Relationship between uteroglobin gene polymorphism and Henoch-Schonlein purpura
10.3760/cma.j.issn.0412-4030.2009.08.010
- VernacularTitle:过敏性紫癜与子宫珠蛋白基因多态性的相关性研究
- Author:
Jianjian ZHU
;
Jing CHEN
;
Jinhua HUANG
- Publication Type:Journal Article
- Keywords:
PtLrpura,Schoenlein-Henoch;
Nephritis;
Uteroglobin;
Polymorphism,single nucleotide
- From:
Chinese Journal of Dermatology
2009;42(8):548-552
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the relationship of uteroglobin gene polymorphism to the sus-ceptibility to, clinical type and pathological type of Henoch-Schsnlein purpura (HSP) and Henoch-Schonlein purpura nephritis (HSPN). Methods Totally, 118 patients with clinically diagnosed HSP, including 80 cases of HSPN and 38 cases without renal involvement were recruited in this study together with 100 normal human healthy controls. Genomic DNA was isolated from peripheral blood leucocytes of all subjects. The uteroglobin G38A polymorphism was determined by PCR-restriction fragment length polymorphism (RFLP). Results The frequencies of genotypes 38GG, 38GA and 38AA in normal human controls did not differ from those in patients with HSP, patients with HSP but without nephritis, patients with HSPN, patients with HSP and joint involvement, patients with HSP and gastrointestinal involvement (all P > 0.05). Also, no sig-nificant difference was observed between patients with HSPN and patients with HSP but without nephritis (P > 0.05). Furthermore, the frequency of genotypes 38GG, 38GA and 38AA had no significant correlation to the clinical phenotype of HSP, the occurrence of gross hematuria and nephrotie syndrome or the degree of renal damage (all P > 0.05). A significant increase was observed in the frequency of genotype 38AA in patients with HSP with elevated serum IgE compared with those with normal serum lgE (58.82% vs 8.43%, χ2 = 21.946, P < 0.05, OR = 15.51, 95% CI range: 4.93% - 48.84%), whereas the frequency of genotype 38GG was significantly increased in patients with HSPN and hypertension than in those with HSPN but without hypertension (75.68% vs 18.60%, χ2 = 26.172, P < 0.05, OR = 13.61, 95% CI range: 5.01% -37.01%). Conclusions The uteroglobin G38A polymorphism seems unrelated to the susceptibility to and degree of renal damage in patients with HSP and HSPN. The genotype 38AA may be associated with elevated level of serum IgE In patients with HSP, while genotype 38GG is associated with a high incidence of hyper-tension in patients with HSPN.
