ArticleRheumatology international2019
Is Henoch-Schönlein purpura a susceptibility factor for functional gastrointestinal disorders in children?
Article in Rheumatology international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Machine learning differentiation of abdominal IgA vasculitis without purpura from appendicitis.Pediatric research · 2026Article
- Predictors of Abdominal Pain Duration in Henoch-Schönlein Purpura and Nomogram Model Development: A Retrospective Study of 220 Cases.Journal of inflammation research · 2025Article
- Clinico-Epidemiological Profile and Outcome of Children with IgA Vasculitis in Aseer Region, Southwestern Saudi Arabia.Healthcare (Basel, Switzerland) · 2021Article
- Systematic Review of Pediatric Functional Gastrointestinal Disorders (Rome IV Criteria).Journal of clinical medicine · 2021Review
- Association between anti-α-1,4-D-polygalacturonic acid antibodies and Henoch-Schönlein purpura in children.The Journal of international medical research · 2019Observational
- Frequency of functional gastrointestinal disorders in children with familial Mediterranean fever.Clinical rheumatology · 2019Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Henoch-Schönlein purpura (HSP), the most common childhood vasculitis is characterized by non-thrombocytopenic palpable purpura, arthritis/arthralgia, abdominal pain and renal involvement. Functional gastrointestinal disorders (FGIDs) are heterogeneous disease spectrum with unclear etiology and include the most common subtypes: functional dyspepsia, irritable bowel syndrome (IBS), functional abdominal pain and functional constipation. Formerly, FGIDs were known as non-organic disorders; however, recent advances revealed that low-grade inflammation may also play a role. We aimed to clarify whether HSP predisposes to FGIDs in pediatric population. Seventy-four children with HSP, diagnosed at least 6 months before the study and 78 healthy controls were enrolled to the study. Patients with red flag signs for organic GI disorders were excluded. Rome IV criteria were utilized for FGIDs diagnosis. We compared the frequencies of FGIDs between HSP patients and healthy subjects. We also examined the parameters including age, abdominal pain, arthralgia, bloody stool, renal involvement and treatment with corticosteroids and laboratory results at HSP diagnosis such as erythrocyte sedimentation rate, C-reactive protein, hemoglobin, leukocytes and platelet counts among patients with and without FGIDs. Overall FGIDs and IBS frequency were 35.1% (n = 26) and 10.8% (n = 8) in HSP patients, 19.2% (n = 15) and 2.6% (n = 2) in healthy controls, respectively. Disease characteristics and laboratory parameters at disease onset were similar between HSP patients with and without FGIDs. Overall FGIDs rate, particularly IBS were statistically higher in HSP patients. We speculate that children with preceding HSP may be predisposed to FGIDs. Since the FGIDs pathogenesis is still remains unclear, further studies are needed to confirm this hypothesis and clarify the etiology. Physicians also should pay attention to FGIDs in HSP patients with ongoing abdominal pain and thus prevent this comorbidity with dietary and psychologic measures.
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