 (COVID-19). We aimed to investigate the use of steroids and its effects. We conducted a retrospective chart review and an analysis of 226 consecutive hospitalized patients with confirmed COVID-19. Patients were divided into those who received steroids (steroid group) and those who did not (no steroid group). Inverse probability weighted analysis was performed to assess the effect of steroids on in-hospital mortality. The steroid group had higher rates of preexisting hypertension and peripheral vascular disease as well as higher lactate dehydrogenase levels, d-dimer levels, and inflammatory markers than the no steroid group (all P <0.05). The steroid group had significantly higher rates of multifocal pneumonia than the no steroid group at admission (75.4% vs. 50.3%, P = 0.001). Notably, the steroid group had higher rates of developing bacterial infection (25% vs. 13.1%, P = 0.041) and fungal infection (12.7% versus 0.7%, P <0.001) during the hospital course than the no steroid group. After adjustment, it was observed that steroids did not decrease or increase in-hospital mortality (odds ratio [95% confidence interval]: 1.02 [0.60-1.73, P = 0.94]). There was an increase in bacterial and fungal infections with steroid use.


Subject(s)
COVID-19/epidemiology , Coinfection/epidemiology , Bacterial Infections/mortality , COVID-19/mortality , Coinfection/mortality , Female , Hospital Mortality , Hospitalization , Humans , Inflammation/mortality , Inflammation/virology , Male , Middle Aged , Mycoses/mortality , New York City/epidemiology , Retrospective Studies , SARS-CoV-2/pathogenicity , Steroids/therapeutic use
5.
Ann Vasc Surg ; 74: 80-87, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1163382

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) causes thromboembolic complications during or post-infection period despite a lack of conventional risk factors. The study aims to learn fundamental changes in COVID-19 patients who underwent embolectomy in terms of clinical characteristics and clot composition. METHODS: In a retrospective cohort study design, we evaluated 21 patients who underwent embolectomy in our clinic between March 12, 2020, and December 31, 2020. Demographics, characteristics, and laboratory values were abstracted and analyzed. Histopathological assessment was held in the pathology department. RESULTS: Of these 21 patients, 11 (52.3%) were SARS-CoV-2 positive and 10 (47.6%) were SARS-CoV-2 negative. There is no statistical difference in terms of anatomic distribution, diagnostic method, length of hospital stay, amputation or mortality levels. Thromboembolic material of COVID-19 patients include significantly less red blood cell (RBC) (21.2-32.6%; P= 0.01), more lymphocyte (14.1-2.6%; P< 0.001), and more leukocyte (27.1-22.1%; P= 0.05). There was no statistical difference between the fibrin ratio. CONCLUSIONS: Inflammatory cells are prominent in arterial thromboembolic material of COVID-19 patients. A combination of hyperinflammation and prothrombotic status may be responsible for this phenomenon.


Subject(s)
COVID-19/complications , Inflammation/pathology , Peripheral Arterial Disease/pathology , Thromboembolism/pathology , Adult , Aged , Aged, 80 and over , Amputation , COVID-19/diagnosis , COVID-19/mortality , Embolectomy , Female , Humans , Inflammation/etiology , Inflammation/mortality , Inflammation/surgery , Length of Stay , Limb Salvage , Male , Middle Aged , Peripheral Arterial Disease/etiology , Peripheral Arterial Disease/mortality , Peripheral Arterial Disease/surgery , Retrospective Studies , Risk Assessment , Risk Factors , Thromboembolism/etiology , Thromboembolism/mortality , Thromboembolism/surgery , Time Factors , Treatment Outcome
6.
Chest ; 159(5): 1793-1802, 2021 05.
Article in English | MEDLINE | ID: covidwho-1046526

ABSTRACT

BACKGROUND: Corticosteroid therapy is used commonly in patients with COVID-19, although its impact on outcomes and which patients could benefit from corticosteroid therapy are uncertain. RESEARCH QUESTION: Are clinical phenotypes of COVID-19 associated with differential response to corticosteroid therapy? STUDY DESIGN AND METHODS: Critically ill patients with COVID-19 from Tongji Hospital treated between January and February 2020 were included, and the main exposure of interest was the administration of IV corticosteroids. The primary outcome was 28-day mortality. Marginal structural modeling was used to account for baseline and time-dependent confounders. An unsupervised machine learning approach was carried out to identify phenotypes of COVID-19. RESULTS: A total of 428 patients were included; 280 of 428 patients (65.4%) received corticosteroid therapy. The 28-day mortality was significantly higher in patients who received corticosteroid therapy than in those who did not (53.9% vs 19.6%; P < .0001). After marginal structural modeling, corticosteroid therapy was not associated significantly with 28-day mortality (hazard ratio [HR], 0.80; 95% CI, 0.54-1.18; P = .26). Our analysis identified two phenotypes of COVID-19, and compared with the hypoinflammatory phenotype, the hyperinflammatory phenotype was characterized by elevated levels of proinflammatory cytokines, higher Sequential Organ Failure Assessment scores, and higher rates of complications. Corticosteroid therapy was associated with a reduced 28-day mortality (HR, 0.45; 95% CI, 0.25-0.80; P = .0062) in patients with the hyperinflammatory phenotype. INTERPRETATION: For critically ill patients with COVID-19, corticosteroid therapy was not associated with 28-day mortality, but the use of corticosteroids showed significant survival benefits in patients with the hyperinflammatory phenotype.


Subject(s)
Adrenal Cortex Hormones/therapeutic use , COVID-19 , Critical Illness , Inflammation , Aged , COVID-19/complications , COVID-19/immunology , COVID-19/mortality , COVID-19/therapy , China/epidemiology , Critical Care/methods , Critical Care/statistics & numerical data , Critical Illness/mortality , Critical Illness/therapy , Female , Humans , Inflammation/mortality , Inflammation/therapy , Male , Middle Aged , Mortality , Organ Dysfunction Scores , Outcome and Process Assessment, Health Care , SARS-CoV-2 , Severity of Illness Index
7.
Clin Immunol ; 223: 108631, 2021 02.
Article in English | MEDLINE | ID: covidwho-919716

ABSTRACT

Although the starting event in COVID-19 is a viral infection some patients present with an over-exuberant inflammatory response, leading to acute lung injury (ALI) and adult respiratory distress syndrome (ARDS). Since IL-6 plays a critical role in the inflammatory response, we assessed the efficacy and safety of tocilizumab (TCZ) in this single-centre, observational study in all Covid-19 in-patient with a proven SARS-CoV-2 rapidly progressing infection to prevent ALI and ARDS. 104 patients with COVID-19 treated with TCZ had a lower mortality rate (5·8%) compared with the regional mortality rate (11%), hospitalized patient's mortality (10%), and slightly lower than hospitalized patients treated with our standard of care alone (6%). We found that TCZ rapidly decreased acute phase reactants, ferritin and liver release of proteins. D-Dimer decreased slowly. We did not observe specific safety concerns. Early administration of IL6-R antagonists in COVID-19 patients with impending hyperinflammatory response, may be safe and effective treatment to prevent, ICU admission and further complications.


Subject(s)
Acute Lung Injury/drug therapy , Antibodies, Monoclonal, Humanized/therapeutic use , COVID-19/drug therapy , Cytokine Release Syndrome/drug therapy , Inflammation/drug therapy , Respiratory Distress Syndrome/drug therapy , SARS-CoV-2/physiology , Acute Lung Injury/mortality , Aged , COVID-19/mortality , Cohort Studies , Cytokine Release Syndrome/mortality , Female , Ferritins/metabolism , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Inflammation/mortality , Male , Middle Aged , Receptors, Interleukin-6/immunology , Respiratory Distress Syndrome/mortality , Survival Analysis
9.
Front Immunol ; 11: 558898, 2020.
Article in English | MEDLINE | ID: covidwho-874473

ABSTRACT

The dysregulated release of cytokines has been identified as one of the key factors behind poorer outcomes in COVID-19. This "cytokine storm" produces an excessive inflammatory and immune response, especially in the lungs, leading to acute respiratory distress (ARDS), pulmonary edema and multi-organ failure. Alleviating this inflammatory state is crucial to improve prognosis. Pro-inflammatory factors play a central role in COVID-19 severity, especially in patients with comorbidities. In these situations, an overactive, untreated immune response can be deadly, suggesting that mortality in COVID-19 cases is likely due to this virally driven hyperinflammation. Administering immunomodulators has not yielded conclusive improvements in other pathologies characterized by dysregulated inflammation such as sepsis, SARS-CoV-1, and MERS. The success of these drugs at reducing COVID-19-driven inflammation is still anecdotal and comes with serious risks. It is also imperative to screen the elderly for risk factors that predispose them to severe COVID-19. Immunosenescence and comorbidities should be taken into consideration. In this review, we summarize the latest data available about the role of the cytokine storm in COVID-19 disease severity as well as potential therapeutic approaches to ameliorate it. We also examine the role of inflammation in other diseases and conditions often comorbid with COVID-19, such as aging, sepsis, and pulmonary disorders. Finally, we identify gaps in our knowledge and suggest priorities for future research aimed at stratifying patients according to risk as well as personalizing therapies in the context of COVID19-driven hyperinflammation.


Subject(s)
Betacoronavirus/immunology , Coronavirus Infections/immunology , Cytokines/immunology , Pneumonia, Viral/immunology , Respiratory Distress Syndrome/immunology , COVID-19 , Coronavirus Infections/mortality , Humans , Immunologic Factors/immunology , Immunologic Factors/therapeutic use , Inflammation/drug therapy , Inflammation/immunology , Inflammation/mortality , Pandemics , Pneumonia, Viral/mortality , Respiratory Distress Syndrome/mortality , Respiratory Distress Syndrome/pathology , Respiratory Distress Syndrome/virology , SARS-CoV-2
10.
Cardiovasc Res ; 116(14): 2197-2206, 2020 12 01.
Article in English | MEDLINE | ID: covidwho-872983

ABSTRACT

The high mortality rate of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection is a critical concern of the coronavirus disease 2019 (COVID-19) pandemic. Strikingly, men account for the majority of COVID-19 deaths, with current figures ranging from 59% to 75% of total mortality. However, despite clear implications in relation to COVID-19 mortality, most research has not considered sex as a critical factor in data analysis. Here, we highlight fundamental biological differences that exist between males and females, and how these may make significant contributions to the male-biased COVID-19 mortality. We present preclinical evidence identifying the influence of biological sex on the expression and regulation of angiotensin-converting enzyme 2 (ACE2), which is the main receptor used by SARS-CoV-2 to enter cells. However, we note that there is a lack of reports showing that sexual dimorphism of ACE2 expression exists and is of functional relevance in humans. In contrast, there is strong evidence, especially in the context of viral infections, that sexual dimorphism plays a central role in the genetic and hormonal regulation of immune responses, both of the innate and the adaptive immune system. We review evidence supporting that ineffective anti-SARS-CoV-2 responses, coupled with a predisposition for inappropriate hyperinflammatory responses, could provide a biological explanation for the male bias in COVID-19 mortality. A prominent finding in COVID-19 is the increased risk of death with pre-existing cardiovascular comorbidities, such as hypertension, obesity, and age. We contextualize how important features of sexual dimorphism and inflammation in COVID-19 may exhibit a reciprocal relationship with comorbidities, and explain their increased mortality risk. Ultimately, we demonstrate that biological sex is a fundamental variable of critical relevance to our mechanistic understanding of SARS-CoV-2 infection and the pursuit of effective COVID-19 preventative and therapeutic strategies.


Subject(s)
COVID-19/mortality , Cardiovascular Diseases/mortality , Health Status Disparities , Inflammation/mortality , SARS-CoV-2/immunology , Animals , COVID-19/diagnosis , COVID-19/immunology , COVID-19/virology , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/virology , Comorbidity , Female , Host-Pathogen Interactions , Humans , Inflammation/diagnosis , Inflammation/immunology , Inflammation/virology , Male , Prognosis , Risk Assessment , Risk Factors , Sex Characteristics , Sex Factors
11.
Inflamm Res ; 69(11): 1077-1085, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-696688

ABSTRACT

BACKGROUND: Decline in mitochondrial function occurs with aging and may increase mortality. We discuss mitochondrial contribution to Covid-19 sepsis, specifically the complex interaction of innate immune function, viral replication, hyper-inflammatory state, and HIF-α/Sirtuin pathways. METHODS: Articles from PubMed/Medline searches were reviewed using the combination of terms "SARS-CoV-2, Covid-19, sepsis, mitochondria, aging, and immunometabolism". RESULTS: Evidence indicates that mitochondria in senescent cells may be dysfunctional and unable to keep up with hypermetabolic demands associated with Covid-19 sepsis. Mitochondrial proteins may serve as damage-associated molecular pattern (DAMP) activating innate immunity. Disruption in normal oxidative phosphorylation pathways contributes to elevated ROS which activates sepsis cascade through HIF-α/Sirtuin pathway. Viral-mitochondrial interaction may be necessary for replication and increased viral load. Hypoxia and hyper-inflammatory state contribute to increased mortality associated with Covid-19 sepsis. CONCLUSIONS: Aging is associated with worse outcomes in sepsis. Modulating Sirtuin activity is emerging as therapeutic agent in sepsis. HIF-α, levels of mitochondrial DNA, and other mitochondrial DAMP molecules may also serve as useful biomarker and need to be investigated. These mechanisms should be explored specifically for Covid-19-related sepsis. Understanding newly discovered regulatory mechanisms may lead to the development of novel diagnostic and therapeutic targets.


Subject(s)
Coronavirus Infections/complications , Coronavirus Infections/pathology , Inflammation/etiology , Inflammation/pathology , Mitochondria/metabolism , Mitochondria/pathology , Mitochondrial Diseases/etiology , Mitochondrial Diseases/pathology , Pneumonia, Viral/complications , Pneumonia, Viral/pathology , Sepsis/etiology , Sepsis/pathology , Aging , COVID-19 , Coronavirus Infections/mortality , Humans , Inflammation/mortality , Mitochondrial Diseases/mortality , Pandemics , Pneumonia, Viral/mortality , Sepsis/mortality
12.
J Thromb Thrombolysis ; 50(4): 825-832, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-696135

ABSTRACT

The new outbreak of Coronavirus Disease 2019 (COVID-19) has emerged as a serious global public health concern. A more in-depth study of blood coagulation abnormality is needed. We retrospectively analyzed 147 consecutive patients with COVID-19 who were admitted to three ICUs in Wuhan from February 9th, 2020 to March 20th, 2020. The baseline coagulation and other characteristics were studied. Our results showed that the prolonged PT, FDP, DD were positively correlated with the levels of neutrophils, ferritin, LDH, total bilirubin, multi-inflammation cytokines, and negatively correlated with the lymphocytes level (p < 0.01). The level of ATIII was significantly negatively correlated with the levels of neutrophils, ferritin, LDH, total bilirubin, IL2R, IL6 and IL8 (p < 0.05). The patients in the ARDS group had a more prominent abnormality in PT, FDP, DD and ATIII, while the patients in the AKI group had more prolonged PT, more severe FDP and DD level, more inferior ATIII and Fib level than those in the non-AKI group (p < 0.01). The value of PT, DD and FDP were positively correlated with the classical APACHE II, SOFA and qSOFA scores, while the ATIII was negatively correlated with them (p < 0.001). The high levels of PT, FDP and DD were correlated with in-hospital mortality (p < 0.001). In conclusion, blood coagulation disorder was prominent in ICU patients with COVID-19 and was correlated with multi-inflammation factors. The abnormality of blood coagulation parameters could be an adverse prognostic indicator for ICU patients with COVID-19.


Subject(s)
Betacoronavirus/pathogenicity , Blood Coagulation Disorders/virology , Blood Coagulation , Coronavirus Infections/therapy , Inflammation Mediators/blood , Inflammation/virology , Intensive Care Units , Pneumonia, Viral/therapy , Aged , Antithrombin III/metabolism , Biomarkers/blood , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/mortality , COVID-19 , Coronavirus Infections/diagnosis , Coronavirus Infections/mortality , Coronavirus Infections/virology , Female , Fibrin Fibrinogen Degradation Products/metabolism , Hospital Mortality , Host-Pathogen Interactions , Humans , Inflammation/blood , Inflammation/diagnosis , Inflammation/mortality , Male , Middle Aged , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/mortality , Pneumonia, Viral/virology , Prognosis , Retrospective Studies , Risk Factors , SARS-CoV-2 , Time Factors
13.
Anesth Analg ; 131(5): 1324-1333, 2020 11.
Article in English | MEDLINE | ID: covidwho-692027

ABSTRACT

Patients with coronavirus disease 2019 (COVID-19) frequently experience a coagulopathy associated with a high incidence of thrombotic events leading to poor outcomes. Here, biomarkers of coagulation (such as D-dimer, fibrinogen, platelet count), inflammation (such as interleukin-6), and immunity (such as lymphocyte count) as well as clinical scoring systems (such as sequential organ failure assessment [SOFA], International Society on Thrombosis and Hemostasis disseminated intravascular coagulation [ISTH DIC], and sepsis-induced coagulopathy [SIC] score) can be helpful in predicting clinical course, need for hospital resources (such as intensive care unit [ICU] beds, intubation and ventilator therapy, and extracorporeal membrane oxygenation [ECMO]) and patient's outcome in patients with COVID-19. However, therapeutic options are actually limited to unspecific supportive therapy. Whether viscoelastic testing can provide additional value in predicting clinical course, need for hospital resources and patient's outcome or in guiding anticoagulation in COVID-19-associated coagulopathy is still incompletely understood and currently under investigation (eg, in the rotational thromboelastometry analysis and standard coagulation tests in hospitalized patients with COVID-19 [ROHOCO] study). This article summarizes what we know already about COVID-19-associated coagulopathy and-perhaps even more importantly-characterizes important knowledge gaps.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Anticoagulants/therapeutic use , Betacoronavirus/pathogenicity , Blood Coagulation/drug effects , Coronavirus Infections/therapy , Inflammation/therapy , Pneumonia, Viral/therapy , Pulmonary Embolism/therapy , Venous Thromboembolism/therapy , Venous Thrombosis/therapy , Anti-Inflammatory Agents/adverse effects , Anticoagulants/adverse effects , Biomarkers/blood , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/mortality , Coronavirus Infections/virology , Evidence-Based Medicine , Fibrin Fibrinogen Degradation Products/analysis , Hospital Mortality , Host-Pathogen Interactions , Humans , Inflammation/blood , Inflammation/mortality , Inflammation/virology , Inflammation Mediators/blood , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/mortality , Pneumonia, Viral/virology , Prognosis , Pulmonary Embolism/blood , Pulmonary Embolism/mortality , Pulmonary Embolism/virology , Risk Factors , SARS-CoV-2 , Venous Thromboembolism/blood , Venous Thromboembolism/mortality , Venous Thromboembolism/virology , Venous Thrombosis/blood , Venous Thrombosis/mortality , Venous Thrombosis/virology
14.
J Hematol Oncol ; 13(1): 94, 2020 07 14.
Article in English | MEDLINE | ID: covidwho-647080

ABSTRACT

BACKGROUND: The COVID-19 pandemic, caused by SARS-CoV-2 virus, has resulted in over 100,000 deaths in the USA. Our institution has treated over 2000 COVID-19 patients during the pandemic in New York City. The pandemic directly impacted cancer patients and the organization of cancer care. Mount Sinai Hospital has a large and diverse multiple myeloma (MM) population. Herein, we report the characteristics of COVID-19 infection and serological response in MM patients in a large tertiary care institution in New York. METHODS: We performed a retrospective study on a cohort of 58 patients with a plasma-cell disorder (54 MM, 4 smoldering MM) who developed COVID-19 between March 1, 2020, and April 30, 2020. We report epidemiological, clinical, and laboratory characteristics including the persistence of viral detection by polymerase chain reaction (PCR) and anti-SARS-CoV-2 antibody testing, treatments initiated, and outcomes. RESULTS: Of the 58 patients diagnosed with COVID-19, 36 were hospitalized and 22 were managed at home. The median age was 67 years; 52% of patients were male and 63% were non-White. Hypertension (64%), hyperlipidemia (62%), obesity (37%), diabetes mellitus (28%), chronic kidney disease (24%), and lung disease (21%) were the most common comorbidities. In the total cohort, 14 patients (24%) died. Older age (> 70 years), male sex, cardiovascular risk, and patients not in complete remission (CR) or stringent CR were significantly (p < 0.05) associated with hospitalization. Among hospitalized patients, laboratory findings demonstrated elevation of traditional inflammatory markers (CRP, ferritin, D-dimer) and a significant (p < 0.05) association between elevated inflammatory markers, severe hypogammaglobulinemia, non-White race, and mortality. Ninety-six percent (22/23) of patients developed antibodies to SARS-CoV-2 at a median of 32 days after initial diagnosis. The median time to PCR negativity was 43 (range 19-68) days from initial positive PCR. CONCLUSIONS: Drug exposure and MM disease status at the time of contracting COVID-19 had no bearing on mortality. Mounting a severe inflammatory response to SARS-CoV-2 and severe hypogammaglobulinemia was associated with higher mortality. The majority of patients mounted an antibody response to SARS-CoV-2. These findings pave a path to the identification of vulnerable MM patients who need early intervention to improve outcomes in future outbreaks of COVID-19.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Multiple Myeloma/complications , Pneumonia, Viral/complications , Tertiary Care Centers , Agammaglobulinemia/mortality , Agammaglobulinemia/pathology , Aged , COVID-19 , Cohort Studies , Coronavirus Infections/mortality , Female , Humans , Immunocompromised Host , Inflammation/mortality , Inflammation/pathology , Male , Middle Aged , Multiple Myeloma/immunology , New York City/epidemiology , Pandemics , Pneumonia, Viral/mortality , Retrospective Studies , Risk Factors , SARS-CoV-2
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