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Titlebook: Interstitial Cystitis; Philip M. Hanno (Professor and Chairman),David R. Book 19901st edition Springer-Verlag London Limited 1990 Urogeni

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Epidemiology of Interstitial Cystitis: 287) were more expansive and used four paragraphs. One reason for the brevity is that with the exception of Oravisto (1975) nearly all the literature made reference only in passing to the issue of epidemiology.
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Mast Cells and Interstitial Cystitisin cytoplasmic granules together with proteoglycan and several proteins such as neutral proteases, acid hydrolases and chemotactic factors. Upon appropriate immunologic or nonimmunologic stimulation the mast cells release their preformed mediators and also generate and release metabolites of arachiodonic acid (see Katz et al. 1985).
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Historical Perspectivesion was one in which edema and the cells of chronic inflammation were found in the interstitial tissue and thus distinguished from parenchymal disease. The best example of that distinction today persists in the kidney, where we still talk of glomerulonephritis and interstitial nephritis. The concept
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Epidemiology of Interstitial Cystitis: 2w of IC cites 12 articles; Messing’s (1984) chapter on IC in Campbell’s textbook (1984) cites 19. Yet the epidemiology literature is summarized in just a few paragraphs. Messing (1984) used two paragraphs; Walsh’s review in an earlier Campbell’s textbook (1978) also used only two; Hanno and Wein (19
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Etiology: Etiologic and Pathogenetic Theories in Interstitial Cystitisases with a known and an unknown etiology (Holm-Bentzen and Lose 1987; Holm-Bentzen et al. 1987c). All the patients present with a variety of urologic symptoms all of a more or less chronic nature: supra-retropubic pain, frequency, nocturia, urgency, dysuria and occasionally hematuria and stranguria
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