Abstract
Adenocystitis is the precancerous lesion that has received the most attention in the field of urology since it was first reported by VonLimberk in 1887. With the availability of endoscopic and tissue biopsy techniques, adenoid cystitis has become a common condition. The pathologic evolution is based on the theory of metastatic epithelial metaplasia and the theory of embryonic tissue remnants. Because adenoid cystitis has too many cancerous metastatic features, the current mainstream thinking in treatment still insists that active intervention with lumpectomy and postoperative perfusion of the bladder with chemotherapeutic drugs can be an active and effective treatment for adenoid cystitis. Good choice of surgical modality is also a key point to note in particular for treatment.
Adenocystitis is the precancerous lesion that has received the most attention in the field of urology since it was first reported by VonLimberk [1] in 1887. With the availability of endoscopic and tissue biopsy techniques, adenocystitis has become a common condition. Because adenocystitis has too many features of cancerous regression, good choice of surgical modality is also the main point that needs special attention for treatment.
1.Clinical symptoms and manifestations
1.1 Clinical diagnosis
The clinical manifestations of adenoid cystitis are linked to the pathological process of the disease, and the clinical symptoms of adenoid cystitis are still mainly bladder irritation signs and hematuria, 9.7% can have difficulty in urination [2], and there are few symptoms of lower urinary tract obstruction. The initial clinical examination, mainly urinary routine, is very important with positive RBCs, no or very few WBCs and negative urine cultures. The confirmatory in-depth examinations are cystoscopic biopsy, ultrasound urodynamics, and urine flow rate examination. Of these, the extent and depth of the biopsy are important and the most critical indicators. It should not be based only on the neoplastic organisms visible on cystoscopy, because adenocystitis is multicentric and diffuse in nature, and a large number of mutated genes may be present in the submucosa before neoplastic organisms are formed. Multi-site biopsy is an important principle.
1.2 Differential diagnosis of adenoid cystitis
Early diagnosis is difficult, mainly because the clinical symptoms of adenoid cystitis are extremely similar to prostatitis and metastatic epithelial carcinoma of the bladder, some of which form masses and are morphologically indistinguishable from bladder cancer (e.g., Figure). However, hematuria and bladder irritation symptoms appear earlier. Bladder cancer has the following clinical features to differentiate it from adenocystitis.
(1) Hematuria with lower abdominal mass.
(2) Cystoscopy shows a broad, hard tumor base with necrotic material or ulcers on the surface.
(3) Hematuria with obvious bladder irritation symptoms, diffuse thickening of bladder wall, no obvious mass on cystoscopy, and extensive erosion and bleeding seen.
(4) Ultrasound and CT reveal only bladder wall thickening. Top and anterior wall infiltrative bladder tumors.
(5) Those with long-term bladder stones. When coexisting with prostatitis, treatment should be differentiated, because adenocystitis and prostatitis are completely different pathogenesis and treatment principles.
2. Evolution of pathological histogenesis
2.1 Etiology
2.1.1 The theory of metastatic epithelial metaplasia
It is believed that in the case of stones, chronic inflammation, obstruction, etc., the mucosal epithelium first forms epithelial buds, which gradually develop into nests of migrating epithelium, i.e. Brunn”s nest, Brunn”s nest protrudes into the basement membrane, and its central cells degenerate to form a sac and cavity, i.e. cystic glandular cystitis. The cells of the surface layer of the cyst wall then form columnar epithelium, glandular cells and secrete, i.e., adenoid cystitis is formed. Since the changes are a series of continuous processes, the coexistence of different various stages of manifestations is seen in the lesion, so it is also called cystic glandular cystitis and glandular cystitis.
2.1.2 Embryonic tissue remnant theory
Inadequate absorption of embryonic glandular remnants in the mesonephric duct results in glandular remnants, preferably in the deltoid region, and residual nested small intestinal epithelial lesions in the bladder, which can occur in any part of the bladder. Residual lesions of the umbilical ureter originate from the umbilical ureteral cord and may be associated with epithelial hyperplasia of the umbilical ureter and glandular metaplasia of the overlying migrating epithelium [3], often occurring in the apical and anterior wall of the bladder,with tumor infiltration into the deep bladder, umbilicus, Retzius space and anterior abdominal wall. During embryonic development, the chemotaxis and aggregation of endothelial cells by the mesoderm promote the migration of vascular endothelial cells and the formation of tubular structures, however, the tubular structures of cannot maintain stability, attracting perivascular cells such as peripheral cells to surround and support endothelial cells, promoting vascular remodeling and maturation, but maintaining vascular integrity and regulating vascular function out of control, the accumulation of endothelial cells to promote vascular injury after the re Endothelialization cannot be completed, forming empty nests and then the subsequent pathological process of adenocystitis. This theory has a reasonable explanation and is theoretically feasible, but it lacks experimental basis and therefore is not widely accepted.
2.1.3 Gram-negative bacterial infection theory
The theory of Gram-negative bacterial infection was proposed in China when a large number of mice were perfused with Gram-negative bacteria and sections were found to have empty nests under the mucosa of the migrating cells, but it is questionable how the inflammatory reaction embodied in the extremely complex and huge abundance of manifestations on the pathological sections [4] could indicate that the empty nests were formed after the induction of adenocystitis, rather than the empty nests produced by the inflammatory reaction itself, and the experimental data did not provide full course of sections of mice at different periods of pathological evolution, and there is no controlled experimental design with empty nests in adenocystitis, so not many people have yet to accept this theory.
2.2 Pathological presentation
Adenoid cystitis is a benign lesion but has a tendency to become malignant; Meliow et al [5] observed the presence of adenoid cystitis in the surrounding tissue of metastatic cell carcinoma and the coexistence of adenoid cystitis was also found between multicentric bladder cancers. It has also been observed that some adenocystitis eventually transforms into adenocarcinoma of the bladder and metastatic cell carcinoma. Recently, some authors [6] have studied the expression of P53 protein and P21 protein in the ras gene to understand the malignant tendency of adenocystitis and suggest that malignant transformation of adenocystitis to cancer is possible. Most people agree that adenocystitis is a precancerous lesion. Therefore, we believe that it is important to treat the nakedly diseased tissue while also aggressively treating the underlying diseased tissue.