2587 Weiss, et al: HSP and infections Personal non-commercial use only. The Journal of Rheumatology Copyright © 2010. All rights reserved. Temporal Association of Streptococcus, Staphylococcus, and Parainfluenza Pediatric Hospitalizations and Hospitalized Cases of Henoch-Schönlein Purpura PAMELA F. WEISS, ANDREW J. KLINK, XIANQUN LUAN, and CHRIS FEUDTNER ABSTRACT. Objective. To determine if hospitalizations for specific infectious exposures are associated with hos- pital admissions for Henoch-Schönlein purpura (HSP). Methods. We conducted a retrospective cohort study using administrative data of children admitted to 40 children’s hospitals between January 1, 2002, and December 31, 2008. We examined the asso- ciation of standardized rates of group A ß-hemolytic Streptococcus (GABS), Staphylococcus aureus, parainfluenza, influenza, adenovirus, and respiratory syncytial virus (RSV)-associated hospital admissions with standardized rates of HSP hospital admissions on a month by month basis using autoregressive moving average process models to account for temporal autocorrelation and cluster- ing by hospital. Results. Among the 3,132 admissions for HSP observed over the 7-year study period, hospital admissions were most frequent September through April, but with substantial variability between hospitals for each month. Accounting for these month by month differences within each hospital, the rate of HSP admissions in a given month increased significantly as the standardized rates of GABS (p = 0.01), S. aureus (p < 0.01), and parainfluenza (p = 0.03) admissions increased. Conclusion. Our results demonstrate a local month by month temporal association between hospi- talization for GABS, S. aureus, and parainfluenza and hospitalization for HSP. Future investigations will be required to determine causality. (First Release Sept 15 2010; J Rheumatol 2010;37:2587–94; doi:10.3899/jrheum.100364) Key Indexing Terms: PEDIATRIC RHEUMATOLOGY EPIDEMIOLOGY VASCULITIS INFECTION HENOCH-SCHÖNLEIN PURPURA From the Division of Rheumatology, Division of General Pediatrics, Healthcare Analytics Unit, and Center for Pediatric Clinical Effectiveness, The Children’s Hospital of Philadelphia; and Department of Pediatrics, Center for Clinical Epidemiology and Biostatistics, and Leonard Davis Institute of Health Economics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. Dr. Weiss was supported by the American College of Rheumatology Research and Education Foundation Clinical Investigator Fellowship Award. P.F. Weiss, MD, MSCE, Division of Rheumatology and Center for Pediatric Clinical Effectiveness, Children’s Hospital of Philadelphia, and Department of Pediatrics, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine; A.J. Klink, MPH, Division of Rheumatology, Center for Pediatric Clinical Effectiveness, Children’s Hospital of Philadelphia; X. Luan, MS, Healthcare Analytics Unit and Center for Pediatric Clinical Effectiveness, Children’s Hospital of Philadelphia; C. Feudtner, MD, MPH, PhD, Division of General Pediatrics and Center for Pediatric Clinical Effectiveness, Children’s Hospital of Philadelphia, and Department of Pediatrics, Center for Clinical Epidemiology and Biostatistics, and Leonard Davis Institute of Health Economics, University of Pennsylvania School of Medicine. Address correspondence to Dr. P.F. Weiss, Room 1539, North Campus, Division of Rheumatology, The Children’s Hospital of Philadelphia, 3535 Market Street, Philadelphia, PA 19104. E-mail: weisspa@email.chop.edu. Accepted for publication July 27, 2010. Henoch-Schönlein purpura (HSP) is an acute vasculitis, affecting 8 to 20 per 100,000 children each year and accounting for half of all childhood vasculitis in the United States 1,2 . According to the European League Against Rheumatism (EULAR), HSP is defined as occurring when there is palpable purpura plus one of the following: diffuse abdominal pain, any biopsy showing predominant IgA dep- osition, arthritis or arthralgias, and renal involvement (any hematuria or proteinuria) 3 . HSP is characterized by promi- nent seasonal variation, with most cases occurring in the winter or spring. While the precise etiology of HSP is unknown, IgA, genetics, and infections each appear to con- tribute to the pathogenesis. Decreased glycosylation of IgA1 increases its propensity to aggregate, activates the alterna- tive complement pathway, and results in tissue deposition 4,5 . Familial genetic aggregation studies 6,7 and an established association with familial Mediterranean fever syndrome 8 lend support for a genetic predisposition for HSP. Additionally, the seasonal nature suggests that antecedent infections contribute to disease pathogenesis in genetically susceptible children. HSP is preceded by an upper respirato- ry tract infection in 30%–50% of cases 9,10,11 , but there is no clear and consistent evidence for an etiologic role of any single organism. Infectious triggers reportedly associated with HSP are numerous and include Group A ß-hemolytic Streptococcus (GABS), Staphylococcus aureus, Kingella kingae, www.jrheum.org Downloaded on November 1, 2021 from