Background SARS-CoV-2 IgG antibody measurements can be used to estimate the proportion of a population exposed or infected and may be informative about the risk of future infection. Previous estimates of the duration of antibody responses vary. Methods We present 6 months of data from a longitudinal seroprevalence study of 3276 UK healthcare workers (HCWs). Serial measurements of SARS-CoV-2 anti-nucleocapsid and anti-spike IgG were obtained. Interval censored survival analysis was used to investigate the duration of detectable responses. Additionally, Bayesian mixed linear models were used to investigate anti-nucleocapsid waning. Results Anti-spike IgG levels remained stably detected after a positive result, e.g., in 94% (95% credibility interval, CrI, 91-96%) of HCWs at 180 days. Anti-nucleocapsid IgG levels rose to a peak at 24 (95% credibility interval, CrI 19-31) days post first PCR-positive test, before beginning to fall. Considering 452 anti-nucleocapsid seropositive HCWs over a median of 121 days from their maximum positive IgG titre, the mean estimated antibody half-life was 85 (95%CrI, 81-90) days. Higher maximum observed anti-nucleocapsid titres were associated with longer estimated antibody half-lives. Increasing age, Asian ethnicity and prior self-reported symptoms were independently associated with higher maximum anti-nucleocapsid levels and increasing age and a positive PCR test undertaken for symptoms with longer anti-nucleocapsid half-lives. Conclusion SARS-CoV-2 anti-nucleocapsid antibodies wane within months, and faster in younger adults and those without symptoms. However, anti-spike IgG remains stably detected. Ongoing longitudinal studies are required to track the long-term duration of antibody levels and their association with immunity to SARS-CoV-2 reinfection.

Background and AimThe study aims to determine and quantify the stratified risk of recurrent pancreatitis (RP) after the first episode of acute pancreatitis in relation to etiology and severity of disease.MethodsA systematic review and meta‐analysis in compliance with PRISMA statement standards was conducted. A search of electronic information sources was conducted to identify all studies investigating the risk of RP after the first episode of acute pancreatitis. Proportion meta‐analysis models using random effects were constructed to calculate the weighted summary risks of RP. Meta‐regression was performed to evaluate the effect of different variables on the pooled outcomes.ResultsAnalysis of 57,815 patients from 42 studies showed that the risk of RP after first episode was 19.8% (95% confidence interval [CI] 17.5–22.1%). The risk of RP was 11.9% (10.2–13.5%) after gallstone pancreatitis, 28.7% (23.5–33.9%) after alcohol‐induced pancreatitis, 30.3% (15.5–45.0%) after hyperlipidemia‐induced pancreatitis, 38.1% (28.9–47.3%) after autoimmune pancreatitis, 15.1% (11.6–18.6%) after idiopathic pancreatitis, 22.0% (16.9–27.1%) after mild pancreatitis, 23.9% (12.9–34.8%) after moderate pancreatitis, 21.6% (14.6–28.7%) after severe pancreatitis, and 6.6% (4.1–9.2%) after cholecystectomy following gallstone pancreatitis. Meta‐regression confirmed that the results were not affected by the year of study (P = 0.541), sample size (P = 0.064), length of follow‐up (P = 0.348), and age of patients (P = 0.138) in the included studies.ConclusionsThe risk of RP after the first episode of acute pancreatitis seems to be affected by the etiology of pancreatitis but not the severity of disease. The risks seem to be higher in patients with autoimmune pancreatitis, hyperlipidemia‐induced pancreatitis, and alcohol‐induced pancreatitis and lower in patients with gallstone pancreatitis and idiopathic pancreatitis.

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