Laboratory trends, hyperinflammation, and clinical outcomes for patients with a systemic rheumatic disease admitted to hospital for COVID-19: a retrospective, comparative cohort study.

Summary Background COVID-19 can induce a hyperinflammatory state, which might lead to poor clinical outcomes. We aimed to assess whether patients with a systemic rheumatic disease might be at increased risk for hyperinflammation and respiratory failure from COVID-19. Methods We did a retrospective, comparative cohort study of patients aged 18 years or older admitted to hospital with PCR-confirmed COVID-19 at Mass General Brigham (Boston, USA). We identified patients by a search of electronic health records and matched patients with a systemic rheumatic disease 1:5 to comparators. We compared individual laboratory results by case status and extracted laboratory results and COVID-19 outcomes for each participant. We calculated the COVID-19-associated hyperinflammation score (cHIS), a composite of six domains (a score of ≥2 indicating hyperinflammation) and used logistic regression to estimate odds ratios (ORs) for COVID-19 outcomes by hyperinflammation and case status. Findings We identified 57 patients with a systemic rheumatic disease and 232 matched comparators who were admitted to hospital with COVID-19 between Jan 30 and July 7, 2020; 38 (67%) patients with a rheumatic disease were female compared with 158 (68%) matched comparators. Patients with a systemic rheumatic disease had higher peak median neutrophil-to-lymphocyte ratio (9·6 [IQR 6·4–22·2] vs 7·8 [4·5–16·5]; p=0·021), lactate dehydrogenase concentration (421 U/L [297–528] vs 345 U/L [254–479]; p=0·044), creatinine concentration (1·2 mg/dL [0·9–2·0] vs 1·0 mg/dL [0·8–1·4], p=0·014), and blood urea nitrogen concentration (31 mg/dL [15–61] vs 23 mg/dL [13–37]; p=0·033) than comparators, but median C-reactive protein concentration (149·4 mg/L [76·4–275·3] vs 116·3 mg/L [58·8–225·9]; p=0·11) was not significantly different. Patients with a systemic rheumatic disease had higher peak median cHIS than comparators (3 [1–5] vs 2 [1–4]; p=0·013). All patients with a peak cHIS of 2 or more had higher odds of admission to intensive care (OR 3·45 [95% CI 1·98–5·99]), mechanical ventilation (66·20 [8·98–487·80]), and in-hospital mortality (16·37 [4·75–56·38]) than patients with a peak cHIS of less than 2. In adjusted analyses, patients with a rheumatic disease had higher odds of admission to intensive care (2·08 [1·09–3·96]) and mechanical ventilation (2·60 [1·32–5·12]) than comparators, but not in-hospital mortality (1.78 [0·79–4·02]). Among patients who were discharged from hospital, risk of rehospitalisation (1·08 [0·37–3·16]) and mortality within 60 days (1·20 [0·58–2·47]) was similar in patients and comparators. Interpretation Patients with a systemic rheumatic disease who were admitted to hospital for COVID-19 had increased risk for hyperinflammation, kidney injury, admission to intensive care, and mechanical ventilation compared with matched comparators. However, among patients who survived, post-discharge outcomes were not significantly different. The cHIS identified patients with hyperinflammation, which was strongly associated with poor COVID-19 outcomes in both patients with a rheumatic disease and comparators. Clinicians should be aware that patients with systemic rheumatic diseases and COVID-19 could be susceptible to hyperinflammation and poor hospital outcomes. Funding None.