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العنوان
Prevalence Of Helicobacter Pylori And Its Pathogenic Gene In Sinonasal Mucosa Of Patients With Chronic Rhinosinusitis/
المؤلف
Abdul Raouf, Amir Aly.
هيئة الاعداد
باحث / Amir Aly Abdul Raouf
amiros-77@yahoo.com
مناقش / Mohamed Hassab
مناقش / Emad Ahmed Magdy
مشرف / Reem Abdel Hameed Harfoush
الموضوع
Otorhinolaryngology.
تاريخ النشر
2013.
عدد الصفحات
77 p.:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
30/5/2013
مكان الإجازة
جامعة الاسكندريه - كلية الطب - Otorhinolaryngology
الفهرس
Only 14 pages are availabe for public view

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Abstract

Chronic Rhinosinusitis is a group of disorders characterized by inflammation of the mucosa of the nose and paranasal sinuses of at least 12 consecutive weeks duration.
The overall prevalence of CRS is 146 per 1000 population It is the fifth most common diagnosis for which an antibiotic is prescribed.
Despite the enormity of the problem, the pathophysiology of chronic rhinosinusitis still eludes the scientific community. Three factors, however, appear crucial for the normal physiologic functioning of the sinuses: patency of the ostiomeatal unit (OMU), normal mucociliary transport, and normal quantity and quality of secretions. Disruption of one or more of these factors can predispose to sinus infection.
Polymicrobial infection is common in chronic sinusitis, which is a synergistic infection and because H. pylori is prevalent in gastric contents, this organism has also been added to the list of potential role players in reflux induced supra esophageal mucosa injury. H. pylori was declared a likely laryngeal pathogen (207) and its presence was also detected in diseased sinonasal tissue.
If the role of H. pylori infection in gastroduodenal disease is unquestionable, the manner by which the organism is transmitted remains unclear. To the established fecal– oral and oral– oral routes, newer routes of transmission have been proposed such as gastric– oral and, more recently, gastric–nasal transmission, the latter is the aim of our investigation.
H. pylori DNA may be encountered in chronically inflamed sinonasal mucosa, possibly as a manifestation of Larynogopharyngeal reflux disease; although at this time we can only speculate on the role of the bacterium at this particular location. The possibility that it plays some etiopathogenic role in rhinosinusitis cannot be dismissed too lightly, as theoretically there is some valid reasoning behind it.
It has been suggested that the reflux of infected gastric juice into the nasopharynx may produce airway mucosal edema and inflammation from the combined activity of peptic-acid injury and local H. pylori infection.