COVID-19

Key clinical point: A single subcutaneous dose of the antibody cocktail REGEN-COV (casirivimab plus imdevimab) is effective in preventing symptomatic and asymptomatic infection in household contacts of COVID-19-positive individuals.

Major finding: The antibody cocktail group developed fewer symptomatic SARS-CoV-2 infections than the placebo group (relative risk reduction, 81.4%). The antibody cocktail effectively prevented symptomatic and asymptomatic infections overall (relative risk reduction, 66.4%).

Study details: In a randomized, double-blind, placebo-controlled trial, unaffected household members (age, 12 years or older) of individuals testing positive for SARS-CoV-2 received either the antibody cocktail (n=753) or placebo (n=752).

Disclosures: The study was funded by Regeneron Pharmaceuticals, F. Hoffmann-LaRoche, and the National Institutes of Health. Several authors were employees and/or stockholders of Regeneron Pharmaceuticals.

Source: O'Brien MP et al. N Engl J Med. 2021 Aug 4. doi: 10.1056/NEJMoa2109682.

Key clinical point: A single subcutaneous dose of the antibody cocktail REGEN-COV (casirivimab plus imdevimab) is effective in preventing symptomatic and asymptomatic infection in household contacts of COVID-19-positive individuals.

Major finding: The antibody cocktail group developed fewer symptomatic SARS-CoV-2 infections than the placebo group (relative risk reduction, 81.4%). The antibody cocktail effectively prevented symptomatic and asymptomatic infections overall (relative risk reduction, 66.4%).

Study details: In a randomized, double-blind, placebo-controlled trial, unaffected household members (age, 12 years or older) of individuals testing positive for SARS-CoV-2 received either the antibody cocktail (n=753) or placebo (n=752).

Disclosures: The study was funded by Regeneron Pharmaceuticals, F. Hoffmann-LaRoche, and the National Institutes of Health. Several authors were employees and/or stockholders of Regeneron Pharmaceuticals.

Source: O'Brien MP et al. N Engl J Med. 2021 Aug 4. doi: 10.1056/NEJMoa2109682.

Key clinical point: A single subcutaneous dose of the antibody cocktail REGEN-COV (casirivimab plus imdevimab) is effective in preventing symptomatic and asymptomatic infection in household contacts of COVID-19-positive individuals.

Major finding: The antibody cocktail group developed fewer symptomatic SARS-CoV-2 infections than the placebo group (relative risk reduction, 81.4%). The antibody cocktail effectively prevented symptomatic and asymptomatic infections overall (relative risk reduction, 66.4%).

Study details: In a randomized, double-blind, placebo-controlled trial, unaffected household members (age, 12 years or older) of individuals testing positive for SARS-CoV-2 received either the antibody cocktail (n=753) or placebo (n=752).

Disclosures: The study was funded by Regeneron Pharmaceuticals, F. Hoffmann-LaRoche, and the National Institutes of Health. Several authors were employees and/or stockholders of Regeneron Pharmaceuticals.

Source: O'Brien MP et al. N Engl J Med. 2021 Aug 4. doi: 10.1056/NEJMoa2109682.

Key clinical point: Dapagliflozin does not improve COVID-19 hospitalization outcomes for patients with cardiometabolic risk factors.

Major finding: Dapagliflozin vs placebo failed to meet the primary composite outcome of organ dysfunction or all-cause death (hazard ratio, 0.80; 95% confidence interval, 0.58-1.10). There was no difference in the rates of new/worsened organ dysfunction, deaths, or clinical improvement between the groups.

Study details: In the DARE-19 phase 3 trial, patients were randomly assigned to receive either dapagliflozin (n=625) or placebo (n=625).

Disclosures: The study was funded by AstraZeneca. R Esterline, J Oscarsson, SB Gasparyan, J Buenconsejo, AM Langkilde, and P Ambery are employees and stockholders of AstraZeneca. M Aboudara, E Akin, WKS Barroso, ADM Feitosa, CRH Filho, A Fonseca, K Gosch, RA Gordon, CP Jaeger, LN Maia, DDF Moia, JRL Soto, F Tang, SL Windsor, O Mukhtar, V Chopra, RVP Soares, V Garla, PE Leaes, FS Silveira, and M Pursley declared no conflict of interests. The remaining authors disclosed relationships with pharmaceutical companies and/or research institutions.

Source: Kosiborod MN et al. Lancet Diabetes Endocrinol. 2021 Jul 21. doi: 10.1016/S2213-8587(21)00180-7.

Key clinical point: Dapagliflozin does not improve COVID-19 hospitalization outcomes for patients with cardiometabolic risk factors.

Major finding: Dapagliflozin vs placebo failed to meet the primary composite outcome of organ dysfunction or all-cause death (hazard ratio, 0.80; 95% confidence interval, 0.58-1.10). There was no difference in the rates of new/worsened organ dysfunction, deaths, or clinical improvement between the groups.

Study details: In the DARE-19 phase 3 trial, patients were randomly assigned to receive either dapagliflozin (n=625) or placebo (n=625).

Disclosures: The study was funded by AstraZeneca. R Esterline, J Oscarsson, SB Gasparyan, J Buenconsejo, AM Langkilde, and P Ambery are employees and stockholders of AstraZeneca. M Aboudara, E Akin, WKS Barroso, ADM Feitosa, CRH Filho, A Fonseca, K Gosch, RA Gordon, CP Jaeger, LN Maia, DDF Moia, JRL Soto, F Tang, SL Windsor, O Mukhtar, V Chopra, RVP Soares, V Garla, PE Leaes, FS Silveira, and M Pursley declared no conflict of interests. The remaining authors disclosed relationships with pharmaceutical companies and/or research institutions.

Source: Kosiborod MN et al. Lancet Diabetes Endocrinol. 2021 Jul 21. doi: 10.1016/S2213-8587(21)00180-7.

Key clinical point: Dapagliflozin does not improve COVID-19 hospitalization outcomes for patients with cardiometabolic risk factors.

Major finding: Dapagliflozin vs placebo failed to meet the primary composite outcome of organ dysfunction or all-cause death (hazard ratio, 0.80; 95% confidence interval, 0.58-1.10). There was no difference in the rates of new/worsened organ dysfunction, deaths, or clinical improvement between the groups.

Study details: In the DARE-19 phase 3 trial, patients were randomly assigned to receive either dapagliflozin (n=625) or placebo (n=625).

Disclosures: The study was funded by AstraZeneca. R Esterline, J Oscarsson, SB Gasparyan, J Buenconsejo, AM Langkilde, and P Ambery are employees and stockholders of AstraZeneca. M Aboudara, E Akin, WKS Barroso, ADM Feitosa, CRH Filho, A Fonseca, K Gosch, RA Gordon, CP Jaeger, LN Maia, DDF Moia, JRL Soto, F Tang, SL Windsor, O Mukhtar, V Chopra, RVP Soares, V Garla, PE Leaes, FS Silveira, and M Pursley declared no conflict of interests. The remaining authors disclosed relationships with pharmaceutical companies and/or research institutions.

Source: Kosiborod MN et al. Lancet Diabetes Endocrinol. 2021 Jul 21. doi: 10.1016/S2213-8587(21)00180-7.

Key clinical point: Canakinumab does not improve survival in hospitalized patients with severe COVID-19.

Major finding: There was no significant difference in survival without invasive mechanical ventilation between days 3 and 29 with canakinumab vs. placebo (88.8% vs. 85.7%; rate difference, 3.1 percentage points; 95% confidence interval [CI], −3.1 to 9.3). COVID-19 mortality also did not differ with canakinumab vs. placebo (4.9% vs 7.2%; rate difference, −2.3 percentage points; 95% CI, −6.7 to 2.2).

Study details: The data come from the randomized, double-blind, placebo-controlled phase 3 CAN-COVID trial (n=454).

Disclosures: The study was sponsored by Novartis Pharma AG, Basel, Switzerland. All authors received funding from Novartis during the conduct of the study. The authors also reported relationships with other pharmaceutical companies.

Source: Caricchio R et al. JAMA. 2021 Jul 20. doi: 10.1001/jama.2021.9508.

Key clinical point: Canakinumab does not improve survival in hospitalized patients with severe COVID-19.

Major finding: There was no significant difference in survival without invasive mechanical ventilation between days 3 and 29 with canakinumab vs. placebo (88.8% vs. 85.7%; rate difference, 3.1 percentage points; 95% confidence interval [CI], −3.1 to 9.3). COVID-19 mortality also did not differ with canakinumab vs. placebo (4.9% vs 7.2%; rate difference, −2.3 percentage points; 95% CI, −6.7 to 2.2).

Study details: The data come from the randomized, double-blind, placebo-controlled phase 3 CAN-COVID trial (n=454).

Disclosures: The study was sponsored by Novartis Pharma AG, Basel, Switzerland. All authors received funding from Novartis during the conduct of the study. The authors also reported relationships with other pharmaceutical companies.

Source: Caricchio R et al. JAMA. 2021 Jul 20. doi: 10.1001/jama.2021.9508.

Key clinical point: Canakinumab does not improve survival in hospitalized patients with severe COVID-19.

Major finding: There was no significant difference in survival without invasive mechanical ventilation between days 3 and 29 with canakinumab vs. placebo (88.8% vs. 85.7%; rate difference, 3.1 percentage points; 95% confidence interval [CI], −3.1 to 9.3). COVID-19 mortality also did not differ with canakinumab vs. placebo (4.9% vs 7.2%; rate difference, −2.3 percentage points; 95% CI, −6.7 to 2.2).

Study details: The data come from the randomized, double-blind, placebo-controlled phase 3 CAN-COVID trial (n=454).

Disclosures: The study was sponsored by Novartis Pharma AG, Basel, Switzerland. All authors received funding from Novartis during the conduct of the study. The authors also reported relationships with other pharmaceutical companies.

Source: Caricchio R et al. JAMA. 2021 Jul 20. doi: 10.1001/jama.2021.9508.

Key clinical point: Inhaled budesonide is associated with a shorter time to recovery but fails to reduce the risk for hospitalization or death in high-risk primary care patients with COVID-19.

Major finding: Budesonide vs usual care was associated with a shorter time to recovery (11.8 days vs 14.7 days). Budesonide was associated with a nonsignificant 2.0% reduction in hospitalization or death compared with usual care.

Study details: The data come from the PRINCIPLE trial, where 2,530 patients were randomly assigned to either inhaled budesonide (n=787), usual care alone (n=1,069), or usual care plus other interventions (n=674).

Disclosures: The study was funded by the National Institute of Health Research and United Kingdom Research Innovation. M Bafadhel, D Richards, BR Saville, N Berry, MA Detry, M Fitzgerald, S de Lusignan, MI Andersson, PJ Barnes, REK Russell, S Ramakrishnan, FDR Hobbs, and CC Butler reported relationships with pharmaceutical companies and/or research institutions. The remaining authors declared no conflict of interests.

Source: Yu LM et al. Lancet. 2021 Aug 10. doi: 10.1016/S0140-6736(21)01744-X.

Key clinical point: Inhaled budesonide is associated with a shorter time to recovery but fails to reduce the risk for hospitalization or death in high-risk primary care patients with COVID-19.

Major finding: Budesonide vs usual care was associated with a shorter time to recovery (11.8 days vs 14.7 days). Budesonide was associated with a nonsignificant 2.0% reduction in hospitalization or death compared with usual care.

Study details: The data come from the PRINCIPLE trial, where 2,530 patients were randomly assigned to either inhaled budesonide (n=787), usual care alone (n=1,069), or usual care plus other interventions (n=674).

Disclosures: The study was funded by the National Institute of Health Research and United Kingdom Research Innovation. M Bafadhel, D Richards, BR Saville, N Berry, MA Detry, M Fitzgerald, S de Lusignan, MI Andersson, PJ Barnes, REK Russell, S Ramakrishnan, FDR Hobbs, and CC Butler reported relationships with pharmaceutical companies and/or research institutions. The remaining authors declared no conflict of interests.

Source: Yu LM et al. Lancet. 2021 Aug 10. doi: 10.1016/S0140-6736(21)01744-X.

Key clinical point: Inhaled budesonide is associated with a shorter time to recovery but fails to reduce the risk for hospitalization or death in high-risk primary care patients with COVID-19.

Major finding: Budesonide vs usual care was associated with a shorter time to recovery (11.8 days vs 14.7 days). Budesonide was associated with a nonsignificant 2.0% reduction in hospitalization or death compared with usual care.

Study details: The data come from the PRINCIPLE trial, where 2,530 patients were randomly assigned to either inhaled budesonide (n=787), usual care alone (n=1,069), or usual care plus other interventions (n=674).

Disclosures: The study was funded by the National Institute of Health Research and United Kingdom Research Innovation. M Bafadhel, D Richards, BR Saville, N Berry, MA Detry, M Fitzgerald, S de Lusignan, MI Andersson, PJ Barnes, REK Russell, S Ramakrishnan, FDR Hobbs, and CC Butler reported relationships with pharmaceutical companies and/or research institutions. The remaining authors declared no conflict of interests.

Source: Yu LM et al. Lancet. 2021 Aug 10. doi: 10.1016/S0140-6736(21)01744-X.

Key clinical point: Presence of pulmonary embolism (PE) is not associated with increased mortality in patients with COVID-19 risk.

Major finding: Risk factors for PE in patients with COVID-19 included male sex, mechanical ventilation, intensive care unit admission, and circulating D-dimer. Patients with PE did not have an increased risk for mortality compared with those without PE (odds ratio, 1.31; P = .25).

Study details: The data come from a meta-analysis of 16 cohort studies involving 5,826 patients with COVID-19.

Disclosures: No funding information was available. The authors declared no conflict of interests.

Source: Gómez CA et al. Sci Rep. 2021 Aug 6. doi: 10.1038/s41598-021-95512-7.

Key clinical point: Presence of pulmonary embolism (PE) is not associated with increased mortality in patients with COVID-19 risk.

Major finding: Risk factors for PE in patients with COVID-19 included male sex, mechanical ventilation, intensive care unit admission, and circulating D-dimer. Patients with PE did not have an increased risk for mortality compared with those without PE (odds ratio, 1.31; P = .25).

Study details: The data come from a meta-analysis of 16 cohort studies involving 5,826 patients with COVID-19.

Disclosures: No funding information was available. The authors declared no conflict of interests.

Source: Gómez CA et al. Sci Rep. 2021 Aug 6. doi: 10.1038/s41598-021-95512-7.

Key clinical point: Presence of pulmonary embolism (PE) is not associated with increased mortality in patients with COVID-19 risk.

Major finding: Risk factors for PE in patients with COVID-19 included male sex, mechanical ventilation, intensive care unit admission, and circulating D-dimer. Patients with PE did not have an increased risk for mortality compared with those without PE (odds ratio, 1.31; P = .25).

Study details: The data come from a meta-analysis of 16 cohort studies involving 5,826 patients with COVID-19.

Disclosures: No funding information was available. The authors declared no conflict of interests.

Source: Gómez CA et al. Sci Rep. 2021 Aug 6. doi: 10.1038/s41598-021-95512-7.

Key clinical point: Administration of convalescent plasma within 7 days of symptom onset fails to prevent disease progression in acutely ill, high-risk patients with COVID-19.

Major finding: There was no difference between the convalescent plasma group and the placebo group in disease progression (30.0% vs 31.9%; risk difference, 1.9 percentage points; 95% credible interval, −6.0 to 9.8).

Study details: The multicenter, single-blind SIREN-C3PO trial included patients with COVID-19 (n=511) randomly assigned to receive either plasma or placebo in the emergency department.

Disclosures: The study was supported by the National Institutes of Health, the Biomedical Advanced Research and Development Authority, and the Operation Warp Speed interagency program. D Beiser, A Burnett R Davenport, L Dumont, V Durkalski-Mauldin, N El Kassar, L Foster, C Greineder, N Haas, J Hah, A Kaplan, B Kea, F Korley, E Lowell, J McDyer, J Quinn, J Reynolds, R Silbergleit, C Van Huysen, and K Yadav declared no conflict of interests. The remaining authors disclosed relationships with pharmaceutical companies and/or research institutions.

Source: Korley FK et al. N Engl J Med. 2021 Aug 18. doi: 10.1056/NEJMoa2103784.

Key clinical point: Administration of convalescent plasma within 7 days of symptom onset fails to prevent disease progression in acutely ill, high-risk patients with COVID-19.

Major finding: There was no difference between the convalescent plasma group and the placebo group in disease progression (30.0% vs 31.9%; risk difference, 1.9 percentage points; 95% credible interval, −6.0 to 9.8).

Study details: The multicenter, single-blind SIREN-C3PO trial included patients with COVID-19 (n=511) randomly assigned to receive either plasma or placebo in the emergency department.

Disclosures: The study was supported by the National Institutes of Health, the Biomedical Advanced Research and Development Authority, and the Operation Warp Speed interagency program. D Beiser, A Burnett R Davenport, L Dumont, V Durkalski-Mauldin, N El Kassar, L Foster, C Greineder, N Haas, J Hah, A Kaplan, B Kea, F Korley, E Lowell, J McDyer, J Quinn, J Reynolds, R Silbergleit, C Van Huysen, and K Yadav declared no conflict of interests. The remaining authors disclosed relationships with pharmaceutical companies and/or research institutions.

Source: Korley FK et al. N Engl J Med. 2021 Aug 18. doi: 10.1056/NEJMoa2103784.

Key clinical point: Administration of convalescent plasma within 7 days of symptom onset fails to prevent disease progression in acutely ill, high-risk patients with COVID-19.

Major finding: There was no difference between the convalescent plasma group and the placebo group in disease progression (30.0% vs 31.9%; risk difference, 1.9 percentage points; 95% credible interval, −6.0 to 9.8).

Study details: The multicenter, single-blind SIREN-C3PO trial included patients with COVID-19 (n=511) randomly assigned to receive either plasma or placebo in the emergency department.

Disclosures: The study was supported by the National Institutes of Health, the Biomedical Advanced Research and Development Authority, and the Operation Warp Speed interagency program. D Beiser, A Burnett R Davenport, L Dumont, V Durkalski-Mauldin, N El Kassar, L Foster, C Greineder, N Haas, J Hah, A Kaplan, B Kea, F Korley, E Lowell, J McDyer, J Quinn, J Reynolds, R Silbergleit, C Van Huysen, and K Yadav declared no conflict of interests. The remaining authors disclosed relationships with pharmaceutical companies and/or research institutions.

Source: Korley FK et al. N Engl J Med. 2021 Aug 18. doi: 10.1056/NEJMoa2103784.

Key clinical point: Addition of baricitinib to standard of care treatment may reduce 28-day mortality risk in patients hospitalized with COVID-19, but does not significantly reduce the frequency of disease progression.

Major finding: There was a 38.2% relative reduction in 28-day all-cause mortality risk with baricitinib vs placebo. There was no significant difference between the baricitinib and placebo groups in the primary composite endpoint of disease progression outcomes (odds ratio, 0.85; P = .18).

Study details: In a phase 3, double-blind trial, hospitalized patients with COVID-19 receiving standard of care were randomly assigned to either baricitinib (n=764) or placebo group (n=761).

Disclosures: The study was funded by Eli Lilly and Company. S de Bono, CE Kartman, V Krishnan, R Liao, MLB Piruzeli, A Cardose, S Chakladar, B Crowe, P Reis, X Zhang, and DH Adams are employees and shareholders of Eli Lilly and Company. RD Pellegrini declared no conflict of interests. Other authors reported relationships with pharmaceutical companies including Eli Lilly and Company.

Source: Marconi VC et al. Lancet Respir Med. 2021 Sep 1. doi: 10.1016/S2213-2600(21)00331-3.

Key clinical point: Addition of baricitinib to standard of care treatment may reduce 28-day mortality risk in patients hospitalized with COVID-19, but does not significantly reduce the frequency of disease progression.

Major finding: There was a 38.2% relative reduction in 28-day all-cause mortality risk with baricitinib vs placebo. There was no significant difference between the baricitinib and placebo groups in the primary composite endpoint of disease progression outcomes (odds ratio, 0.85; P = .18).

Study details: In a phase 3, double-blind trial, hospitalized patients with COVID-19 receiving standard of care were randomly assigned to either baricitinib (n=764) or placebo group (n=761).

Disclosures: The study was funded by Eli Lilly and Company. S de Bono, CE Kartman, V Krishnan, R Liao, MLB Piruzeli, A Cardose, S Chakladar, B Crowe, P Reis, X Zhang, and DH Adams are employees and shareholders of Eli Lilly and Company. RD Pellegrini declared no conflict of interests. Other authors reported relationships with pharmaceutical companies including Eli Lilly and Company.

Source: Marconi VC et al. Lancet Respir Med. 2021 Sep 1. doi: 10.1016/S2213-2600(21)00331-3.

Key clinical point: Addition of baricitinib to standard of care treatment may reduce 28-day mortality risk in patients hospitalized with COVID-19, but does not significantly reduce the frequency of disease progression.

Major finding: There was a 38.2% relative reduction in 28-day all-cause mortality risk with baricitinib vs placebo. There was no significant difference between the baricitinib and placebo groups in the primary composite endpoint of disease progression outcomes (odds ratio, 0.85; P = .18).

Study details: In a phase 3, double-blind trial, hospitalized patients with COVID-19 receiving standard of care were randomly assigned to either baricitinib (n=764) or placebo group (n=761).

Disclosures: The study was funded by Eli Lilly and Company. S de Bono, CE Kartman, V Krishnan, R Liao, MLB Piruzeli, A Cardose, S Chakladar, B Crowe, P Reis, X Zhang, and DH Adams are employees and shareholders of Eli Lilly and Company. RD Pellegrini declared no conflict of interests. Other authors reported relationships with pharmaceutical companies including Eli Lilly and Company.

Source: Marconi VC et al. Lancet Respir Med. 2021 Sep 1. doi: 10.1016/S2213-2600(21)00331-3.

Key clinical point: Individuals with asthma have a 17% lower risk for COVID-19 infection than those without asthma.

Major finding: Individuals with asthma had a lower risk for COVID-19 infection (risk ratio [RR], 0.83; P = .01), but not for COVID-19-related hospitalization (RR, 1.18; P = .08), intensive care unit admission (RR, 1.21; P = .09), and ICU admission (RR, 1.06; P = .65).

Study details: The data come from a meta-analysis of 51 studies involving 965,551 individuals with and without asthma who tested positive for COVID-19.

Disclosures: This study was self-funded. The authors declared no conflict of interests.

Source: Sunjaya AP et al. Eur Respir J. 2021 Aug 24. doi: 10.1183/13993003.01209-2021.

Key clinical point: Individuals with asthma have a 17% lower risk for COVID-19 infection than those without asthma.

Major finding: Individuals with asthma had a lower risk for COVID-19 infection (risk ratio [RR], 0.83; P = .01), but not for COVID-19-related hospitalization (RR, 1.18; P = .08), intensive care unit admission (RR, 1.21; P = .09), and ICU admission (RR, 1.06; P = .65).

Study details: The data come from a meta-analysis of 51 studies involving 965,551 individuals with and without asthma who tested positive for COVID-19.

Disclosures: This study was self-funded. The authors declared no conflict of interests.

Source: Sunjaya AP et al. Eur Respir J. 2021 Aug 24. doi: 10.1183/13993003.01209-2021.

Key clinical point: Individuals with asthma have a 17% lower risk for COVID-19 infection than those without asthma.

Major finding: Individuals with asthma had a lower risk for COVID-19 infection (risk ratio [RR], 0.83; P = .01), but not for COVID-19-related hospitalization (RR, 1.18; P = .08), intensive care unit admission (RR, 1.21; P = .09), and ICU admission (RR, 1.06; P = .65).

Study details: The data come from a meta-analysis of 51 studies involving 965,551 individuals with and without asthma who tested positive for COVID-19.

Disclosures: This study was self-funded. The authors declared no conflict of interests.

Source: Sunjaya AP et al. Eur Respir J. 2021 Aug 24. doi: 10.1183/13993003.01209-2021.

Key clinical point: Infection with the SARS-CoV-2 Delta (B.1.617.2) variant carries a significantly higher risk for hospitalization and attending hospital for emergency care than the Alpha (B.1.1.7) variant.

Major finding: The Delta variant was associated with more than twice the risk of being admitted to hospital (adjusted hazard ratio [aHR], 2·26; 95% confidence interval [CI], 1·32-3·89) and nearly 1.5 times the risk of seeking emergency care (aHR, 1·45; 95% CI, 1·08-1·95) compared with the Alpha variant.

Study details: A cohort study included 43,338 COVID-19-positive cases in England who were found to be infected with either the Alpha or Delta SARS-CoV-2 variant through whole-genome sequencing.

Disclosures: The study was funded by Medical Research Council, UK Research and Innovation, Department of Health and Social Care, and National Institute for Health Research. GD's employer, Public Health England was funded by GlaxoSmithKline for a research project related to seasonal influenza and antiviral treatment but had no relation to COVID-19. The remaining authors declared no conflict of interests.

Source: Twohig KA et al. Lancet Infect Dis. 2021 Aug 27. doi: 10.1016/S1473-3099(21)00475-8.

Key clinical point: Infection with the SARS-CoV-2 Delta (B.1.617.2) variant carries a significantly higher risk for hospitalization and attending hospital for emergency care than the Alpha (B.1.1.7) variant.

Major finding: The Delta variant was associated with more than twice the risk of being admitted to hospital (adjusted hazard ratio [aHR], 2·26; 95% confidence interval [CI], 1·32-3·89) and nearly 1.5 times the risk of seeking emergency care (aHR, 1·45; 95% CI, 1·08-1·95) compared with the Alpha variant.

Study details: A cohort study included 43,338 COVID-19-positive cases in England who were found to be infected with either the Alpha or Delta SARS-CoV-2 variant through whole-genome sequencing.

Disclosures: The study was funded by Medical Research Council, UK Research and Innovation, Department of Health and Social Care, and National Institute for Health Research. GD's employer, Public Health England was funded by GlaxoSmithKline for a research project related to seasonal influenza and antiviral treatment but had no relation to COVID-19. The remaining authors declared no conflict of interests.

Source: Twohig KA et al. Lancet Infect Dis. 2021 Aug 27. doi: 10.1016/S1473-3099(21)00475-8.

Key clinical point: Infection with the SARS-CoV-2 Delta (B.1.617.2) variant carries a significantly higher risk for hospitalization and attending hospital for emergency care than the Alpha (B.1.1.7) variant.

Major finding: The Delta variant was associated with more than twice the risk of being admitted to hospital (adjusted hazard ratio [aHR], 2·26; 95% confidence interval [CI], 1·32-3·89) and nearly 1.5 times the risk of seeking emergency care (aHR, 1·45; 95% CI, 1·08-1·95) compared with the Alpha variant.

Study details: A cohort study included 43,338 COVID-19-positive cases in England who were found to be infected with either the Alpha or Delta SARS-CoV-2 variant through whole-genome sequencing.

Disclosures: The study was funded by Medical Research Council, UK Research and Innovation, Department of Health and Social Care, and National Institute for Health Research. GD's employer, Public Health England was funded by GlaxoSmithKline for a research project related to seasonal influenza and antiviral treatment but had no relation to COVID-19. The remaining authors declared no conflict of interests.

Source: Twohig KA et al. Lancet Infect Dis. 2021 Aug 27. doi: 10.1016/S1473-3099(21)00475-8.

Decreased motor function, as well as other adverse outcomes, are linked to post–COVID-19 syndrome in patients with Parkinson’s disease, new research suggests.

Results from a small, international retrospective case study show that about half of participants with Parkinson’s disease who developed post–COVID-19 syndrome experienced a worsening of motor symptoms and that their need for anti-Parkinson’s medication increased.

“In our series of 27 patients with Parkinson’s disease, 85% developed post–COVID-19 symptoms,” said lead investigator Valentina Leta, MD, Parkinson’s Foundation Center of Excellence, Kings College Hospital, London.

The most common long-term effects were worsening of motor function and an increase in the need for daily levodopa. Other adverse effects included fatigue; cognitive disturbances, including brain fog, loss of concentration, and memory deficits; and sleep disturbances, such as insomnia, Dr. Leta said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Long-term sequelae

Previous studies have documented worsening of motor and nonmotor symptoms among patients with Parkinson’s disease in the acute phase of COVID-19. Results of these studies suggest that mortality may be higher among patients with more advanced Parkinson’s disease, comorbidities, and frailty.

Dr. Leta noted that long-term sequelae with so-called long COVID have not been adequately explored, prompting the current study.

The case series included 27 patients with Parkinson’s disease in the United Kingdom, Italy, Romania, and Mexico who were also affected by COVID-19. The investigators defined post–COVID-19 syndrome as “signs and symptoms that develop during or after an infection consistent with COVID-19, continue for more than 12 weeks, and are not explained by an alternative diagnosis.”

Because some of the symptoms are also associated with Parkinson’s disease, symptoms were attributed to post–COVID-19 only if they occurred after a confirmed severe acute respiratory infection with SARS-CoV-2 or if patients experienced an acute or subacute worsening of a pre-existing symptom that had previously been stable.

Among the participants, 59.3% were men. The mean age at the time of Parkinson’s disease diagnosis was 59.0 ± 12.7 years, and the mean Parkinson’s disease duration was 9.2 ± 7.8 years. The patients were in Hoehn and Yahr stage 2.0 ± 1.0 at the time of their COVID-19 diagnosis.

Charlson Comorbidity Index score at COVID-19 diagnosis was 2.0 ± 1.5, and the levodopa equivalent daily dose (LEDD) was 1053.5 ± 842.4 mg.
 

Symptom worsening

“Cognitive disturbances” were defined as brain fog, concentration difficulty, or memory problems. “Peripheral neuropathy symptoms” were defined as having feelings of pins and needles or numbness.

By far, the most prevalent sequelae were worsening motor symptoms and increased need for anti-Parkinson’s medications. Each affected about half of the study cohort, the investigators noted.

Dr. Leta added the non-Parkinson’s disease-specific findings are in line with the existing literature on long COVID in the general population. The severity of COVID-19, as indicated by a history of hospitalization, did not seem to correlate with development of post–COVID-19 syndrome in patients with Parkinson’s disease.

In this series, few patients had respiratory, cardiovascular, gastrointestinal, musculoskeletal, or dermatologic symptoms. Interestingly, only four patients reported a loss of taste or smell.

The investigators noted that in addition to viral illness, the stress of prolonged lockdown during the pandemic and reduced access to health care and rehabilitation programs may contribute to the burden of post–COVID-19 syndrome in patients with Parkinson’s disease.

Study limitations cited include the relatively small sample size and the lack of a control group. The researchers noted the need for larger studies to elucidate the natural history of COVID-19 among patients with Parkinson’s disease in order to raise awareness of their needs and to help develop personalized management strategies.
 

Meaningful addition

Commenting on the findings, Kyle Mitchell, MD, movement disorders neurologist, Duke University, Durham, N.C., said he found the study to be a meaningful addition in light of the fact that data on the challenges that patients with Parkinson’s disease may face after having COVID-19 are limited.

“What I liked about this study was there’s data from multiple countries, what looks like a diverse population of study participants, and really just addressing a question that we get asked a lot in clinic and we see a fair amount, but we don’t really know a lot about: how people with Parkinson’s disease will do during and post COVID-19 infection,” said Dr. Mitchell, who was not involved with the research.

He said the worsening of motor symptoms and the need for increased dopaminergic medication brought some questions to mind.

“Is this increase in medications permanent, or is it temporary until post-COVID resolves? Or is it truly something where they stay on a higher dose?” he asked.

Dr. Mitchell said he does not believe the worsening of symptoms is specific to COVID-19 and that he sees individuals with Parkinson’s disease who experience setbacks “from any number of infections.” These include urinary tract infections and influenza, which are associated with worsening mobility, rigidity, tremor, fatigue, and cognition.

“People with Parkinson’s disease seem to get hit harder by infections in general,” he said.

The study had no outside funding. Dr. Leta and Dr. Mitchell have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Decreased motor function, as well as other adverse outcomes, are linked to post–COVID-19 syndrome in patients with Parkinson’s disease, new research suggests.

Results from a small, international retrospective case study show that about half of participants with Parkinson’s disease who developed post–COVID-19 syndrome experienced a worsening of motor symptoms and that their need for anti-Parkinson’s medication increased.

“In our series of 27 patients with Parkinson’s disease, 85% developed post–COVID-19 symptoms,” said lead investigator Valentina Leta, MD, Parkinson’s Foundation Center of Excellence, Kings College Hospital, London.

The most common long-term effects were worsening of motor function and an increase in the need for daily levodopa. Other adverse effects included fatigue; cognitive disturbances, including brain fog, loss of concentration, and memory deficits; and sleep disturbances, such as insomnia, Dr. Leta said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Long-term sequelae

Previous studies have documented worsening of motor and nonmotor symptoms among patients with Parkinson’s disease in the acute phase of COVID-19. Results of these studies suggest that mortality may be higher among patients with more advanced Parkinson’s disease, comorbidities, and frailty.

Dr. Leta noted that long-term sequelae with so-called long COVID have not been adequately explored, prompting the current study.

The case series included 27 patients with Parkinson’s disease in the United Kingdom, Italy, Romania, and Mexico who were also affected by COVID-19. The investigators defined post–COVID-19 syndrome as “signs and symptoms that develop during or after an infection consistent with COVID-19, continue for more than 12 weeks, and are not explained by an alternative diagnosis.”

Because some of the symptoms are also associated with Parkinson’s disease, symptoms were attributed to post–COVID-19 only if they occurred after a confirmed severe acute respiratory infection with SARS-CoV-2 or if patients experienced an acute or subacute worsening of a pre-existing symptom that had previously been stable.

Among the participants, 59.3% were men. The mean age at the time of Parkinson’s disease diagnosis was 59.0 ± 12.7 years, and the mean Parkinson’s disease duration was 9.2 ± 7.8 years. The patients were in Hoehn and Yahr stage 2.0 ± 1.0 at the time of their COVID-19 diagnosis.

Charlson Comorbidity Index score at COVID-19 diagnosis was 2.0 ± 1.5, and the levodopa equivalent daily dose (LEDD) was 1053.5 ± 842.4 mg.
 

Symptom worsening

“Cognitive disturbances” were defined as brain fog, concentration difficulty, or memory problems. “Peripheral neuropathy symptoms” were defined as having feelings of pins and needles or numbness.

By far, the most prevalent sequelae were worsening motor symptoms and increased need for anti-Parkinson’s medications. Each affected about half of the study cohort, the investigators noted.

Dr. Leta added the non-Parkinson’s disease-specific findings are in line with the existing literature on long COVID in the general population. The severity of COVID-19, as indicated by a history of hospitalization, did not seem to correlate with development of post–COVID-19 syndrome in patients with Parkinson’s disease.

In this series, few patients had respiratory, cardiovascular, gastrointestinal, musculoskeletal, or dermatologic symptoms. Interestingly, only four patients reported a loss of taste or smell.

The investigators noted that in addition to viral illness, the stress of prolonged lockdown during the pandemic and reduced access to health care and rehabilitation programs may contribute to the burden of post–COVID-19 syndrome in patients with Parkinson’s disease.

Study limitations cited include the relatively small sample size and the lack of a control group. The researchers noted the need for larger studies to elucidate the natural history of COVID-19 among patients with Parkinson’s disease in order to raise awareness of their needs and to help develop personalized management strategies.
 

Meaningful addition

Commenting on the findings, Kyle Mitchell, MD, movement disorders neurologist, Duke University, Durham, N.C., said he found the study to be a meaningful addition in light of the fact that data on the challenges that patients with Parkinson’s disease may face after having COVID-19 are limited.

“What I liked about this study was there’s data from multiple countries, what looks like a diverse population of study participants, and really just addressing a question that we get asked a lot in clinic and we see a fair amount, but we don’t really know a lot about: how people with Parkinson’s disease will do during and post COVID-19 infection,” said Dr. Mitchell, who was not involved with the research.

He said the worsening of motor symptoms and the need for increased dopaminergic medication brought some questions to mind.

“Is this increase in medications permanent, or is it temporary until post-COVID resolves? Or is it truly something where they stay on a higher dose?” he asked.

Dr. Mitchell said he does not believe the worsening of symptoms is specific to COVID-19 and that he sees individuals with Parkinson’s disease who experience setbacks “from any number of infections.” These include urinary tract infections and influenza, which are associated with worsening mobility, rigidity, tremor, fatigue, and cognition.

“People with Parkinson’s disease seem to get hit harder by infections in general,” he said.

The study had no outside funding. Dr. Leta and Dr. Mitchell have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Decreased motor function, as well as other adverse outcomes, are linked to post–COVID-19 syndrome in patients with Parkinson’s disease, new research suggests.

Results from a small, international retrospective case study show that about half of participants with Parkinson’s disease who developed post–COVID-19 syndrome experienced a worsening of motor symptoms and that their need for anti-Parkinson’s medication increased.

“In our series of 27 patients with Parkinson’s disease, 85% developed post–COVID-19 symptoms,” said lead investigator Valentina Leta, MD, Parkinson’s Foundation Center of Excellence, Kings College Hospital, London.

The most common long-term effects were worsening of motor function and an increase in the need for daily levodopa. Other adverse effects included fatigue; cognitive disturbances, including brain fog, loss of concentration, and memory deficits; and sleep disturbances, such as insomnia, Dr. Leta said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Long-term sequelae

Previous studies have documented worsening of motor and nonmotor symptoms among patients with Parkinson’s disease in the acute phase of COVID-19. Results of these studies suggest that mortality may be higher among patients with more advanced Parkinson’s disease, comorbidities, and frailty.

Dr. Leta noted that long-term sequelae with so-called long COVID have not been adequately explored, prompting the current study.

The case series included 27 patients with Parkinson’s disease in the United Kingdom, Italy, Romania, and Mexico who were also affected by COVID-19. The investigators defined post–COVID-19 syndrome as “signs and symptoms that develop during or after an infection consistent with COVID-19, continue for more than 12 weeks, and are not explained by an alternative diagnosis.”

Because some of the symptoms are also associated with Parkinson’s disease, symptoms were attributed to post–COVID-19 only if they occurred after a confirmed severe acute respiratory infection with SARS-CoV-2 or if patients experienced an acute or subacute worsening of a pre-existing symptom that had previously been stable.

Among the participants, 59.3% were men. The mean age at the time of Parkinson’s disease diagnosis was 59.0 ± 12.7 years, and the mean Parkinson’s disease duration was 9.2 ± 7.8 years. The patients were in Hoehn and Yahr stage 2.0 ± 1.0 at the time of their COVID-19 diagnosis.

Charlson Comorbidity Index score at COVID-19 diagnosis was 2.0 ± 1.5, and the levodopa equivalent daily dose (LEDD) was 1053.5 ± 842.4 mg.
 

Symptom worsening

“Cognitive disturbances” were defined as brain fog, concentration difficulty, or memory problems. “Peripheral neuropathy symptoms” were defined as having feelings of pins and needles or numbness.

By far, the most prevalent sequelae were worsening motor symptoms and increased need for anti-Parkinson’s medications. Each affected about half of the study cohort, the investigators noted.

Dr. Leta added the non-Parkinson’s disease-specific findings are in line with the existing literature on long COVID in the general population. The severity of COVID-19, as indicated by a history of hospitalization, did not seem to correlate with development of post–COVID-19 syndrome in patients with Parkinson’s disease.

In this series, few patients had respiratory, cardiovascular, gastrointestinal, musculoskeletal, or dermatologic symptoms. Interestingly, only four patients reported a loss of taste or smell.

The investigators noted that in addition to viral illness, the stress of prolonged lockdown during the pandemic and reduced access to health care and rehabilitation programs may contribute to the burden of post–COVID-19 syndrome in patients with Parkinson’s disease.

Study limitations cited include the relatively small sample size and the lack of a control group. The researchers noted the need for larger studies to elucidate the natural history of COVID-19 among patients with Parkinson’s disease in order to raise awareness of their needs and to help develop personalized management strategies.
 

Meaningful addition

Commenting on the findings, Kyle Mitchell, MD, movement disorders neurologist, Duke University, Durham, N.C., said he found the study to be a meaningful addition in light of the fact that data on the challenges that patients with Parkinson’s disease may face after having COVID-19 are limited.

“What I liked about this study was there’s data from multiple countries, what looks like a diverse population of study participants, and really just addressing a question that we get asked a lot in clinic and we see a fair amount, but we don’t really know a lot about: how people with Parkinson’s disease will do during and post COVID-19 infection,” said Dr. Mitchell, who was not involved with the research.

He said the worsening of motor symptoms and the need for increased dopaminergic medication brought some questions to mind.

“Is this increase in medications permanent, or is it temporary until post-COVID resolves? Or is it truly something where they stay on a higher dose?” he asked.

Dr. Mitchell said he does not believe the worsening of symptoms is specific to COVID-19 and that he sees individuals with Parkinson’s disease who experience setbacks “from any number of infections.” These include urinary tract infections and influenza, which are associated with worsening mobility, rigidity, tremor, fatigue, and cognition.

“People with Parkinson’s disease seem to get hit harder by infections in general,” he said.

The study had no outside funding. Dr. Leta and Dr. Mitchell have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.