{"doi":"10.1002/art.41447","title":"COVID‐19 in Rheumatic Diseases: A Research Agenda","abstract":"Although only a few months have passed since the coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS–Cov-2) began, we have learned a lot about the infection and the outcomes in individuals with rheumatic diseases. Herein, I summarized recent findings as well as remaining gaps in knowledge concerning the epidemiology and outcomes of COVID-19 in rheumatic diseases. I also outlined a clinical research agenda for the coming months. Much of the research addressing this issue has come from European cities heavily impacted early on during the pandemic. Researchers quickly mobilized to systematically survey entire clinic populations or disease cohorts, identifying COVID-19 cases and their outcomes. Across the >3,000 people included in these studies, the prevalence of COVID-19 was very low, and no deaths were recorded (1). In several cohorts, including 1 nationwide cohort of patients with inflammatory bowel disease treated with tumor necrosis factor inhibitor (TNFi) or thiopurine, the prevalence of COVID-19 was similar to that in the general population (2, 3). The survey described by Favalli and colleagues in this issue of Arthritis & Rheumatology provides further reassurance (4). The researchers contacted 955 individuals with inflammatory conditions seen in a biologics clinic in Pavia, Italy, achieving a remarkably high response rate of 98% over a short period. They found that <1% of patients had been diagnosed as having COVID-19, and no patient required mechanical ventilation or died. A recent study from China examined 42 families of people with rheumatic diseases in whom at least 1 person had COVID-19. Matching people with rheumatic disease to family members, they found a higher susceptibility to infection among those with rheumatic diseases. However, this was a small study, so no definitive conclusions can be drawn (5). Taken together, these studies suggest that the risk of contracting COVID-19 is either similar to or only slightly increased in people with rheumatic diseases. Indeed, the extremely high transmission rates in vulnerable populations in institutionalized settings, such as homeless shelters, prisons, and nursing homes, illustrate that initial infection is most strongly associated with high-risk exposures rather than underlying conditions or immunosuppression. Population-based studies and large case series in people with rheumatic diseases have shown that older age and the presence of comorbidities such as diabetes or cardiovascular, kidney, and lung disease increase the risk of hospitalization, mechanical ventilation, and death (1, 6). Comorbidities occur at higher rates in people with rheumatic disease, either as a result of organ manifestations of the underlying disease (e.g., lupus nephritis, interstitial lung disease) or as a complication of treatment (e.g., glucocorticoid-induced diabetes). This puts many of our patients in a high-risk group for severe COVID-19 outcomes like respiratory failure, although overall mortality rates have been low. Moreover, COVID-19 mortality rates in rheumatic diseases have been lower than in populations with cancer or organ transplants (1). Although more data are needed to look at specific drug categories, available studies provide some reassurance. For example, data from 600 patients in the COVID-19 Global Rheumatology Alliance (GRA) registry, a case-reporting registry for rheumatologists, show that most immunosuppressive drugs, including biologic DMARDs and targeted synthetic drugs, are not associated with a significantly higher risk of hospitalization (6). A case series of 86 patients with autoimmunity hospitalized due to COVID-19 in New York had similar findings (7). Studies using age- and sex-matched control designs also suggest comparable risks of hospitalization and mortality regardless of exposure to most immunosuppressive medications (8). Interestingly, moderate-to-high–dose glucocorticoids are the one class of medicati","journal":"Arthritis & Rheumatology","year":2020,"id":90158,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":8,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9638,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":24102,"name":"Jinoos Yazdany","orcid":"0000-0002-3508-4094","position":0,"is_corresponding":true}],"reference_count":10,"raw_metadata":null,"created_at":"2026-07-18T22:02:48.683291Z","pmid":"32705748","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}