Southern medical journal · 2010
Relationship of the intensity of Helicobacter pylori and severity of inflammation with beta-2 microglobulin levels in serum according to the updated Sydney System.
Клиническое исследованиеСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Dincer Nazmiye, Topal Firdevs, Karaman Kerem, Kurt Mevlut, Akbulut Sabiye, Cosgun Yasemin, Dolek Yasemin
Аннотация
OBJECTIVE: Helicobacter pylori (HP) is a cause of chronic gastritis. Beta-2 microglobulin has been used as a simple inflammatory indicator in some diseases. We investigate the usability of beta-2 microglobulin as a simple marker that may reflect the severity of inflammation and intensity of HP in gastric mucosa.
MATERIALS AND METHODS: A total of 114 patients was included in the study, who applied to an outpatient gastroenterology clinic with complaint of dyspepsia. Serum beta-2 microglobulin levels were evaluated in 109 patients. Esophagogastroduodenoscopy was performed on patients included in the study, and histological analysis was performed by obtaining two specimens from each of antrum, corpus, and incisura angularis. All specimens were evaluated according to the updated Sydney System.
RESULTS: No statistically significant result was found between serum beta-2 microglobulin levels and the intensity of HP and the severity of inflammation of gastric mucosa. However, it was observed that the serum beta-2 microglobulin level in specimens taken from corpus was found to be higher in patients with moderate-severe HP intensities compared to those with lower HP intensities.
CONCLUSIONS: Although HP is the cause of the chronic active gastritis characterized with the infiltration of lymphocytes, plasma cells, and neutrophils, it is accompanied by local involvement apart from diseases with a course of systemic involvement. We suggest that the serum beta-2 microglobulin level cannot be used as a simple marker of HP intensity and severity of inflammation in gastric endoscopic biopsies.
MATERIALS AND METHODS: A total of 114 patients was included in the study, who applied to an outpatient gastroenterology clinic with complaint of dyspepsia. Serum beta-2 microglobulin levels were evaluated in 109 patients. Esophagogastroduodenoscopy was performed on patients included in the study, and histological analysis was performed by obtaining two specimens from each of antrum, corpus, and incisura angularis. All specimens were evaluated according to the updated Sydney System.
RESULTS: No statistically significant result was found between serum beta-2 microglobulin levels and the intensity of HP and the severity of inflammation of gastric mucosa. However, it was observed that the serum beta-2 microglobulin level in specimens taken from corpus was found to be higher in patients with moderate-severe HP intensities compared to those with lower HP intensities.
CONCLUSIONS: Although HP is the cause of the chronic active gastritis characterized with the infiltration of lymphocytes, plasma cells, and neutrophils, it is accompanied by local involvement apart from diseases with a course of systemic involvement. We suggest that the serum beta-2 microglobulin level cannot be used as a simple marker of HP intensity and severity of inflammation in gastric endoscopic biopsies.