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Clin Exp Rheumatol. 2016 May-Jun;34(3 Suppl 97):S84-8. Epub 2016 Feb 1.

Interleukin 1 beta (IL1ß) rs16944 genetic variant as a genetic marker of severe renal manifestations and renal sequelae in Henoch-Schönlein purpura.

Author information

1
Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
2
Medicine Department, Hospital Universitario San Cecilio, Granada, Spain.
3
Rheumatology Department, Hospital Universitario La Princesa, IIS-Princesa, Madrid, Spain.
4
Epidemiology and Computational Biology Department, School of Medicine, University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IDIVAL, Santander, Spain.
5
Division of Rheumatology, Hospital Universitario Lucus Augusti, Lugo, Spain.
6
Nephrology Department, Hospital Universitario San Cecilio, Granada, Spain.
7
Dermatology Department, Hospital Universitario La Princesa, IIS-Princesa, Madrid, Spain.
8
Rheumatology Department, Hospital Universitario Virgen del Rocío, Sevilla, Spain.
9
Rheumatology Department, Hospital Universitario de Basurto, Bilbao, Spain.
10
Institute of Parasitology and Biomedicine López-Neyra, CSIC, Granada, Spain.
11
Epidemiology, Genetics & Atherosclerosis Res.Group, Systemic Inflammatory Diseases, IDIVAL; School of Medicine, Univ.of Cantabria, Santander, Spain; and Cardiovascular Pathophysiology & Genomics Research, Univ.of Witwatersrand, Johannesburg, South Africa.

Abstract

OBJECTIVES:

Data from a small series suggested that the Interleukin 1 beta (IL1ß) rs16944 polymorphism may be associated with severe renal involvement and persistent renal damage (renal sequelae) in Henoch-Schönlein purpura (HSP). To confirm this association, we assessed the largest cohort of Caucasian HSP patients ever considered for genetic studies.

METHODS:

338 Spanish HSP patients and 635 sex and ethnically matched controls were recruited in this study. All patients were required to have had at least 6 months' follow-up. Patients and controls were genotyped for IL1β rs16944 by TaqMan genotyping assay.

RESULTS:

No differences between IL1β rs16944 genotype or allele frequencies were found either in the case/control study or when HSP patients were stratified according to the age at disease onset, presence of nephritis or gastrointestinal manifestations. Nevertheless, 4 (25%) of the 16 HSP patients who developed severe renal manifestations carried the TT genotype versus 29 (9%) of 322 who did not develop this complication (p=0.01, OR=5.48, 95% CI: 1.01-28.10). Accordingly, patients carrying the mutant T allele had an increased risk of developing severe nephropathy (p=0.016, OR=2.35, 95% CI: 1.09-5.07). Additionally, a significant increase of the TT genotype was observed in patients with persistent renal damage when compared with those patients without this complication (25% versus 8.6%, respectively; p=0.0035, OR=4.90, 95% CI: 1.26- 18.51). Moreover, renal sequelae were more common in patients carrying the mutant T allele (p=0.0076, OR=2.20, 95% CI: 1.17-4.14).

CONCLUSIONS:

Our results support that the IL1ß rs16944 polymorphism may be a potential marker of severe renal manifestations and renal sequelae in HSP.

PMID:
26842496
[Indexed for MEDLINE]

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