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Gout and the risk of COVID-19 diagnosis and death in the UK Biobank: a population-based study

Topless et al., The Lancet Rheumatology, doi:10.1016/S2665-9913(21)00401-X
Jan 2022  
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Mortality 23% Improvement Relative Risk Colchicine for COVID-19  Topless et al.  Prophylaxis Is prophylaxis with colchicine beneficial for COVID-19? Retrospective 341,398 patients in the United Kingdom Lower mortality with colchicine (not stat. sig., p=0.12) c19early.org Topless et al., The Lancet Rheumatology, Jan 2022 Favorscolchicine Favorscontrol 0 0.5 1 1.5 2+
Colchicine for COVID-19
5th treatment shown to reduce risk in September 2020, now with p = 0.00000031 from 56 studies.
Lower risk for mortality, ICU, hospitalization, and recovery.
No treatment is 100% effective. Protocols combine treatments.
5,100+ studies for 111 treatments. c19early.org
UK Biobank retrospective showing a higher risk of COVID-19 cases and mortality for patients with gout. Among patients with gout, mortality risk was lower for those on colchicine, OR 1.06 [0.60-1.89], compared to those without colchicine, OR 1.38 [1.08-1.76].
Although the 23% lower mortality is not statistically significant, it is consistent with the significant 28% lower mortality [17‑37%] from meta analysis of the 43 mortality results to date.
risk of death, 23.2% lower, OR 0.77, p = 0.12, relative odds for patients with gout, model 2, RR approximated with OR.
Effect extraction follows pre-specified rules prioritizing more serious outcomes. Submit updates
Topless et al., 28 Jan 2022, retrospective, database analysis, United Kingdom, peer-reviewed, 6 authors, dosage not specified.
This PaperColchicineAll
Gout and the risk of COVID-19 diagnosis and death in the UK Biobank: a population-based study
Ruth K Topless, MD Angelo Gaffo, Lisa K Stamp, Philip C Robinson, Nicola Dalbeth, Prof Tony R Merriman
The Lancet Rheumatology, doi:10.1016/s2665-9913(21)00401-x
Background There is a paucity of data on outcomes for people with gout and COVID-19. We aimed to assess whether gout is a risk factor for diagnosis of COVID-19 and COVID-19-related death, and to test for sex-and drug-specific differences in risk. Methods We used data from the UK Biobank, which included 15 871 people with gout. We used multivariable-adjusted logistic regression in the following analyses using a case-control study design: to test for an association between gout and COVID-19 diagnosis in the entire UK Biobank cohort (n=459 837); to test for an association between gout and COVID-19-related death in people who were known to have died or survived with COVID-19 (n=15 772); to test for an association between gout and COVID-19-related death in the entire UK Biobank cohort (n=459 837); and to assess risk of COVID-19-related death in a subset of patients from the UK Biobank cohort with prescription data, stratified by prescription of urate-lowering therapy and colchicine (n=341 398). Models 1 and 2 were adjusted for age group, sex, ethnicity, Townsend deprivation index, BMI, and smoking status. Model 2 was also adjusted for diagnosis of 16 other diseases that are established comorbidities of gout or established risk factors for COVID-19-related death. Findings Gout was associated with diagnosis of COVID-19 (odds ratio [OR] 1•20, 95% CI 1•11-1•29) but not with risk of COVID-19-related death in the cohort of patients diagnosed with COVID-19 (1•20, 0•96-1•51). In the entire cohort, gout was associated with COVID-19-related death (1•29, 1•06-1•56); women with gout had an increased risk of COVID-19-related death (1•98, 1•34-2•94), whereas men with gout did not (1•16, 0•93-1•45). We found no significant differences in the risk of COVID-19-related death according to prescription of urate-lowering therapy or colchicine. When patients with gout were stratified by vaccination status, the risk of diagnosis with COVID-19 was significant in the non-vaccinated group (1•21, 1•11-1•30) but not the vaccinated group (1•09, 0•65-1•85). Interpretation Gout is a risk factor for COVID-19-related death in the UK Biobank cohort, with an increased risk in women with gout, which was driven by risk factors independent of the metabolic comorbidities of gout.
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