الفهرس 
Goblet cellsOnly 14 pages are availabe for public view
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Abstract
A prospective study of 140 surgically resected appendices was performed. The study comprised a histopathological study of the various pathological lesions found in those 140 appendices, an interesting study of the distribution and the role of goblet, mast and argentaffin cells in appendicitis and ultimately a correlation was made between the pathological findings found and the clinical data of those 140 patients. - The histopathological study revealed findings that were included in three group; group I which included normal and minor changes such as lynrphoid hyperplasia (5%) fibrosis, (6.4%), haemorrhage (2.9%) and faecolith (1.4%). These changes, though minor, they in most instances appeared to play a role in the pathogenesis of appendicitis. On the other hand group I1 included inflammation and related conditions. Appendicitis was diagnosed in 80 appendices (57.1%); 50 cases of acute appendicitis (35.8%) , 12 cases of acute appendicitis complicated by perforation (8.6%) and 5 by gangrene(3.6%), 12 cases of chronic appendicitis(8.6%) and finally one case of subacute appendicitis (0.7%). The remaining 7 appendices showed ulceration (2.9%), necrosis (0.7%). stricture (0.7%) and secondary periappendicitis (0.7%). Acute appendicitis was the most frequent lesion in this study (35.8%). It was predominantly a disease of the second and third decades of life with male preponderance. Aetiologically, the obstructive form was found in (26%) of the 50 cases of acute appendicitis. Non obstructive acute appendicitis was found in (74%) of the cases. The several aetiological factors proposed for the initiation of the latter form were studied depending on the pathological findings, age incidence and clinical data. Immunological mechanisms, dietary factors operating through a neural mechanism and infective aetiology have been all suggested in the pathogenesis of non obstructive acute appendicitis. On correlating these factors with the age incidence of the cases of appendicitis in this study it appeared that none of these factors can be responsi hle alone for acute appendicitis i .e. it is probably a mu1 ti factorial disease. Pathologically it took various forms, or more accurately stages. These included acute cattarhal appendicitis, focal ulcerative appendicitis,early acute and classical acute suppurative appendicitis and finally acute perforating and gangrenous appendicitis. Suhncute appendicitis as revealed by this study did exsist. It represented a more subsiding form of appendicitis. The outstanding feature in its diagnosis was the transmural eosinophilic infiltrate amounting to 5 or more/H.P.F. Certainly occasional neutrophils lymphocytes, and plasma cells were important for the diagnosis to exclude other causes of transmural eosinophilia. chronic appendicitis as revealed by this study do exist and was found in 12 cases (8.6%). Periappendicitis in the absence of intrinsic inflammation was found in only one case and actually is a very important clinical entity since it directs the attention of the surgeon to the pesence of extraqppendiceal disease that could threaten the patient’s life even after appendectomy, such as urologic disorders, pelvic inflammatory disease, inflammatory bowel disease, colonic neoplasms, diverticular disease and others. The third group included unusual pathological lesions (20.6%) which included granulomatous diseases; such as Cro hn ’s disease xanthogranuloma, foreign body granuloma, and granuloma. Crohn’s disease (1.4%) isolated to the appendix was found to be a documented pathological’entity and may mimic clinically acute appendicitis. This group also included parasitic diseases of which pure entrobiasis (5%) and schistosomiasis (5%) were the most frequent. Entrobius vernlic~lnris was a common incidenal finding in (1 1.4%) of the 140 appendices. These worms were frequent in children and young adults. Their role in the pathogenesis of acute appendicitis as revealed by this study was disputed. TTowever their presence was certainly the cause of the preoperative clinical symptoms giving a false impression of acute appendicitis. ~cliistosoniinsis of the appendix was not uncommon representing 10.7 (Im) of the 140 cases. Acute schistosomal appendicitis as revealed by this study do exist and took two forms. Acute granulomatous and acute obstructive bilharzial appendicitis. A third form as revealed by this study was the coexistence of acute granulomatous bilharzial reaction and acute suppurative appendicitis. chronic schistosomal appendicitis was also another form of schistosomal affection of the appendix. Other forms of bilharzial affection included polyp in bilharzial appendix , periappendiceal bilharzial nodules and bilharzial appendix. Other lesions included in group I11 were tumours and tumour like lesions. They comprised one case of mucocele, hyperplastic polyp, angiolipoma and carcinoid tumour and two cases of malignant infiltration from colonic lymphomas. Unfortunately they were so infrequent that a sufficient study was not possible. The second component of this work was to study the distribution and role of goblet, mast and argentaffin cells in appendicitis. Actually this study was somewhat unique as up to our knoweldge no similar study was carried on inflammed appendices. This part of the work was somewhat difficult because of the limited f’;lcilitics. therefore the study gave a rough idea on thc distribution and role of these cells rather than accurate and definite facts. The role of goblet cells in appendicitis seemed to be more prominent in cases of acute cattarha1 and parasitic appendicitis. The increased goblet cell population seen in those cases suggested a protective role by producing a protective layer of mucin against any mucosal irritant, e.g impacted faecal material, schistosomal ova, entrobius worm or foreign body in the lumen of the appendix. The depletion of goblet cell population in cases of acute suppurative appendicitis was accompanied by hyperplasia of the absorptive columnar cells which are known to have a secretory and an immunological function as well creating another line of defence mechanism against the invading micro-organism. Additionally the adenomatous changes and basal cell proliferation seen in association with some cases of acute suppurative appendicitis suggested that it could be the pathological counterpart of ulcerative colitis. Similarly mast cells which were found to be increased in cases of appendicitis and a component of the inflammatory reaction suggested that they play an important role at the first line protection of the appendiceal mucosa against any injurious substance by influencing the inflammatory response through the release of their chemical mediators. On the other hand the increased argentaffin cell population particularly the subepithelial type had two aspects, either it occured as a component of the inflammatory reaction the same as mast cells and others by releasing their contents of chemical mediators i.e a protective function or their proliferation preceded the development of appendicitis and were alternatively the initiating event of appendicitis i.e a causal factor. Unfortunately a distinction between the two roles could not be confirmed. Finally the correlation between the pathological findings and clinical data made in this study aimed at assessing the degree of error in the clinical diagnosis and the significance of routine histopa thological examination of resected appendices. In this respect an operational error was made in (50%) of the cases. Additionally a first choice preoperative diagnosis of acute appendicitis was only correct in 69 of 130 cases (53.7%) suggested to have acute appendicitis. Additionally a variety of interesting and uncommon lesions were identified in 35 of 140 cases studied (25%) and were missed by the surgeon. These included entrobiasis, schistosomiasis, ascariasis and entameobiasis , granulomas, angiolipoma and hyperplastic polyp. Some of these conditions when diagnosed would certainly account for the recurrence of symptoms following appendectomy or warrant a search for extra-appendiceal disease as in the case of Crohn’s disease. Finally the pathological examination of the appendix also revealed lesions that explained to the surgeon the presence of symptoms in the absence of any apparent inflammation of the appendix at operation e.g the inspissated faecal casts in the lumen, entrobius worms, schistosomiasis, fibrous obliteration, faecolith and haemorrhage seen in our appendices are all conditions that produce appendicular pain even though appendicitis is not present.