Helicobacter pylori (+) kronik aktif gastrit ve duodenal ülserli hastalarda, cagA pozitifliği ile serum gastrin ve TNF-alfa ilişkisi
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Tarih
1999
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Dergi ISSN
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Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Kronik aktif gastritin (KAG) temel nedeni olan Helicobacter pylori (H. pylori) peptik ülser gelişiminde en önemli faktörlerden biri olup mide adenokarsinomu ve primer gastrik B hücreli lenfomada da kofaktör olarak kabul edilmektedir. Bu çalışmada KAG ve duodenal ülser (DÜ) patogenezinde H. pylori'nin cag A(+) suşu, gastrin hormonu ve bir inflamatuvar mediatör olan TNF-alfanın ilişkisini ortaya koymak amacı ile H. pylori pozitif bulunan 21 KAG, 31 DÜ'li hasta ve endoskopik ve histolojik olarak patoloji saptanmayan 18 kontrol olgusu incelendi. Tüm olgulardan endoskopik işlem öncesi serum gastrin, TNF-alfa düzeyi ile cag A antikoru ölçümü için kan örneği alındı. Her üç parametre aynı kan örneğinde çalışıldı. KAG'li olguların %33.3'ünde (7/21), DÜ'li olguların %64.5'inde (20/31) cagA antikoru saptandı ( p<0.05). Olgular serum gastrin düzeyi açısından karşılaştırıldığında KAG (74.1±26 pg/ml) ile DÜ (69.5±22 pg/ml) arasında anlamlı fark bulunmaz iken, her iki grubun kontrol grubundan (44.9±5.7 pg/ml) anlamlı derecede yüksek olduğu görüldü (p<0.001). Serum TNF-alfa düzeyi KAG'li vakalarda (38±34pg/ml) kontrol grubundan (18±9 pg/ml) daha yüksek bulundu (p<0.05). cag A(+) olgular ile cag A(-) olgular arasında serum gastrin ve TNF-alfa düzeyi açısından anlamlı bir fark saptanmadı (pı0.05) Sonuç olarak; cag A pozitif H. pylori suşları ile DÜ arasında pozitif ilişki vardır. H. pylori enfeksiyonunda serum gastrin düzeyi yüksektir. Bu yükseklik, bakterinin yol açtığı kronik gastrit ve DÜ ile, bakterinin cag A içerip içermemesinden bağımsızdır. Serum TNF alfa düzeyi ile gastrin hormonu ve cag A antikoru arasında korelasyon olmaması hem gastrin salınımının hem de inflamatuvar sitokin yanıtının cag A' dan bağımsız olduğunu düşündürmektedir.
Helicobacter pylori (H.pylori) infection, which is strongly associated with non-autoimmune chronic active gastritis and peptic ulcer disease, is also considered to be a co-factor in gastric adenocarcinoma and primer gastric B cell lyphoma. in order to examine the relationship between cag A (+) strain of H. pylori with gastrin and TNF-alpha, an inflammatory mediator, in both chronic active gastritis (CAG) and duodenal ulcer (DU) pathogenesis, 21 patients with CAG and 31 patients with DU disease were investigated in addition to 18 patients who had no pathological findings on either upper gastrointestinal endoscopy or histological examination. Prior to endoscopy, sera were collected from all of cases in order to evaluate gastrin and TNF-alpha and also for cag A antibody measurements. These three parameters were studied from the same blood sample. Cag A antibody was found in 33.3% (7/21) of patients with CAG and in 64.5% (20/31) of patients with DU disease (p<0.05). When the cases with CAG (74.1±26pg/ml) and with DU (69.5±22pg/ml) were compared there was no significant difference between gastrin levels of the patient groups but both were significantly higher than the gastrin level (44.9±5.7pg/ml) of the control group (p<0.001). the serum TNF-alpha level of cases with CAG (38±34pg/ml) was higher than control group (18±9pg/ml) (p< 0.05). There was no significant/difference between the serum gastrin and TNF-alpha levels of cag A(+) and cagA(-) cases. According to these results, there seems to be a positive relationship between cag A positive H. pylori strains and DU. Serum gastrin levels are high in H. pylori infection. This finding does not depend on the presence of cagA antibody of H. pylori and is also not related with CAG and DU, which are caused by H. pylori. As there is no correlation between the serum TNF-alpha level, gastrin level and presence of cagA antibody, we conclude that both the secretion of gastrin and the inflammatory cytokin response are free from the effect of cag A antibody.
Helicobacter pylori (H.pylori) infection, which is strongly associated with non-autoimmune chronic active gastritis and peptic ulcer disease, is also considered to be a co-factor in gastric adenocarcinoma and primer gastric B cell lyphoma. in order to examine the relationship between cag A (+) strain of H. pylori with gastrin and TNF-alpha, an inflammatory mediator, in both chronic active gastritis (CAG) and duodenal ulcer (DU) pathogenesis, 21 patients with CAG and 31 patients with DU disease were investigated in addition to 18 patients who had no pathological findings on either upper gastrointestinal endoscopy or histological examination. Prior to endoscopy, sera were collected from all of cases in order to evaluate gastrin and TNF-alpha and also for cag A antibody measurements. These three parameters were studied from the same blood sample. Cag A antibody was found in 33.3% (7/21) of patients with CAG and in 64.5% (20/31) of patients with DU disease (p<0.05). When the cases with CAG (74.1±26pg/ml) and with DU (69.5±22pg/ml) were compared there was no significant difference between gastrin levels of the patient groups but both were significantly higher than the gastrin level (44.9±5.7pg/ml) of the control group (p<0.001). the serum TNF-alpha level of cases with CAG (38±34pg/ml) was higher than control group (18±9pg/ml) (p< 0.05). There was no significant/difference between the serum gastrin and TNF-alpha levels of cag A(+) and cagA(-) cases. According to these results, there seems to be a positive relationship between cag A positive H. pylori strains and DU. Serum gastrin levels are high in H. pylori infection. This finding does not depend on the presence of cagA antibody of H. pylori and is also not related with CAG and DU, which are caused by H. pylori. As there is no correlation between the serum TNF-alpha level, gastrin level and presence of cagA antibody, we conclude that both the secretion of gastrin and the inflammatory cytokin response are free from the effect of cag A antibody.
Açıklama
Anahtar Kelimeler
Cerrahi
Kaynak
Turkish Journal of Gastroenterology
WoS Q Değeri
Scopus Q Değeri
Cilt
10
Sayı
4
