Johannes C Nossent1,2, Warren Raymond3,4, Helen Keen3,4, David B Preen3,4, Charles A Inderjeeth3,4. 1. From the Department of Rheumatology, Sir Charles Gairdner Hospital; the Rheumatology Group, School of Medicine, University of Western Australia; Department of Rheumatology, Fiona Stanley Hospital; and the School of Population and Global Health, University of Western Australia, Perth, Australia. johannes.nossent@uwa.edu.au. 2. J.C. Nossent, MD, PhD, Department of Rheumatology, Sir Charles Gairdner Hospital, and the Rheumatology Group, School of Medicine, University of Western Australia; W. Raymond, BSc, Rheumatology Group, School of Medicine, University of Western Australia; H. Keen, MBBS, PhD, Rheumatology Group, School of Medicine, University of Western Australia, and the Department of Rheumatology, Fiona Stanley Hospital; D.B. Preen, PhD, School of Population and Global Health, University of Western Australia; C.A. Inderjeeth, MBBS, MPH, Department of Rheumatology, Sir Charles Gairdner Hospital, and the Rheumatology Group, School of Medicine, University of Western Australia. johannes.nossent@uwa.edu.au. 3. From the Department of Rheumatology, Sir Charles Gairdner Hospital; the Rheumatology Group, School of Medicine, University of Western Australia; Department of Rheumatology, Fiona Stanley Hospital; and the School of Population and Global Health, University of Western Australia, Perth, Australia. 4. J.C. Nossent, MD, PhD, Department of Rheumatology, Sir Charles Gairdner Hospital, and the Rheumatology Group, School of Medicine, University of Western Australia; W. Raymond, BSc, Rheumatology Group, School of Medicine, University of Western Australia; H. Keen, MBBS, PhD, Rheumatology Group, School of Medicine, University of Western Australia, and the Department of Rheumatology, Fiona Stanley Hospital; D.B. Preen, PhD, School of Population and Global Health, University of Western Australia; C.A. Inderjeeth, MBBS, MPH, Department of Rheumatology, Sir Charles Gairdner Hospital, and the Rheumatology Group, School of Medicine, University of Western Australia.
Abstract
OBJECTIVE: Clinical data suggest that infections can trigger IgA vasculitis (IgAV), but longterm observations are lacking. We compared rates, types, and microorganisms for serious infection before and after diagnosis for children with IgAV and non-exposed controls. METHODS: Using population-based administrative linked health datasets we estimated incidence rates (IR) for serious infection per 1000 person-months for patients with IgAV (n = 504, age 5 yrs, 59.1% males) and controls matched for age, sex, and year of presentation (n = 1281, age 6 yrs, 66% males). Time zero (T0) was the date of IgAV diagnosis or equivalent date in controls, lookback (median 38 mos) was the period prior to T0, and followup (median 239 mos) was the period after T0. RESULTS: During lookback, prevalence of serious infection was similar in patients with IgAV and controls (11.5% vs 9.5%, respectively), but patients with IgAV had a higher rate of upper respiratory tract infections [incidence rate ratio (IRR) 1.79; 95% CI 1.39-2.31] with shorter time between first serious infection and T0 (27 vs 43 mos; p = 0.02). During followup, patients were at a constant increased risk for serious infections (IRR 1.46, 95% CI 1.35-1.58). These rates were higher during followup: sepsis (IRR 12.6), pneumonia (IRR 6.19), upper respiratory tract infections (IRR 2.36), and skin infections (IRR 1.85). There was little overlap between patients with serious infections in the lookback and followup periods. CONCLUSION: In patients with childhood IgAV there is an increased longterm risk for a broader spectrum of infections, which is unrelated to serious infections prior to diagnosis or treatment. This suggests disease-specific factors may have a lasting effect on immune competence in childhood IgAV.
OBJECTIVE: Clinical data suggest that infections can trigger IgA vasculitis (IgAV), but longterm observations are lacking. We compared rates, types, and microorganisms for serious infection before and after diagnosis for children with IgAV and non-exposed controls. METHODS: Using population-based administrative linked health datasets we estimated incidence rates (IR) for serious infection per 1000 person-months for patients with IgAV (n = 504, age 5 yrs, 59.1% males) and controls matched for age, sex, and year of presentation (n = 1281, age 6 yrs, 66% males). Time zero (T0) was the date of IgAV diagnosis or equivalent date in controls, lookback (median 38 mos) was the period prior to T0, and followup (median 239 mos) was the period after T0. RESULTS: During lookback, prevalence of serious infection was similar in patients with IgAV and controls (11.5% vs 9.5%, respectively), but patients with IgAV had a higher rate of upper respiratory tract infections [incidence rate ratio (IRR) 1.79; 95% CI 1.39-2.31] with shorter time between first serious infection and T0 (27 vs 43 mos; p = 0.02). During followup, patients were at a constant increased risk for serious infections (IRR 1.46, 95% CI 1.35-1.58). These rates were higher during followup: sepsis (IRR 12.6), pneumonia (IRR 6.19), upper respiratory tract infections (IRR 2.36), and skin infections (IRR 1.85). There was little overlap between patients with serious infections in the lookback and followup periods. CONCLUSION: In patients with childhood IgAV there is an increased longterm risk for a broader spectrum of infections, which is unrelated to serious infections prior to diagnosis or treatment. This suggests disease-specific factors may have a lasting effect on immune competence in childhood IgAV.
Entities:
Keywords:
CHILDREN; INFECTION RISK; IgA VASCULITIS
Authors: Khalid Almutairi; Charles Inderjeeth; David B Preen; Helen Keen; Katrina Rogers; Johannes Nossent Journal: Rheumatol Int Date: 2021-02-23 Impact factor: 2.631