الفهرس 
Respiratory EpitheliumOnly 14 pages are availabe for public view
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Abstract
Introduction: Chronic exposure to harmful substances is thought to cause bronchial mucosal cells to undergo pathological and morphological changes. The cell injury elicits a compensatory and inflammatory response. Mucosal basal cells respond by proliferation to generate mucus-secreting goblet cells and columnar epithelial cells are replaced by stratified squamous epithelium (metaplasia), cellular atypia and increased mitotic activity which leads to mucosal dysplasia signals the development of neoplasia. Aim of work: This work was planned to study the epithelial changes that may occur in the bronchial mucosa in patients exposed to risk(s) for bronchial carcinoma as inflammation, squamous metaplasia, atypia, dysplasia or neoplasia. Patients and methods: This study was carried out at Thoracic Medicine Department in collaboration with Pathology and Radiology Departments, Mansoura University Hospitals during January 2004 and September 2008. It included 59 subjects (51 males and 8 females) in 3 groups: Group I included 38 subjects at risk for bronchial carcinoma (36 males and 2 females) with a mean age of 55.02 10.92 years. Group II included 15 patients diagnosed as bronchial carcinoma (10 males and 5 females) with a mean age of 55.06 10.47 years (positive control group). Group III included 6 non smoker apparently healthy volunteers (5 males and 1 female) with a mean age of 49.50 11.72 years (negative control group). All groups were subjected to the following: Clinical evaluation, Routine laboratory investigations, Plain x-ray chest P-A and lateral views and high resolution CT of chest, Spirometric pulmonary function testing and arterial blood gases analysis. Slide examination after staining with haematoxylin and eosin and immunohistochemical staining using monoclonal antibodies for P53 and for TTF-1. Results: Normal cellular pattern and cytological examination of sputum were found in 23.7% of cases (9 out of 38) in high risk group for bronchial carcinoma, in 6.7% of cases (1 out of 15) with bronchial carcinoma and in all 6 cases of the control group. Excess neutrophils in sputum were found in 13.2% of cases (5 out of 38 cases) in high risk group for bronchial carcinoma and nearly similar percent (13.3%) of cases (2 out of 15) with bronchial carcinoma (as both groups of patients were smokers). With no neutrophils were detected in the control non- smoker group. Immunohistochemical staining of sputum with monoclonal antibodies against p53 was positive in 60% (9 out of 15 cases) in bronchial carcinoma versus 2.6% (1 out of 38 cases) in high risk group for bronchial carcinoma versus none in healthy non smoker volunteers. These differences were statistically significant (P < 0.05). No apparent abnormality was detected with FOB in 20 cases out of 37 (54.1%) in high risk group versus one case out of 15 cases (6.7%) in bronchial carcinoma versus all 6 healthy non smokers. Normal cellular patterns were found in 32 cases out of 37 (86.5%) in high risk group for bronchial carcinoma versus 13.3% of cases (2 out of 15) in bronchial carcinoma versus all 6 non smoker healthy volunteers. Immunohistochemical staining monoclonal antibodies against p53 was positive in 60% (9 out of 15 cases) in bronchial carcinoma versus 2.7% (1 out of 37 cases) in high risk group for bronchial carcinoma. These differences were statistically significant (P < 0.05). Immunohistochemical staining monoclonal antibodies against TTF-1 was positive 33.3% (5 out of 15 cases) in bronchial carcinoma versus 0% in high risk group for bronchial carcinoma and non smoker group. These differences were statistically significant (P < 0.05). Conclusions: P53 expression can be used as a biological marker for early detection of bronchial carcinoma and it can detect malignancy months to years before it can be detected clinically, radiologically. TTF-1 is helpful in diagnosing bronchial carcinoma cell type and can be used for early detection of adenocarcinoma.