UNASSIGNED: A previous report has shown that cyclooxygenase-2 inhibitors can prevent the recurrence of cystitis glandularis postoperatively. Herein, we present a case of cystitis glandularis in which the tumor volume was markedly reduced by preoperative oral administration of a cyclooxygenase-2 inhibitor.
UNASSIGNED: A 45-year-old man with voiding difficulty and lower abdominal pain during urination was referred to our hospital. Cystoscopy revealed multiple cystitis glandularis-like edematous masses on the trigone and the neck of the bladder, completely involving the bilateral ureteral orifices. Cyclooxygenase-2 inhibitor was orally administered at the patient\'s request. Six weeks later, the tumor volume was markedly reduced, bilateral ureteral orifices were identified, and the voiding difficulty and pain on urination disappeared. Complete transurethral resection of the residual tumor was performed, and the pathological diagnosis was intestinal-type cystitis glandularis.
UNASSIGNED: Cyclooxygenase-2 inhibition can be considered a useful therapeutic strategy for cystitis glandularis.

•we report the case of a 36-year-old female patient who presented to our hospital with a diagnosis of cystitis glandularis manifesting as a vesicovaginal fistula. She underwent cystoscopic biopsy at a local hospital, but anti-inflammatory treatment was ineffective, and the patient was experiencing low urination frequency and urgency, as well as pain. The patient underwent laparoscopic repair of a cystoscopy-confirmed vesicovaginal fistula. After surgery, the patient experienced a paroxysm of Crohn\'s disease with multiple small bowel fistulas and erosion of the external iliac vessels that ruptured to form an external iliac vessel small bowel fistula. The fistula was confirmed by surgical exploration, and the patient eventually died.

Cystitis glandularis is a rare benign condition, occurring in only 1% of the general population, and it tends to affect males more frequently. This pathology is characterized by reactive metaplasia of the bladder\'s urothelium, which results from chronic and recurrent irritation of the bladder wall. Symptoms are nonspecific and primarily marked by an irritative urinary syndrome accompanied by hematuria. We present a case of a young male patient with cystitis glandularis, discovered as a result of bilateral uretero-hydronephrosis detected during an ultrasound examination subsequent to an irritative urinary syndrome. The diagnosis was initially suggested by a CT scan; it was ultimately histologically confirmed following the endoscopic resection of the tumor.

BACKGROUND: Cystitis glandularis is a proliferative disease of the bladder epithelium usually presenting in the setting of chronic inflammation, characterized by the formation of glands in the bladder mucosa and submucosa. Intestinal metaplasia is a described process in cystitis glandularis characterized by the presence of intestinal cells and mucin production which is rare as compared to cystitis glandularis.
METHODS: We present a case of cystitis glandularis with intestinal metaplasia located in the bladder and concomitantly in the prostatic urethra. Patient underwent transurethral resection of the lesion which was unusually found in the prostatic urethra.
UNASSIGNED: Florid cystitis glandularis is a rare condition found in women more than in men. It usually presents with irritative lower urinary tract symptoms or hematuria which leads to its eventual diagnosis. It is usually causes by inflammation to the bladder mucosa due to infections or irritation. Patients are diagnosed through Transurethral resection of these bladder lesions found in the trigone and bladder neck region. Surgery is the standard treatment of choice. However, medical treatment may also be used to treat underlying inflammatory conditions using antibiotics, steroids, and non-steroidal anti-inflammatory agents. Radical or partial cystectomy may be performed for severe refractory cases.
CONCLUSIONS: This article describes the rare occurrence of florid cystitis glandularis in the prostatic urethra and provides an overview on diagnosis, etiology, and management of the disease.

BACKGROUND: Cystitis glandularis (CG) is a proliferative lesion of the bladder mucosa, and the incidence rate of CG has increased year by year. Considering the potential function of β-sitosterol in CG, we aim to fathom its effect and mechanism of CG.
METHODS: Primary human cells isolated from CG patients and following transfection as needed, were treated with different concentrations of β-sitosterol. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and transwell assay was used to test the cell migration. Meanwhile, co-immunoprecipitation was employed to evaluate the interaction between 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and NLR family pyrin domain containing 3 (NLRP3). Additionally, pyroptosis-associated proteins and HMGCR expressions were tested using western blot or quantitative real-time reverse transcription polymerase chain reaction.
RESULTS: β-sitosterol suppressed cell viability and migration, enhanced cell pyroptosis, and upregulated expressions of NLRP3, Cleaved Caspase-1, interleukin-1β (IL-1β), gasdermin D-N-terminal domain (GSDMD-N), and HMGCR in CG primary cells (p < 0.05). HMGCR silencing promoted cell viability and migration, inhibited cell pyroptosis, and downregulated expressions of NLRP3, Cleaved Caspase-1, IL-1β, and GSDMD-N in β-sitosterol-affected CG primary cells (p < 0.05). HMGCR interacted with NLRP3.
CONCLUSIONS: β-sitosterol alleviates the proliferation and migration of CG-associated cells by targeting HMGCR to induce NLRP3-dependent pyroptosis. These findings confirmed the therapeutic effect of β-sitosterol on treating CG.

This study presents the case of man who underwent ultrasonography (US) for the diagnosis and follow-up of cystitis glandularis with severe intestinal metaplasia. We believe that our study makes a significant contribution to the literature because the findings of cystitis glandularis that forms a mass is relatively rare.

UNASSIGNED: Cystitis glandularis is a common bladder epithelial lesion characterized by hyperplasia and metaplasia of the bladder mucosa epithelium. The pathogenesis of cystitis glandularis of the intestinal type is unknown and less common. When cystitis glandularis (intestinal type) is extremely severely differentiated, it is called florid cystitis glandularis (the occurrence is extremely rare).
UNASSIGNED: Both patients were middle-aged men. In patient 1, the lesion was also seen in the posterior wall and was diagnosed more than 1 year ago as cystitis glandularis with urethral stricture. Patient 2 was examined for symptoms such as hematuria and was found to have an occupied bladder; both were treated surgically, and the postoperative pathology was diagnosed as florid cystitis glandularis (intestinal type), with mucus extravasation.
UNASSIGNED: The pathogenesis of cystitis glandularis (intestinal type) is unknown and less common. When cystitis glandularis of the intestinal type is extremely severely differentiated, we call it florid cystitis glandularis. It is more common in the bladder neck and trigone. The clinical manifestations are mainly symptoms of bladder irritation, or hematuria as the main complaint, which rarely leads to hydronephrosis. Imaging is nonspecific and the diagnosis depends on pathology. Surgical excision of the lesion is possible. Due to the malignant potential of cystitis glandularis of intestinal type, postoperative follow-up is required.

Cystitis glandularis (CG) is a rare chronic bladder hyperplastic disease that mainly manifests by recurrent frequent urination, dysuria and gross hematuria. The current lack of unified diagnosis and treatment criteria makes it essential to comprehensively describe the inflammatory immune environment in CG research.
Here, we performed scRNA-sequencing in CG patients for the first time, in which four inflamed tissues as well as three surrounding normal bladder mucosa tissues were included. Specifically, we isolated 18,869 cells to conduct bioinformatic analysis and performed immunofluorescence experiments.
Our genetic results demonstrate that CG does not have the classic chromosomal variation observed in bladder tumors, reveal the specific effects of TNF in KRT15 epithelial cells, and identify a new population of PIGR epithelial cells with high immunogenicity. In addition, we confirmed the activation difference of various kinds of T cells during chronic bladder inflammation and discovered a new group of CD27-Switch memory B cells expressing a variety of immunoglobulins.
CG was regarded as a rare disease and its basic study is still weak.Our study reveals, for the first time, the different kinds of cell subgroups in CG and provides the necessary basis for the clinical treatment of cystitis glandularis. Besides, our study significantly advances the research on cystitis glandularis at the cellular level and provides a theoretical basis for the future treatment of cystitis glandularis.

BACKGROUND: Paraneoplastic neurological syndrome (PNS) is an unusual event. PNS caused by cystitis glandularis (CG) or a bladder tumor is extremely rare; hence, missed diagnosis or misdiagnosis can easily occur. To date, approximately 21 cases have been reported in PubMed.
METHODS: We report a case of PNS caused by CG and describe the clinical and imaging features. The main clinical feature was advanced cognitive impairment, and early clinical features were memory impairment, decreased computational ability, and abnormal behavior. Later clinical features were dementia, vomiting, inability to eat and walk, urinary incontinence, and hematuria. Imaging features on cranial magnetic resonance imaging were diffuse white matter lesions. Paraneoplastic tumor markers were normal. A total abdominal computed tomography scan showed multiple thickened areas on the bladder wall with local prominence. Cystoscopy revealed a volcanic protuberance on the posterior wall of the bladder with a diameter of 6 cm and no pedicle. The postoperative pathological diagnosis was CG. The patient recovered well following resection of CG. PNS cases caused by previous bladder tumors can be retrieved from PubMed to describe the clinical signs and prognosis of PNS.
CONCLUSIONS: The main clinical feature of PNS caused by CG was dementia, and the imaging features were diffuse cerebral white matter lesions. Resection of CG lesions is the fundamental treatment for PNS induced by CG. This case highlights the importance of etiological treatment.

Cystitis Glandularis (CG) is an unusual proliferative disease of the bladder. This condition was associated with chronic inflammation or chronic obstruction. This condition usually presents as microscopic finding and the presence of large macroscopic lesion is a rare feature. Until now, the course of disease from transitional to cystitis glandularis is still unclear and the uncertainty of CG to potentially develop into adenocarcinoma has once been documented. Herewith, we report our experience with 2 years old boy with cystitis glandularis presenting with LUTS obstructive symptoms, hematuria and bladder mass. Ultrasound examination revealed bilateral hydronephrosis with hydroureter and bladder wall thickness suggesting the sign of obstruction and chronic inflammation. Cystoscopy examination was performed to ensure the diagnosis with the result revealing protruding mass partially obstructing the bladder trigone, both ureteral orifice and posterior urethra. Transurethral resection was performed and the administration of COX-2 inhibitor and oral steroid therapy were given. Post-operative course was uneventful with the improvement in symptom and uroflowmetry revealed promising result. This case represented an entity of rare and interesting case of cystitis glandularis causing severe obstructive symptoms and urinary bladder mass which appropriate therapy of endoscopic intervention, COX-2 inhibitor and oral steroid resulted in promising outcome. Follow up of 1 year resulted in reduced LUTS symptoms such as straining and difficulty of urination.