I. Is adenocystitis a common disease?
Adenoid cystitis has been gaining attention from urologists and pathologists since it was first reported by Stoerck in 1899 and has been reported significantly more recently, but is not necessarily a common disease. authoritative books such as Campell’sUrology and Wu Jieping Urology do not have a separate chapter on the disease, but only mention it in the context of uroepithelial tumors. More descriptions are common in books on related pathology, mostly on the diagnostic aspects of the characteristic manifestations, and clinical manifestations and treatment are mostly reported in clinical papers. A search in medline with cystisglandularis or cystiscystica in the title of the article retrieved only 101 relevant articles, compared with 695 articles in Chinese (1994-2010). There is a lack of studies on the incidence and prevalence of this disease. The prevalence of clinically significant adenoid cystitis in the US population has been reported to be 0.9C1.9%. Weiner et al. reported 100 autopsies with a normal bladder on visual inspection, in which Brunn’s nest and cystic cystitis were found in 89% and 60% of cases, respectively. Adenoid cystitis can be seen in any age group, preferably in women and rarely in children.
Are Brunn’s nest, cystitiscystica and cystitisglandularis the same disease?
Brunn’s nest (sometimes called VonBrunn’s nest), cystitiscystica, and adenocystitis are three common proliferative lesions of the bladder mucosa that are interconnected and commonly associated with inflammatory bladder disease as well as benign and malignant tumors. VonBrunn’s nest is a nest-like structure formed when the bladder’s migratory epithelium is subjected to various chronic irritations and grows in a bud-like pattern towards the submucosa, which is then divided by the surrounding connective tissue envelope and separated from the migratory epithelium.VonBrunn’s nest consists of well-differentiated migratory epithelium with epithelial cells arranged perpendicular to the surrounding basement membrane . Sometimes the epithelial nests are cystic in the center, and if the cystic surface is covered with migratory epithelium and the fluid within the cyst is a light yellow mucus component, it is called cystic cystitis. In the lamina propria, glandular formation is seen, and sometimes the luminal surface may evolve into a mucous columnar epithelium similar to the intestinal mucosa, with infiltration of lymphocytes and plasma cells, and histological analysis shows that the glands secrete intestinal-type mucus, called adenoid cystitis. In some cases, intestinal mucus is seen in the urine. In most cases, there is a coexistence of VonBrunn’s nest, cystic and glandular metaplasia, which can be collectively referred to as adenocystitis or cystic cystitis. These hyperplastic lesions can also be seen in the ureter or renal pelvis. In contrast, polypoid cystitis develops as an ectoplasmic growth of the migrating epithelium. There are two types of adenoid cystitis, typical and intestinal, the latter being less common. The typical type is a gland that may consist of cuboidal and columnar epithelium covered by several layers of urogenital migratory epithelium. The intestinal type consists of a mucus-secreting columnar epithelium with a nucleus located at the base, and commonly cupped cells. It has also been classified into four types: migratory cell type, intestinal epithelial type, prostatic epithelial type, and mixed type.
Is the cause of adenoid cystitis clear?
Most of the literature suggests that adenoid cystitis is caused by chronic inflammation due to long-term chronic irritation from factors such as stones, infection, obstruction, urinary catheterization, and tumors. parker et al. reported 32 cases of cystic cystitis and 8 cases of adenoid cystitis, 95% of which had infection, stones, and obstruction. delnay et al. reported that about 23% of patients with urinary catheterization had adenoid cystitis. Kaplan and King reported 2.4% of children with adenocystitis who had recurrent urinary tract infections. It is more common in girls, and some patients also have vesicoureteral reflux.
Another view is that adenoid cystitis is caused by abnormal embryologic development. During embryonic development, the cloaca separates into the urogenital sinus and rectum, and the separation of the rectum from the urogenital sinus results in the retention of the umbilical ureter or intestinal epithelium, which eventually leads to the development of adenoid cystitis. This has also been disputed, as adenovaginitis and adenovaginitis can also occur in the ureter and renal pelvis.
Some other possible causes include vitamin deficiencies, toxin allergies, viral infections, carcinogens, IgA-mediated immune responses, and hormonal imbalances. Approximately 75% of patients with pelvic adiposity have adenocystitis, and the mechanism remains to be further explored.
Fourth, is adenoid cystitis a precancerous lesion?
Given that 50-100% of bladders on autopsy have varying degrees of Brunn’s nest, cystic cystitis and presentation, some scholars believe that the above histologic changes may be normal variants of the bladder mucosa rather than precancerous lesions. It is noteworthy that these autopsy bladders were largely normal to the naked eye and only microscopic histological alterations were present.
Most investigators consider adenocystitis to be a precancerous lesion associated with adenocarcinoma of the bladder. Adenocarcinoma of the bladder triangle often originates from adenocystitis or cystic cystitis. Adenocystitis can often be found around carcinoma in situ or other invasive bladder tumors. In five larger series of bladder adenocarcinoma studies, approximately 10-42% of cases were associated with adenocystitis. slmon et al. studied 38 total bladder cancer specimens and found atypical hyperplasia, cystic cystitis and Brunn’s nest in 89% of cases and concluded that there were three possible relationships with the tumor:
1, mucinous proliferative changes preceded the presence of tumor;
2, both occur simultaneously;
3, the tumor occurs before the mucoproliferative changes.
Therefore, some scholars have proposed the hypothesis that it may be the stimulation of the tumor that leads to the heterogeneous proliferation of bladder mucosa and the formation of glandular inflammation in the tumor area and surrounding tissues, or it may be the malignant change on the basis of glandular cystitis.
In view of these controversies, it has been suggested that adenoid cystitis with diffuse gross lesions, widely diffuse histological nests of cells, and molecular biological indicators suggesting active proliferation has a higher chance of carcinogenesis and should be considered precancerous. lu et al. found high expression of bcl-2 in patients with adenoid cystitis and an association with carcinogenesis. Zhou Xing et al. reported that the expression rate of ras and p21 positive proteins in patients with adenocystitis was as high as 70.5%, of which 42.5% were malignant, suggesting that high expression of ras and p21 could be a sign of the onset of malignancy in adenocystitis. murphy et al. found that mAbDas1 could predict the possibility of malignant transformation in adenocystitis. Such patients should be closely monitored with regular follow-up (including urine cytology, cystoscopy and biopsy). It has been found that the duration of exposure to toxicants, duration of disease, concomitant bladder stones and dyspareunia may also be important risk factors for carcinogenesis.
The above controversy may be caused by the fact that there is no universally accepted understanding of precancerous lesions. According to pathology, precancerous lesions are those that appear before malignant tumors and have some degree of morphological atypical hyperplasia, but do not have malignant characteristic changes, or are considered to be more likely to develop into cancer; WHO stipulates that all kinds of lesions with more than 20% chance of developing into malignant are precancerous. Any lesions that may develop into cancer are included as precancerous lesions, regardless of their likelihood and the length of time before they become cancerous, and are classified as precancerous lesions without restriction, which is a bit overly generalized and lacks practical value. Chronic cystitis can cause squamous and glandular metaplasia of the bladder mucosa, and these pathological changes can further develop into squamous or adenocarcinoma, so it is obviously unreasonable to define chronic cystitis as precancerous. There is a lack of long-term systematic scientific follow-up data on adenoid cyst, and the current evidence is insufficient to suggest that any histologic adenoid cystitis is precancerous. Although there is no consensus among scholars that adenocystitis is precancerous, aggressive treatment and careful follow-up are well accepted and advocated.
Most reports suggest an association between adenocystitis and adenocarcinoma, but there are also many reports suggesting an association between adenocystitis and metastatic and squamous carcinoma. Among the 104 patients with adenocystitis, 80 had simple adenocystitis; among the 24 cases with carcinoma, 11 had adenocystitis evolving into metastatic cell carcinoma.KittredZe (1964) and Salm (1967) reported one case of adenocystitis coexisting with mucinous adenocarcinoma of the bladder and squamous carcinoma of the bladder, respectively.Donald et al. reported two cases of PeterFegen et al. reported three patients with coexisting adenocarcinoma and metastatic cell carcinoma of the bladder, suggesting that the adenocarcinoma may have evolved from the adenocyst and the two tumor tissues may have co-evolved from the metastatic cells. It has been shown that long-term chronic inflammation can lead to the formation of adenocystitis, squamous metaplasia and metastatic atypical hyperplasia in the bladder mucosa, so the above adenocarcinoma, squamous carcinoma, metastatic cell carcinoma and adenocystitis may coexist, and their origins and interrelationships may be extremely complex, and which one comes first needs further investigation.
V. Is it easy to diagnose adenocystitis?
Adenoid cystitis can be clinically manifested mainly by various symptoms such as urinary frequency, urgency, painful urination, lower abdominal and perineal pain, difficulty in urination and microscopic hematuria, etc. It occurs in the bladder triangle, bladder neck and around the ureteral orifice, and is similar to other non-specific inflammatory diseases of the bladder without specificity. It has been suggested that there are characteristic cystoscopic manifestations: papillary masses with generally translucent ends and no vascular branches, and edema visible around the papillae, which can occur singly or in groups.
In fact, adenoid cystitis has several types of presentation on cystoscopy.
(1) papillary hyperplasia (also called follicular edema): the bladder mucosa shows papillary hyperplasia with a tipped surface that is congested and edematous, and the tipped size varies.
(2) Laminar hyperplasia type: bladder mucus shows villi-like or lamellar hyperplasia.
(3) Chronic inflammatory type: the bladder mucosa shows restricted congestion, roughness, small erosive surfaces and follicles.
(4) Mixed type: multiple types co-exist. The above presentation types are easily confused with follicular cystitis, inflammatory pseudotumor, eosinophilic cystitis, interstitial cystitis, and tuberculous cystitis, and cases of misdiagnosis of bladder cancer are not uncommon. The characteristic manifestations are only significant for the papillary hyperplasia type and less significant for the lamellar hyperplasia and chronic inflammatory types. Due to the diversity of morphological manifestations, it is difficult to make a specific diagnosis from imaging examinations such as ultrasound, CT, MRI and IVU. Xiao Yajun et al. observed 30 cases of bladder tumors and 11 cases of adenoid cystitis with hydrogen peroxide cystography ultrasonography, and concluded that adenoid cystitis lesions had no obvious bleeding, necrosis, and a smooth surface. There was no microscopic oxygen bubble attachment after hydrogen peroxide contrast and no significant enhancement of surface echogenic reflection, which could be differentiated from bladder tumors, but had limited clinical application.
The main basis for confirming the diagnosis of adenocystitis is a combination of cystoscopy and biopsy. Early cystoscopy plus biopsy is advocated for those with suspected causative factors and clinical manifestations, provided that the urinary routine is normal or there is no infection (within 1 week), with a view to early diagnosis and early treatment to avoid prolonging the course of the disease and worsening the lesion. Pathological biopsy can be combined with immunohistochemical results if necessary.
VI. Is there a specific treatment for adenoid cystitis?
There is no satisfactory treatment for adenoid cystitis, with a high recurrence rate in some cases and a wide range of treatments with varying efficiency. The first choice is to remove the cause (long-term antibiotic treatment, removal of mechanical irritation), on the basis of which there are also mucosal stripping of the bladder, partial cystectomy, total cystectomy (with some form of urinary diversion), bladder enlargement, ureteral bladder reimplantation, intravesical instillation of various drugs (such as mitomycin, thiotepa, birubicin, hydroxycamptothecin, 1% silver nitrate, procaine + gentamicin and BCG vaccine, but also immunomodulators such as interleukin-2, interferon, etc.), transurethral electrocautery or laser therapy, and radiation therapy. There is also transurethral electrodesis or electrocautery combined with bladder irrigation.
BCG is usually instilled at a dose of 100 mg + 40 ml of saline, and the treatment is carried out according to the method of bladder cancer instillation, once a week for 6 times.
The bladder perfusion of chemotherapy drugs is the same as the bladder tumor perfusion method, and the drug dose and duration of treatment can be adjusted appropriately according to the disease. It has been suggested that there is no need for “overtreatment” of bladder irrigation with anticancer drugs after elective resection, and that bladder irrigation with drugs is usually used for recurrent patients.
The infusion dose of 1% silver nitrate solution is 40ml, once every 1~2 weeks, and half a year is a course of treatment.
Radiation therapy is often performed with a linear gas pedal at a dose of 4000-4500 Gy (60% of the tumor treatment dose) in 16-18 doses, either daily or every other day, and the symptoms can be relieved after 3-6 months of treatment.
Since adenocystitis is a persistent disease and some of the lesions reach deep into the sub lamina propria of the bladder, all of the diseased mucosa and adjacent normal mucosa should be excised during electrodesiccation vaporization according to the type of lesion, the depth and extent of lesion involvement, and the depth should reach the sub lamina propria. For extensive diffuse lesions, electrocautery or laser treatment is not advocated because complete and complete excision of the lesion is more difficult, while cautery of large areas can aggravate bladder irritation. For extensive intravesical lesions involving the triangle and bladder neck, or if local adenocarcinoma has been detected, radical cystectomy should be performed, but the choice of surgery should be carefully considered in terms of the extent of the lesion, the severity of the disease, and the patient’s quality of life in the future.
To improve the outcome of adenocystitis treatment, the appropriate treatment (including the combination of multiple treatment modalities) should be selected based on the presence or absence of clear predisposing factors, concomitant underlying disease, and the type, location, extent, and type of pathology of the lesion.
The following principles should be followed in the choice of treatment for adenocystitis.
(1) Removal of predisposing factors and resolution of the underlying disease are the basic therapeutic tools, and after these treatments, some patients may heal spontaneously.
(2) Transurethral resection or electrocautery is the main treatment method and is more suitable for redundant organisms larger than 0.5 cm.
(3) Patients with unknown etiology and diffuse lesions should be treated with bladder perfusion chemotherapy.
(4) Patients with extensive lesions and active hyperplasia should be monitored, followed up regularly and treated as bladder cancer if necessary.
(5) Patients with a long history, extensive lesions, severe symptoms, and high suspicion of malignancy or malignancy can undergo partial cystectomy or total cystectomy. Total cystectomy should be performed with caution.
(6) The combined application of multiple treatments can improve the therapeutic effect.