Is helicobacter pylori infection one of the actual causes of vitamin B12 deficiency?
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Tarih
2011
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Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Amaç: Bu çalışmanın amacı vitamin B12 eksikliğindeki H. pylori enfeksiyonu oranını ve h. pylori enfeksiyonunun gerçekten vitamin B12 eksikliğinin asıl sebebi olup olmadığını belirlemektir. Materyal ve Metod: 40 vitamin B12 eksikliği olan hastayı ve 25 sağlıklı kişiyi değerlendirdik. Bu hastaların B12 eksikliği sebebi bilinmiyordu. H. pylori için endoskopik değerlendirme ve patolojik inceleme uyguladık. Vitamin B12 eksikliği olan grupta %50 atrofik gastrit belirledik, fakat kontrol grubunda endoskopik olarak hiçbir atrofik gastrit gözlemlemedik. Bulgular: Patolojik incelemelere göre hasta grubunda 40 hastadan 11’inde (%27,5), kontrol grubunda ise 25 hastadan 16’sında (%64) H. pylori pozitifliği vardı (p0,01). Hasta grubunun patolojik incelemesi ayrıca 11 hastanın hafif (%27,5), 5 hastanın orta (%12,5), 3 hastanın ise ağır (%7,5) atrofisi olduğunu ortaya koydu. Zıt olarak kontrol grubunda, 3 hastanın sadece hafif (%12) atrofisi vardı. Gastroskopik değerlendirmede ayrıca H. pylori (-) 29 hastadan 17’sinde (%58,6) ve H. pylori () 11 hastadan 3’ünde (%27.3) atrofik gastrit olduğunu bulduk. Sonuç: Vitamin B12 eksikliği olan hastaların gastrik mukozasında daha düşük H. pylori oranı vardı. Diğer yandan, gastroskopik ve patolojik incelemeye göre hasta grubunun daha yüksek atrofik gastrit oranı vardı. Hasta grubunda H. pylori pozitifliği yaşla birlikte progresif olarak azalmıştı. Takip eden yıllarda gastrik mukozadaki atrofi sonucu H. pylori yok olmuştu. Biz, atrofik mukozanın, H. pylorinin kolonizasyonu için uygun olmadığı sonucuna vardık.
Aim: Aim of this study is to determine Helicobacter pylori infection rate in Vitamin B12 deficiency and determine whether H.pylori infection is really actual cause of Vitamin B12 deficiency. Material and Methods: We evaluated 40 vitamin B12 deficient patients and 25 healthy subjects. Those patients did not have known cause of vitamin B12 deficiency. We performed endoscopic evaluation and pathological examination for H.pylori. We determined 50% atrophic gastritis in vitamin B12 deficient group, but we did not observe any atrophic gastritis in the control group endoscopically. Results: There were H.pylori positivity in 11/40 (27.5%) in the patients group but 16/25 (64) in the control group in pathological examination (p<0.01). Pathological examination of patient group also illustrated that 11 patients had mild atrophy in 11 (27.5%), 5 had moderate atrophy (12.5%) and 3 patient (7.5%) had severe atrophy. In contrast, 3 patients had only mild atrophy (12%) in the control group. We also found that H.pylori (-) 17/29 (58.6%) patients and H.pylori () 3/11 (27.3%) patients had atrophic gastritis in gastroscopic evaluation. Conclusion: Patients who have vitamin B12 deficiency had lower ratio of H.pylori in gastric mucosa. On the other hand, the patient group had higher ratio of atrophic gastritis in pathological and gastroscopic examination. H.pylori positivity had been decreased progressively with aging in patients group. H.pylori has disappeared in following years as a result of atrophy in gastric mucosa. We conluded that atrophic mucosa is not suitable for colonization of H.pylori infection.
Aim: Aim of this study is to determine Helicobacter pylori infection rate in Vitamin B12 deficiency and determine whether H.pylori infection is really actual cause of Vitamin B12 deficiency. Material and Methods: We evaluated 40 vitamin B12 deficient patients and 25 healthy subjects. Those patients did not have known cause of vitamin B12 deficiency. We performed endoscopic evaluation and pathological examination for H.pylori. We determined 50% atrophic gastritis in vitamin B12 deficient group, but we did not observe any atrophic gastritis in the control group endoscopically. Results: There were H.pylori positivity in 11/40 (27.5%) in the patients group but 16/25 (64) in the control group in pathological examination (p<0.01). Pathological examination of patient group also illustrated that 11 patients had mild atrophy in 11 (27.5%), 5 had moderate atrophy (12.5%) and 3 patient (7.5%) had severe atrophy. In contrast, 3 patients had only mild atrophy (12%) in the control group. We also found that H.pylori (-) 17/29 (58.6%) patients and H.pylori () 3/11 (27.3%) patients had atrophic gastritis in gastroscopic evaluation. Conclusion: Patients who have vitamin B12 deficiency had lower ratio of H.pylori in gastric mucosa. On the other hand, the patient group had higher ratio of atrophic gastritis in pathological and gastroscopic examination. H.pylori positivity had been decreased progressively with aging in patients group. H.pylori has disappeared in following years as a result of atrophy in gastric mucosa. We conluded that atrophic mucosa is not suitable for colonization of H.pylori infection.
Açıklama
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Genel ve Dahili Tıp
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Düzce Tıp Fakültesi Dergisi
WoS Q Değeri
Scopus Q Değeri
Cilt
13
Sayı
3
