ABSTRACT
Background H. pylori infection causes diverse clinical outcomes, including dyspepsia, peptic ulceration, gastric carcinoma and mucosa associated lymphoid tissue [MALT] lymphoma. Up-remulation of COX-2 has been observed in H. pylori gastritis in response to inflammatory cytokines. IL-8 is a major activator for neutrophils which contribute to mucosal damage in H. pylori infected patients. A wide-spread use of non-invasive simple diagnostic method is indicated for diagnosis and follow-up of H. pylori infection
Aims: Assessment of COX-2 and IL-8 immuno-express.ion in gastric mucosa in correlations to H. pylori infection in patients suffering from dyspepsia and evaluation of different available diagnostic modalities for detection of H. pylori infection in Sohag city, Egypt
Methods: The study included 62 patients complaining of dyspepsia. Stool samples were examined for detection of H. pylori stool antigen [HpSA] using enzyme immunoassay [ElA]. Antral endoscopical biopsies were taken for culture, and histopathological evaluation using Giemsa stain. Immunohistochemical expressions of IL-8 and COX-2 in tissue sections were evaluated
Results: H. pylori infection was detected in 42/62 [67.7%] of patients with dyspepsia by using the gold standard method [culture and Giemsa stain]. The diagnostic accuracy of HpSA was 83.8% which made it a good non-invasive alternative for detection ofH. pylori infection in our community. COX-2 was expressed in 90.5% ofH. pylori positive and in 55% of H. pylori negative cases [P < 0.003]. IL-8 was expressed in 83.3% ofH. pylori positive and in 50% ofH. pylori negative cases [P < 0.003]
Conclusions: Wherever endoscopy is not indicated, HpSA EIA is a non invasive, rapid, easily performed, reliable method for diagnosis ofH. pylori infection. H. pylori infection causes enhancement of COX-2 and IL-8, and this may have a role in the progression of gastritis to more advanced lesions?
ABSTRACT
Aim: The aim of this study is to analyse the incidence and highlight the risk factors associated with facial nerve dysfunction after conservative primary parotidectomy
Methods: The study included 41 patients, who were initially with normal facial nerve function and had been treated by conservative primary parotidectomy [42 procedures] for parotid neoplasms in Sohag University Hospital, during the period from March 2002 to March 2005. Facial nerve function was assessed on admission before surgery; and then at one day, one month and six months following the parotidectomy. Extent of the surgery, size of the parotid neoplasm, and histopathological type of the neoplasm were correlated with the incidence of postoperative facial nerve dysfunction
Results: The rate of postoperative facial nerve dysfunction was 35.7% in the first post-operative day, 19% and 4.8% at one month and six months, respectively. Cases treated with total parotidectomy with or without neck dissection showed poorer facial nerve function [p < 0.001], [p < 0.01], and [p < 0.04] at one day, one month, and 6months, respectively. Overall, neoplasms with size >/= 5 cm had a higher prevalence of facial nerve paresis [p < 0.03 at one day, and 0.04 at one month postoperative]. Patients with malignant parotid neoplasms had more tendency to develop facial nerve dysfunction [p < 0.02], [p < 0.001], and [p < 0.03] at one day, one month, and 6months, respectively
Conclusion: In our study, the following were associated with higher risk of facial nerve dysfunction: extensive surgery; large sized neoplasms; parotid cancer, when treated with · total parotidectomy or combined with neck dissection; chronic sialadenitis; and vascular malformation