Henoch-Schonlein Purpuralı Çocuklarda Angiotensin Konverting Enzim Gen Polimorfîzmi. (Turkish)

Objective: We examined the insertion (I) and deletion (D) polymorphism of angiotensin converting enzyme (ACE) gene polymorphism in 54 children with HSP to investigate the associated with presentation, prognosis and progression of children with Henoch-Schönlein purpura (HSP). Materal and Methods: Blood samples were collected from patients and obtained into EDTA. Genomic DNA from peripheral blood lymphocytes was purified. The ACE l/D gene polymorphism was detected by PCR with primer sequences derived. Results: The percent of ACE genotypes II, ID and D D in all patients was detected 4 %, 74 % and 22 % respectively. Patients were divided into 3 groups as HSP nephritis (n=14), HSP with minor urinary anomaly (n=18) and HSP without renal involvement (n=22). The distribution of ACE genotypes II. ID and DD respectively in HSP nephritis was 7 %, 57 %, 36 %; in HSP with minor urinary anomaly was 0 %, 89 %, 1! %; and in HSP without renal involvement was 5 %, 72 %, 23 % detected. No association was found between the ACE genotypes and the presence of renal involvement (x2=4.39, p=0.356). The distribution of ACE allels I and D respectively in HSP nephritis was 36 % cmd 64 %; in HSP with minor urinary anomaly was 44 % and 56 % and in HSP without renal involvement was 41 % and 59 % detected. No association was found between the ACE allels and the presence of renal involvement (x2=0.500, p=0.780). Conclusion: In conclusion these results does not support a statistically significantly association between renal involvement and DD genotype or D aile I in children with HSP. However D allele was detected in 96 % patients and DD genotype was higher in patients with HSP nephritis than patients without renal involvement. According these results we showed that D allel is a facilitative and I allel is a protective factor for development and renal involvement of disease. However larger studies are required to confirm these results. [ABSTRACT FROM AUTHOR]

Amaç: Henoch-Schönlein purpuralı (HSP) 54 çocukta anjiotensin konverting enzinı (ACE) gen polimorfizminin hastalığın kliniği, progııozu ve klinik seyri ile olan ilişkisini araştırmak amacıyla ACE geninin insersiyon (I) ve delesyon (D) polimorfızınini araştırdık. Gereç ve Yöntem: Hasta kan örnekleri EDTA'lı tüpe alındı. Lökosit DNA'sı elde edilerek PCR yöntemiyle ACE HD polimorfızmleri belirlendi. Bulgular: Hastaların tiimiinde ACE genotipleri II. ID ve DD 'nin oranları sırasıyla % 4, % 74 ve % 22 olarak saptandı. Hastalar HSP nefriti olanlar (n=14), HSP'li ve hafif idrar bulguları olanlar (n=18) ve böbrek tutulumu olmayanlar (ıı=22) olmak iizere üç grııba ayrıldı. ACE genotipleri II. İD ve DD 'nin dağılımları sırasıyla HSP nefritinde % 7, % 57, % 36: hafif idrar bulguları olanlarda % 0. % 89, % 11; böbrek tutulumu olmayanlarda % 5, % 72, % 23 olarak saptandı. Renal tutulum varlığı ile ACE genotipleri arasında istatistiksel olarak anlamlı bir ilişki saptanmadı (x2=4.39, p=0.356). ACE allelleri I ve D'nin dağılımları sırasıyla HSP nefritinde % 36 ve % 64, hafif idrar bulguları olanlarda % 44 ve % 56, böbrek tutulumu olmayanlarda ise % 41 ve % 59 olarak saptandı. Böbrek tutulumu ile ACE allelleri arasında istatistiksel olarak anlamlı bir ilişki saptanmadı (x2=0.500, p=0.780). Sonuç: Bu veriler HSP'li çocuklarda böbrek tutulumu ile DD genotipi veya D alleli arasında istatistiksel olarak anlamlı bir ilişkiyi desteklememektedir. Bununla birlikte D alleli hastaların % 96'sında saptandı ve D D genotipi de HSP nefritli hastalarda böbrek tutulumu olmayanlara göre daha yüksek bulundu. Bu sonuçlara göre hastalığın oluşumunda ve renal tutulumda D ailelinııı kolaylaştırıcı ve 1 allelinin ise koruyucu faktör olduğunu gösterdik, fakat bu bulguları destekleyen daha biiyiik çalışmalar gereklidir. [ABSTRACT FROM AUTHOR]

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