NOTE: This dataset has been retired and marked as historical-only. This dataset is a companion to the COVID-19 Daily Cases and Deaths dataset (https://data.cityofchicago.org/d/naz8-j4nc). The major difference in this dataset is that the case, death, and hospitalization corresponding rates per 100,000 population are not those for the single date indicated. They are rolling averages for the seven-day period ending on that date. This rolling average is used to account for fluctuations that may occur in the data, such as fewer cases being reported on weekends, and small numbers. The intent is to give a more representative view of the ongoing COVID-19 experience, less affected by what is essentially noise in the data. All rates are per 100,000 population in the indicated group, or Chicago, as a whole, for “Total” columns. Only Chicago residents are included based on the home address as provided by the medical provider. Cases with a positive molecular (PCR) or antigen test are included in this dataset. Cases are counted based on the date the test specimen was collected. Deaths among cases are aggregated by day of death. Hospitalizations are reported by date of first hospital admission. Demographic data are based on what is reported by medical providers or collected by CDPH during follow-up investigation. Denominators are from the U.S. Census Bureau American Community Survey 1-year estimate for 2018 and can be seen in the Citywide, 2018 row of the Chicago Population Counts dataset (https://data.cityofchicago.org/d/85cm-7uqa). All data are provisional and subject to change. Information is updated as additional details are received and it is, in fact, very common for recent dates to be incomplete and to be updated as time goes on. At any given time, this dataset reflects cases and deaths currently known to CDPH. Numbers in this dataset may differ from other public sources due to definitions of COVID-19-related cases and deaths, sources used, how cases and deaths are associated to a specific date, and similar factors. Data Source: Illinois National Electronic Disease Surveillance System, Cook County Medical Examiner’s Office, U.S. Census Bureau American Community Survey

NOTE: This dataset has been retired and marked as historical-only.

Only Chicago residents are included based on the home ZIP Code, as provided by the medical provider, or the address, as provided by the Cook County Medical Examiner.

Cases with a positive molecular (PCR) or antigen test are included in this dataset. Cases are counted on the date the test specimen was collected. Deaths are those occurring among cases based on the day of death. Hospitalizations are based on the date of first hospitalization. Only one hospitalization is counted for each case. Demographic data are based on what is reported by medical providers or collected by CDPH during follow-up investigation.

Because of the nature of data reporting to CDPH, hospitalizations will be blank for recent dates They will fill in on later updates when the data are received, although, as for cases and deaths, may continue to be updated as further data are received.

All data are provisional and subject to change. Information is updated as additional details are received and it is, in fact, very common for recent dates to be incomplete and to be updated as time goes on. At any given time, this dataset reflects data currently known to CDPH.

Numbers in this dataset may differ from other public sources due to definitions of COVID-19-related cases, deaths, and hospitalizations, sources used, how cases, deaths and hospitalizations are associated to a specific date, and similar factors.

Data Source: Illinois National Electronic Disease Surveillance System, Cook County Medical Examiner’s Office

NOTE: This dataset has been retired and marked as historical-only.

Weekly rates of COVID-19 cases, hospitalizations, and deaths among people living in Chicago by vaccination status and age.

Rates for fully vaccinated and unvaccinated begin the week ending April 3, 2021 when COVID-19 vaccines became widely available in Chicago. Rates for boosted begin the week ending October 23, 2021 after booster shots were recommended by the Centers for Disease Control and Prevention (CDC) for adults 65+ years old and adults in certain populations and high risk occupational and institutional settings who received Pfizer or Moderna for their primary series or anyone who received the Johnson & Johnson vaccine.

Chicago residency is based on home address, as reported in the Illinois Comprehensive Automated Immunization Registry Exchange (I-CARE) and Illinois National Electronic Disease Surveillance System (I-NEDSS).

Outcomes: • Cases: People with a positive molecular (PCR) or antigen COVID-19 test result from an FDA-authorized COVID-19 test that was reported into I-NEDSS. A person can become re-infected with SARS-CoV-2 over time and so may be counted more than once in this dataset. Cases are counted by week the test specimen was collected. • Hospitalizations: COVID-19 cases who are hospitalized due to a documented COVID-19 related illness or who are admitted for any reason within 14 days of a positive SARS-CoV-2 test. Hospitalizations are counted by week of hospital admission. • Deaths: COVID-19 cases who died from COVID-19-related health complications as determined by vital records or a public health investigation. Deaths are counted by week of death.

Vaccination status: • Fully vaccinated: Completion of primary series of a U.S. Food and Drug Administration (FDA)-authorized or approved COVID-19 vaccine at least 14 days prior to a positive test (with no other positive tests in the previous 45 days). • Boosted: Fully vaccinated with an additional or booster dose of any FDA-authorized or approved COVID-19 vaccine received at least 14 days prior to a positive test (with no other positive tests in the previous 45 days). • Unvaccinated: No evidence of having received a dose of an FDA-authorized or approved vaccine prior to a positive test.

CLARIFYING NOTE: Those who started but did not complete all recommended doses of an FDA-authorized or approved vaccine prior to a positive test (i.e., partially vaccinated) are excluded from this dataset.

Incidence rates for fully vaccinated but not boosted people (Vaccinated columns) are calculated as total fully vaccinated but not boosted with outcome divided by cumulative fully vaccinated but not boosted at the end of each week. Incidence rates for boosted (Boosted columns) are calculated as total boosted with outcome divided by cumulative boosted at the end of each week. Incidence rates for unvaccinated (Unvaccinated columns) are calculated as total unvaccinated with outcome divided by total population minus cumulative boosted, fully, and partially vaccinated at the end of each week. All rates are multiplied by 100,000.

Incidence rate ratios (IRRs) are calculated by dividing the weekly incidence rates among unvaccinated people by those among fully vaccinated but not boosted and boosted people.

Overall age-adjusted incidence rates and IRRs are standardized using the 2000 U.S. Census standard population.

Population totals are from U.S. Census Bureau American Community Survey 1-year estimates for 2019.

All data are provisional and subject to change. Information is updated as additional details are received and it is, in fact, very common for recent dates to be incomplete and to be updated as time goes on. This dataset reflects data known to CDPH at the time when the dataset is updated each week.

Numbers in this dataset may differ from other public sources due to when data are reported and how City of Chicago boundaries are defined.

For all datasets related to COVID-19, see https://data.cityofchic

COVID-19 is a disease caused by the novel Coronavirus SARS-CoV-2 causing an acute respiratory disease that can eventually lead to severe acute respiratory syndrome (SARS). An exacerbated inflammatory response is characteristic of SARS-CoV-2 infection, which leads to a cytokine release syndrome also known as cytokine storm associated with the severity of the disease. Considering the importance of this event in the immunopathology of COVID-19, this study analyses cytokine levels of hospitalized patients to identify cytokine profiles associated with severity and mortality. Using a machine learning approach, 3 clusters of COVID-19 hospitalized patients were created based on their cytokine profile. Significant differences in the mortality rate were found among the clusters, associated to different CXCL10/IL-38 ratio. The balance of a CXCL10 induced inflammation with an appropriate immune regulation mediated by the anti-inflammatory cytokine IL-38 appears to generate the adequate immune context to overrule SARS-CoV-2 infection without creating a harmful inflammatory reaction. This study supports the concept that analyzing a single cytokine is insufficient to determine the outcome of a complex disease such as COVID-19, and different strategies incorporating bioinformatic analyses considering a broader immune profile represent a more robust alternative to predict the outcome of hospitalized patients with SARS-CoV-2 infection.

This dataset includes aggregated weekly data on the percent of emergency department visits and the percent of hospital inpatient admissions due to influenza-like illness (ILI), COVID-19, influenza, RSV, and acute respiratory illness. The Illinois Department of Public Health (IDPH) collects data for Emergency Department visits to all 185 acute care hospitals in Illinois. The data are submitted from IDPH to the CDC’s BioSense Platform for access and analysis by health departments via the ESSENCE system.

The CDC National Syndromic Surveillance Program (NSSP) utilizes diagnostic codes and clinical terms to create definitions for diagnosed COVID-19, influenza, RSV, and acute respiratory illness. For more information on diagnostic codes and clinical terms used, visit: https://www.cdc.gov/nssp/php/onboarding-resources/companion-guide-ed-data-respiratory-illness.html

The data is characterized by selected demographic groups including age group and race/ethnicity.

The dataset also includes percent of weekly outpatient visits due to ILI as reported by several outpatient clinics throughout Chicago that participate in CDC’s Influenza-like Illness Surveillance Network (ILINet).

For more information on ESSENCE, see https://www.dph.illinois.gov/data-statistics/syndromic-surveillance

For more information on ILINet, see https://www.cdc.gov/fluview/overview/index.html#cdc_generic_section_3-outpatient-illness-surveillance

All data are provisional and subject to change. Information is updated as additional details are received. At any given time, this dataset reflects data currently known to CDPH. Numbers in this dataset may differ from other public sources.

BackgroundThe use of IL-6 blockers in COVID-19 hospitalized patients has been associated with a reduction in mortality compared to standard care. However, many uncertainties remain pertaining to optimal intervention time, administration schedule, and predictors of response. To date, data on the use of subcutaneous sarilumab is limited and no randomized trial results are available.MethodsOpen label randomized controlled trial at a single center in Spain. We included adult patients admitted with microbiology documented COVID-19 infection, imaging confirmed pneumonia, fever and/or laboratory evidence of inflammatory phenotype, and no need for invasive ventilation. Participants were randomly assigned to receive sarilumab, a single 400 mg dose in two 200 mg subcutaneous injections, added to standard care or standard care, in a 2:1 proportion. Primary endpoints included 30-day mortality, mean change in clinical status at day 7 scored in a 7-category ordinal scale ranging from death (category 1) to discharge (category 7), and duration of hospitalization. The primary efficacy analysis was conducted on the intention-to-treat population.ResultsA total of 30 patients underwent randomization: 20 to sarilumab and 10 to standard care. Most patients were male (20/30, 67%) with a median (interquartile range) age of 61.5 years (56–72). At day 30, 2/20 (10%) patients died in the sarilumab arm vs. none (0/10) in standard care (Log HR 15.11, SE 22.64; p = 0.54). At day 7, no significant differences were observed in the median change in clinical status (2 [0–3]) vs. 3 [0–3], p = 0.32). Median time to discharge (days) was similar (7 [6–11] vs. 6 [4–12]; HR 0.65, SE 0.26; p = 0.27). No significant differences were detected in the rate of progression to invasive and noninvasive mechanical ventilation.Conclusions and RelevanceOur pragmatic pilot study has failed to demonstrate the benefit of adding subcutaneous sarilumab to standard care for mortality by 30 days, functional status at day 7, or hospital stay. Findings herein do not exclude a potential effect of sarilumab in severe COVID-19 but adequately powered blinded randomized phase III trials are warranted to assess the impact of the subcutaneous route and a more selected target population.Trial Registrationwww.ClinicalTrials.gov, Identifier: NCT04357808.

BackgroundCoronavirus disease 2019 (COVID-19) have brought great disaster to mankind, and there is currently no globally recognized specific drug or treatment. Severe COVID-19 may trigger a cytokine storm, manifested by increased levels of cytokines including interleukin-17 (IL-17), so a new strategy to treat COVID-19 may be to use existing IL-17 inhibitors, which have demonstrated efficacy, safety and tolerability in the treatment of psoriasis. However, the use of IL-17 inhibitors in patients with psoriasis during the COVID-19 pandemic remains controversial due to reports that IL-17 inhibitors may increase the risk of respiratory tract infections.ObjectivesThe systematic review and meta-analysis aimed to evaluate the effect of IL-17 inhibitors on the risk of COVID-19 infection, hospitalization, and mortality in patients with psoriasis.MethodsDatabases (including Embase, PubMed, SCI-Web of Science, Scopus, CNKI, and the Cochrane Library) were searched up to August 23, 2022, for studies exploring differences in COVID-19 outcomes between psoriasis patients using IL-17 inhibitors and those using non-biologics. Two authors independently extracted data and assessed the risk of bias in a double-blind manner. The risk ratios (RRs) and 95% confidence intervals (CIs) were calculated and heterogeneities were determined by the Q test and I2 statistic. And the numbers needed to treat (NNTs) were calculated to assess the clinical value of IL-17 inhibitors in preventing SARS-CoV-2 infection and treating COVID-19.ResultsNine observational studies involving 7,106 participants were included. The pooled effect showed no significant differences in the rates of SARS-CoV-2 infection (P = 0.94; I2 = 19.5%), COVID-19 hospitalization (P = 0.64; I2 = 0.0%), and COVID-19 mortality (P = 0.32; I2 = 0.0%) in psoriasis patients using IL-17 inhibitors compared with using non-biologics. Subgroup analyses grouped by age and COVID-19 cases, respectively, revealed consistent results as above. Meanwhile, the pooled NNTs showed no significant differences between the two groups in the clinical value of preventing SARS-CoV-2 infection and treating COVID-19.ConclusionThe use of IL-17 inhibitors in patients with psoriasis does not increase the risk of SARS-CoV-2 infection or worsen the course of COVID-19.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42022335195.

BackgroundCytokine release triggered by a hyperactive immune response is thought to contribute to severe acute respiratory syndrome coronavirus 2019 (SARS-CoV-2)–related respiratory failure. Bruton tyrosine kinase (BTK) is involved in innate immunity, and BTK inhibitors block cytokine release. We assessed the next-generation BTK inhibitor zanubrutinib in SARS-CoV-2–infected patients with respiratory distress.MethodCohort 1 had a prospective, randomized, double-blind, placebo-controlled design; cohort 2 had a single-arm design. Adults with SARS-CoV-2 requiring hospitalization (without mechanical ventilation) were randomized in cohort 1. Those on mechanical ventilation ≤24 hours were enrolled in cohort 2. Patients were randomized 1:1 to zanubrutinib 320 mg once daily or placebo (cohort 1), or received zanubrutinib 320 mg once daily (cohort 2). Co-primary endpoints were respiratory failure-free survival rate and time to return to breathing room air at 28 days. Corollary studies to assess zanubrutinib’s impact on immune response were performed.ResultsSixty-three patients in cohort 1 received zanubrutinib (n=30) or placebo (n=33), with median treatment duration of 8.5 and 7.0 days, respectively. The median treatment duration in cohort 2 (n=4) was 13 days; all discontinued treatment early. In cohort 1, respiratory failure-free survival and the estimated rates of not returning to breathing room air by day 28 were not significantly different between treatments. Importantly, serological response to coronavirus disease 2019 (COVID-19) was not impacted by zanubrutinib. Lower levels of granulocyte colony-stimulating factor, interleukin (IL)-10, monocyte chemoattractant protein-1, IL-4, and IL-13 were observed in zanubrutinib-treated patients. Moreover, single-cell transcriptome analysis showed significant downregulation of inflammatory mediators (IL-6, IL-8, macrophage colony-stimulating factor, macrophage inflammatory protein-1α, IL-1β) and signaling pathways (JAK1, STAT3, TYK2), and activation of gamma-delta T cells in zanubrutinib-treated patients.ConclusionsMarked reduction in inflammatory signaling with preserved SARS-CoV-2 serological response was observed in hospitalized patients with COVID-19 respiratory distress receiving zanubrutinib. Despite these immunological findings, zanubrutinib did not show improvement over placebo in clinical recovery from respiratory distress. Concurrent administration of steroids and antiviral therapy to most patients may have contributed to these results. Investigation of zanubrutinib may be warranted in other settings where cytokine release and immune cell exhaustion are important.Clinical Trial Registrationhttps://www.clinicaltrials.gov/study/NCT04382586, identifier NCT04382586.

IntroductionSARS-CoV-2 elicits a hyper-inflammatory response that contributes to increased morbidity and mortality in patients with COVID-19. In the case of HIV infection, despite effective anti-retroviral therapy, people living with HIV (PLWH) experience chronic systemic immune activation, which renders them particularly vulnerable to the life-threatening pulmonary, cardiovascular and other complications of SARS-CoV-2 co-infection. The focus of the study was a comparison of the concentrations of systemic indicators o\f innate immune dysfunction in SARS-CoV-2-PCR-positive patients (n=174) admitted with COVID-19, 37 of whom were co-infected with HIV.MethodsParticipants were recruited from May 2020 to November 2021. Biomarkers included platelet-associated cytokines, chemokines, and growth factors (IL-1β, IL-6, IL-8, MIP-1α, RANTES, PDGF-BB, TGF-β1 and TNF-α) and endothelial associated markers (IL-1β, IL-1Ra, ICAM-1 and VEGF).ResultsPLWH were significantly younger (p=0.002) and more likely to be female (p=0.001); median CD4+ T-cell count was 256 (IQR 115 -388) cells/μL and the median HIV viral load (VL) was 20 (IQR 20 -12,980) copies/mL. Fractional inspired oxygen (FiO2) was high in both groups, but higher in patients without HIV infection (p=0.0165), reflecting a greater need for oxygen supplementation. With the exception of PDGF-BB, the levels of all the biomarkers of innate immune activation were increased in SARS-CoV-2/HIV-co-infected and SARS-CoV-2/HIV-uninfected sub-groups relative to those of a control group of healthy participants. The magnitudes of the increases in the levels of these biomarkers were comparable between the SARS-CoV-2 -infected sub-groups, the one exception being RANTES, which was significantly higher in the sub-group without HIV. After adjusting for age, sex, and diabetes in the multivariable model, only the association between HIV status and VEGF was statistically significant (p=0.034). VEGF was significantly higher in PLWH with a CD4+ T-cell count >200 cells/μL (p=0.040) and those with a suppressed VL (p=0.0077).DiscussionThese findings suggest that HIV co-infection is not associated with increased intensity of the systemic innate inflammatory response during SARS-CoV-2 co-infection, which may underpin the equivalent durations of hospital stay, outcome and mortality rates in the SARS-CoV-2/HIV-infected and -uninfected sub-groups investigated in the current study. The apparent association of increased levels of plasma VEGF with SARS-CoV-2/HIV co-infection does, however, merit further investigation.

This study aimed to detect, analyze, and correlate the clinical characteristics, blood coagulation functions, blood calcium levels, and inflammatory factors in patients with mild and severe COVID-19 infections. The enrolled COVID-19 infected patients were from Wuhan Jin Yin-tan Hospital (17 cases, Wuhan, China), Suzhou Infectious Disease Hospital (87 cases, Suzhou, China), and Xuzhou Infectious Disease Hospital (14 cases, Xuzhou, China). After admission, basic information was collected; X-ray and chest CT images were obtained; and data from routine blood tests, liver and kidney function, myocardial enzymes, electrolytes, blood coagulation function, (erythrocyte sedimentation rate) ESR, C-reactive protein (CRP), IL-6, procalcitonin (PCT), calcitonin, and other laboratory tests were obtained. The patients were grouped according to the clinical classification method based on the pneumonia diagnosis and treatment plan for new coronavirus infection (trial version 7) in China. The measurements from mild (56 cases) and severe cases (51 cases) were compared and analyzed. Most COVID-19 patients presented with fever. Chest X-ray and CT images showed multiple patchy and ground glass opacities in the lungs of COVID 19 infected patients, especially in patients with severe cases. Compared with patients with mild infection, patients with severe infection were older (p = 0.023) and had a significant increase in AST and BUN. The levels of CK, LDH, CK-MB, proBNP, and Myo in patients with severe COVID-19 infection were also increased significantly compared to those in patients with mild cases. Patients with severe COVID-19 infections presented coagulation dysfunction and increased D-dimer and fibrin degradation product (FDP) levels. Severe COVID-19 patients had low serum calcium ion (Ca2+) concentrations and high calcitonin and PCT levels and exhibited serious systemic inflammation. Ca2+ in COVID-19 patients was significantly negatively correlated with PCT, calcitonin, D-dimer, PFDP, ESR, CRP and IL-6. D-dimer in COVID-19 patients was a significantly positively correlated with CRP and IL-6. In conclusion, patients with severe COVID-19 infection presented significant metabolic dysfunction and abnormal blood coagulation, a sharp increase in inflammatory factors and calcitonin and procalcitonin levels, and a significant decrease in Ca2+. Decreased Ca2+ and coagulation dysfunction in COVID-19 patients were significantly correlated with each other and with inflammatory factors.

Il set di dati contiene gli ultimi dati pubblici disponibili sul COVID-19, tra cui un aggiornamento quotidiano sulla situazione, la curva epidemiologica e la distribuzione geografica globale (UE/SEE e Regno Unito, in tutto il mondo). Il 12 febbraio 2020 il nuovo coronavirus è stato denominato sindrome respiratoria acuta grave da coronavirus 2 (SARS-CoV-2), mentre la malattia ad esso associata è ora denominata COVID-19. L'ECDC sta monitorando da vicino l'epidemia e fornisce valutazioni dei rischi per guidare gli Stati membri dell'UE e la Commissione europea nelle loro attività di risposta.

Optimal timing for intubating patients with coronavirus disease 2019 (COVID-19) has been debated throughout the pandemic. Early use of high-flow nasal cannula (HFNC) can help reduce the need for intubation, but delay can result in poorer outcomes. This study examines trends in laboratory parameters and serum severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA levels of patients with COVID-19 in relation to HFNC failure. Patients requiring HFNC within three days of hospitalization between July 1 and September 30, 2021 were enrolled. The primary outcome was HFNC failure (early failure ≤Day 3; late failure ≥Day 4), defined as transfer to intensive care just before/after intubation or in-hospital death. We examined changes in laboratory markers and SARS-CoV2-RNAemia on Days 1, 4, and 7, together with demographic data, oxygenation status, and therapeutic agents. We conducted a univariate logistic regression with the explanatory variables defined as 10% change rate in each laboratory marker from Day 1 to 4. We utilized the log-rank test to assess the differences in HFNC failure rates, stratified based on the presence of SARS-CoV2 RNAemia. Among 122 patients, 17 (13.9%) experienced HFNC failure (early: n = 6, late: n = 11). Seventy-five patients (61.5%) showed an initial SpO2/FiO2 ratio ≤243, equivalent to PaO2/FiO2 ratio ≤200, and the initial SpO2/FiO2 ratio was significantly lower in the failure group (184 vs. 218, p = 0.018). Among the laboratory markers, a 10% increase from Day 1 to 4 of lactate dehydrogenase (LDH) and interleukin (IL)-6 was associated with late failure (Odds ratio [OR]: 1.42, 95% confidence interval [CI]: 1.09–1.89 and OR: 1.04, 95%CI: 1.00–1.19, respectively). Furthermore, in patients with persistent RNAemia on Day 4 or 7, the risk of late HFNC failure was significantly higher (Log-rank test, p

BackgroundTo prevent COVID-19 progression, low-cost alternatives that are available to all patients are needed. Diverse forms of thermotherapy have been proposed to prevent progression to severe/critical COVID-19.ObjectiveThe aim of this study is to evaluate the efficacy and safety of local thermotherapy to prevent disease progression in hospitalized adult patients with mild-to-moderate COVID-19.MethodsA multicenter, open-label, parallel-group, randomized, adaptive trial is used to evaluate the efficacy and safety of local thermotherapy to prevent disease progression in hospitalized adult patients with mild-to-moderate COVID-19. Eligible hospitalized adult patients with symptoms of COVID-19 with ≤5 days from symptom onset, meeting criteria for mild or moderate COVID-19, were randomly assigned to the intervention consisting of local thermotherapy via an electric heat pad in the thorax (target temperature range 39.5–42°C) continuously for 90 min, twice daily, for 5 days, or standard care. The main outcome was the proportion of patients who progressed to severe-to-critical COVID-19 or death. Patients were randomized in a 1:1 ratio through a centralized computer-generated sequence of minimization with a random component of 20%. Participants and medical staff were not blinded to the intervention.ResultsOne-hundred and five participants (thermotherapy n = 54, control n = 51) with a median age of 53 (IQR: 41–64) years were included for analysis after the early cessation of recruitment due to the closure of all temporal COVID-19 units (target sample size = 274). The primary outcome of disease progression occurred in 31.4% (16/51) of patients in the control group vs. 25.9% (14/54) of those receiving thermotherapy (risk difference = 5.5%; 95%CI: −11.8–22.7, p = 0.54). Thermotherapy was well tolerated with a median total duration of thermotherapy of 900 (IQR: 877.5–900) min. Seven (13.7%) patients in the control group and seven (12.9%) in the thermotherapy group had at least one AE (p = 0.9), none of which were causally attributed to the intervention. No statistically significant differences in serum cytokines (IL-1β, IL-6, IL-8, IL-10, IL-17, and IFN-γ) were observed between day 5 and baseline among groups.ConclusionLocal thermotherapy was safe and well-tolerated. A non-statistically significant lower proportion of patients who experienced disease progression was found in the thermotherapy group compared to standard care. Local thermotherapy could be further studied as a strategy to prevent disease progression in ambulatory settings.Clinical Trial registration: www.clinicaltrials.gov, identifier: NCT04363541.