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PubMed1998

The treatment of interstitial cystitis with supratrigonal cystectomy and ileocystoplasty: difference in outcome between classic and nonulcer disease.

PURPOSE: Interstitial cystitis is a chronic debilitating condition that mainly affects women. Accumulated evidence indicates that interstitial cystitis is a heterogeneous syndrome. The nonulcer type seems to respond less favorably to various conservative treatments than the classic type. Supratrigonal cystectomy with ileocystoplasty is established treatment for interstitial cystitis refractory to conservative treatment. We evaluate whether classic interstitial cystitis responds differently than nonulcer disease to subtotal bladder resection and ileocystoplasty. MATERIALS AND METHODS: We evaluated 13 patients 27 to 79 years old with interstitial cystitis who underwent supratrigonal cystectomy and ileocystoplasty due to failure to respond to conservative treatment. RESULTS: In all 10 patients with classic interstitial cystitis symptoms were relieved after ileocystoplasty. In the 3 patients with nonulcer interstitial cystitis pain remained, while the frequency of voiding somewhat decreased. In these patients trigonal resection and urinary diversion with a Kock pouch resolved the symptoms. CONCLUSIONS: Our study confirms that supratrigonal cystectomy with ileocystoplasty results in a good outcome in classic interstitial cystitis. However, this method seems to be unsuitable for nonulcer disease. Identification of the relevant subtype of interstitial cystitis is of crucial importance for selecting the appropriate method of lower urinary tract reconstruction.

Adult↗
PubMed2003

The role of beta-catenin signaling in the malignant potential of cystitis glandularis.

PURPOSE: Chronic inflammation is a risk factor for malignant transformation in the bladder. The pro-inflammatory cytokine tumor necrosis factor-alpha (TNFalpha) is a mediator of such inflammation that induces nuclear localization of the adherens junction component beta-catenin. This mechanism has a key role in the initiation and progression of the premalignant lesion Barrett's metaplasia of the esophagus. Cystitis glandularis is a metaplastic lesion of the bladder urothelium occurring in the presence of chronic inflammation and in up to 13% of asymptomatic bladders. Two subtypes are described (typical and intestinal/colonic) with uncertain malignant potential. Etiologically and histologically cystitis glandularis mimics Barrett's metaplasia. We investigated the roles of beta-catenin and TNFalpha in cystitis glandularis. MATERIALS AND METHODS: Immunohistochemistry and immunofluorescence were used to demonstrate the expression and localization of E-cadherin, beta-catenin and TNFalpha in 9 sections of typical cystitis glandularis and 4 of intestinal/colonic cystitis glandularis. Appropriate controls were used for all experiments. RESULTS: Immunohistochemistry demonstrated normal membranous expression of E-cadherin and beta-catenin in all cystitis glandularis sections with increased TNFalpha expression. Immunofluorescence showed nuclear localization of beta-catenin in the intestinal/colonic subtype only, which was not observed in typical cystitis glandularis. CONCLUSIONS: The presence of nuclear beta-catenin suggests that intestinal/colonic cystitis glandularis shares the same signaling pathway with the premalignant lesion Barrett's metaplasia of the esophagus and the intestinal/colonic subtype of cystitis glandularis may have the potential to progress to malignancy. This finding has important implications for the management of this lesion.

Adenocarcinoma↗
PubMed1998

Comparison of Escherichia coli strains recovered from human cystitis and pyelonephritis infections in transurethrally challenged mice.

Urinary tract infection, most frequently caused by Escherichia coli, is one of the most common bacterial infections in humans. A vast amount of literature regarding the mechanisms through which E. coli induces pyelonephritis has accumulated. Although cystitis accounts for 95% of visits to physicians for symptoms of urinary tract infections, few in vivo studies have investigated possible differences between E. coli recovered from patients with clinical symptoms of cystitis and that from patients with symptoms of pyelonephritis. Epidemiological studies indicate that cystitis-associated strains appear to differ from pyelonephritis-associated strains in elaboration of some putative virulence factors. With transurethrally challenged mice we studied possible differences using three each of the most virulent pyelonephritis and cystitis E. coli strains in our collection. The results indicate that cystitis strains colonize the bladder more rapidly than do pyelonephritis strains, while the rates of kidney colonization are similar. Cystitis strains colonize the bladder in higher numbers, induce more pronounced histologic changes in the bladder, and are more rapidly eliminated from the mouse urinary tract than pyelonephritis strains. These results provide evidence that cystitis strains differ from pyelonephritis strains in this model, that this model is useful for the study of the uropathogenicity of cystitis strains, and that it would be unwise to use pyelonephritis strains to study putative virulence factors important in the development of cystitis.

Animals↗
PubMed2000

The association of elevated urinary total to sulfated glycosaminoglycan ratio and high molecular mass hyaluronic acid with interstitial cystitis.

PURPOSE: A decrease in the glycosaminoglycan (GAG) layer on the urothelium is believed to be one of the possible causes of interstitial cystitis. Consequently, GAG-like substances and hyaluronic acid (HA) have been prescribed for treating this condition. To delineate the possible role of GAG and HA in the interstitial cystitis disease process, we compared the urinary levels of total GAGs (sulfated + non-sulfated), sulfated GAGs and HA in interstitial cystitis patients and normal controls. We also examined different HA species present in the urine of interstitial cystitis patients. MATERIALS AND METHODS: The total GAG and sulfated GAG levels in urine specimens of normal individuals (n = 20) and interstitial cystitis patients (n = 25) were determined by utilizing the carbazole reaction assay and the Farndale method, respectively, and were expressed as microg./mg. creatinine. Urinary HA levels were measured by applying the HA test and were expressed as ng./mg. creatinine. Gel filtration column chromatography was used to examine the profile of urinary GAGs and HA species. RESULTS: Total urinary GAGs were 2.5 to 4-fold elevated in interstitial cystitis patients with moderate to severe symptoms (Group 2; 76.2 +/- 24.8) when compared with those in normal individuals (19.9 +/- 2.5) and patients with mild symptoms (Group 1; 30.4 +/- 5.1) (p <0.001). Three urinary GAG peaks were detected in both normal and interstitial patients. However, each GAG peak from interstitial cystitis patient urine was 3 to 5-fold higher than that from normal patient urine. The sulfated GAG levels, however, remained unchanged among normal individuals (1.4 +/- 0.22), Group 1 (2.2 +/- 0.96) and Group 2 (1.6 +/- 0.38) patients (p >0.05). Consequently, the ratio of total GAGs to sulfated GAGs was elevated 3 to 3.5-fold in Group 2 patients (49.9 +/- 13.9) in comparison to that in normal individuals (16.7 +/- 2.5) and group 1 patients (14.4 +/- 4.6) (p <0.001). Urinary HA levels were marginally elevated in Group 2 patients (821. 4 +/- 247.9) when compared with those in the normal group (337.3 +/- 106.1) and Group 1 patients (540.9 +/- 166.5). In addition, a distinct high molecular mass HA species was present only in Group 2 patients. CONCLUSIONS: The increased ratio of total GAGs to sulfated GAGs and marginally elevated HA levels in urine indicate that the GAG layer is altered in interstitial cystitis patients. However, these results are in contrast to the accepted concept that a reduction in urothelial GAGs causes interstitial cystitis. The high molecular mass HA species detected in patients with severe symptoms may play a role in the pathophysiology of this disease.

Adult↗
PubMed2001

Nonbladder related symptoms in patients with interstitial cystitis.

PURPOSE: Clinical experience and epidemiological studies suggest that patients with interstitial cystitis have multiple nonbladder related symptoms. However, to our knowledge this finding has not been tested with a validated questionnaire and matched controls. With the University of Wisconsin scale, we compare the scores for patients with interstitial cystitis to those for control subjects. This validated questionnaire includes 7 bladder and 18 reference symptoms not related to the bladder. MATERIALS AND METHODS: A total of 35 female patients with interstitial cystitis and 35 age matched female controls completed the University of Wisconsin questionnaire. RESULTS: For the 7 bladder symptoms the difference between interstitial cystitis and control groups was extremely significant (p = 0.0001). Patients with interstitial cystitis had higher scores than controls for 2 reference symptoms, including other pelvic discomfort, backache, dizziness, chest pain, aches in joints, abdominal cramps, nausea, heart pounding and headache (p <0.01). However, they did not have higher scores for blind spots and/or blurred vision, numbness and/or tingling in fingers or toes, swollen ankles, feeling of suffocation, sore throat, cough, flu, nasal congestion and ringing in ears. The majority of patients with interstitial cystitis had a 0 score for all but 2 of the reference symptoms. CONCLUSIONS: Patients with interstitial cystitis had increased scores for 9 reference symptoms but did not indiscriminately report high scores for generalized complaints. This result suggests that in some cases of interstitial cystitis the pathophysiology may affect other organ systems besides the bladder. Alternatively, some of these symptoms may result from changes in sleep pattern or other factors associated with interstitial cystitis.

Arthralgia↗
PubMed2001

Augmented stretch activated adenosine triphosphate release from bladder uroepithelial cells in patients with interstitial cystitis.

PURPOSE: Extracellular adenosine triphosphate (ATP) has been shown to mediate inflammation and nociception and, therefore, it may have a role in symptoms associated with interstitial cystitis. We theorized that the bladder uroepithelium releases ATP in response to stretch and, furthermore, this process is augmented in interstitial cystitis. MATERIALS AND METHODS: We quantitated ATP using the luciferin-luciferase assay. Urinary ATP levels were compared in 35 patients with interstitial cystitis and in 33 normal controls after pH correction. Cultured interstitial cystitis and normal urothelial cells from the bladder biopsies of 5 patients each were stretched with the Flexcell 2000 machine (Flexcell International Corp., McKeesport, Pennsylvania) and supernatant ATP concentrations were measured. RESULTS: Mean urinary ATP plus or minus standard error of mean was significantly higher in patients with interstitial cystitis than in controls (L value 985 +/- 161 versus 377 +/- 27, p = 0.0007). Supernatant ATP released by stretched interstitial cystitis cells was stretch intensity dependent when comparing 0%, 10% and 20% elongation, and was also significantly higher in stretched interstitial cystitis than in stretched normal cells. CONCLUSIONS: Adenosine triphosphate was significantly elevated in the urine of individuals with interstitial cystitis and the stretch activated release of ATP was augmented in interstitial cystitis urothelium. Increased extracellular ATP may have a role in mechanosensory transduction and to our knowledge it represents a novel hypothesis.

Adenosine Triphosphate↗
PubMed2001

Increased urinary leukotriene E4 and eosinophil protein X excretion in patients with interstitial cystitis.

PURPOSE: The role of cysteinyl containing leukotriene C4, D4 and E4, and eosinophil protein X in interstitial cystitis is unknown. Leukotriene E4, the end product of cysteinyl containing leukotrienes, and eosinophil protein X are markers of the activation of mast cells and eosinophils, respectively. Cysteinyl containing leukotrienes are potent and specific chemoattractants for eosinophils. We compared the urinary excretion of leukotriene E4 and eosinophil protein X in patients with interstitial cystitis and in healthy controls. MATERIALS AND METHODS: Morning spot urine samples from nine patients with interstitial cystitis who fulfilled National Institute of Diabetes and Digestive and Kidney Diseases criteria were collected on the day of cystoscopy with biopsies. Aliquots of urine specimens were immediately centrifuged and the supernatants were stored at -80C until use. Urine samples from 9 healthy women served as controls. Urinary leukotriene E4 and eosinophil protein X were measured by enzyme immunoassay and radioimmunoassay, respectively. All determinations were performed in duplicate and normalized to urine creatinine. RESULTS: Leukotriene E4 and eosinophil protein X were significantly increased in the morning urine of patients with interstitial cystitis compared with controls. The mean urinary excretion of leukotriene E4 plus or minus standard deviation was 148.8 +/- 62.5 and 62.2 +/- 17.5 ng./mmol. creatinine in patients and controls (p = 0.003), while the mean urinary excretion of eosinophil protein X was 109.7 +/- 70.4 and 43.7 +/- 22.0 microg./mmol. creatinine, respectively (p = 0.01). All urine cultures were negative. The mean mast cell count in detrusor biopsies in the interstitial cystitis group was 41 cells per mm.2 (range 5 to 84). Eosinophilic granulocytes were occasionally observed in the submucosa but not in the detrusor. CONCLUSIONS: Our study shows that patients with interstitial cystitis and detrusor mastocytosis have increased urinary leukotriene E4 and eosinophil protein X. It is possible that cysteinyl containing leukotrienes and eosinophil protein X are involved in the pathogenesis of interstitial cystitis. Urinary leukotriene E4 and eosinophil protein X may be useful markers for assessing the grade of activation of mast cells and eosinophils in patients with interstitial cystitis and/or for confirming the diagnosis. However, it remains to be investigated whether the increase in urinary leukotriene E4 and eosinophil protein X correlates with interstitial cystitis symptoms.

Adult↗
PubMed2001

[Hemorrhagic cystitis: etiology and treatment].

Haemorrhagic cystitis consists of acute or insidious diffuse bleeding from the bladder mucosa. Although the aetiology of haemorrhagic cystitis is varied, the two predominant causes are chemical and irradiation. The chemical compounds most frequently responsible for haemorrhagic cystitis are oxaphosphorines (cyclophosphamide, ifosfamide). Haemorrhagic cystitis may also be due to toxic or infectious causes (bacterial, fungal, parasitic or viral). Finally, haemorrhagic cystitis can occur in the context of a systemic disease or may be isolated and idiopathic. Prevention of haemorrhagic cystitis, based on general measures and specific measures, is essential, but is not always effective. In the case of proven haemorrhagic cystitis, various treatment options are available, including and can associate clot extraction, continuous bladder irrigation, bladder instillations of haemostatic factors, formalin, hyperbaric oxygen therapy, arterial embolization or salvage surgery. Although therapeutic management is usually effective, it can sometimes be difficult due to the severity of the bleeding and its repercussions on the patient's general state. Deaths are not exceptional, emphasizing the seriousness of haemorrhagic cystitis. Based on a review of the literature, the authors review the aetiology and treatment of haemorrhagic cystitis.

Cystitis↗
PubMed2002

A comparison of multiple urine markers for interstitial cystitis.

PURPOSE: We measured several urine markers in 24-hour specimens from patients with interstitial cystitis and healthy controls. For each marker we determined whether the urine level was significantly different in interstitial cystitis and control cases, and whether the marker level correlated with the symptom score. MATERIALS AND METHODS: Study participants included 36 female patients with interstitial cystitis and 36 age matched female volunteers. Multiple urine aliquots were obtained to measure the various markers. RESULTS: Certain markers were significantly increased in interstitial cystitis, including anti-proliferative factor, epidermal growth factor, insulin-like growth factor (IGF) binding protein-3 and interleukin (IL)-6. Markers significantly decreased in interstitial cystitis were heparin-binding epidermal growth factor-like growth factor, cyclic guanosine monophosphate and methylhistamine. Other markers were not significantly different in the interstitial cystitis and control groups, including total glycosaminoglycans, epitectin, hyaluronic acid, IL-8, IL-1 and nitrates plus nitrites. IGF-1 was undetectable in 24-hour urine samples but spot voided samples from the same interstitial cystitis population had IGF-1 levels similar to previously reported levels. The only significant association of marker with symptom score was a positive correlation of IL-6 with nocturia. For all markers the conclusions were the same whether the marker was normalized to creatinine or to 24 hours. CONCLUSIONS: This study confirmed several previously reported urine alterations in interstitial cystitis, including increased anti-proliferative factor, epidermal growth factor, IGF binding protein-3 and IL-6, and decreased heparin-binding epidermal growth factor-like growth factor and cyclic guanosine monophosphate. Of all markers studied anti-proliferative factor had the least overlap in the interstitial cystitis and control groups, and so it is the most likely candidate to become a diagnostic test.

Adult↗
PubMed1997

Multiple urinary cytokine levels of bacterial cystitis.

PURPOSE: We have examined urinary cytokine levels to define the inflammatory response in patients with bacterial cystitis or microhematuria relative to normal subjects. Cytokines examined include interleukin-1beta (IL-1beta), IL-1alpha, tumor necrosis factor (TNF alpha), IL-6 and IL-4. Unique features of this study include a) a simultaneous study of several relevant cytokines b) a study of the inflammatory response at both low and high counts of bacterial infection and c) an assessment of whether microhematuria without bacterial cystitis or pyuria is associated with cytokine elevation compared to normals. MATERIALS AND METHODS: Enzyme immunoassays were utilized for each cytokine. Patients studied include those with bacterial cystitis (n = 49), patients with microhematuria (n = 11), and normal subjects (n = 36). Cytokine levels were also determined for patients with low count bacterial cystitis (1,000-50,000 organisms; n = 15) and compared to high count bacterial cystitis (>100,000 organisms; n = 34) and normal subjects. Statistical analysis was carried out using the Kruskal-Wallis test followed by pairwise testing with Newman-Keuls test. RESULTS: a) The means for normal, microhematuria and bacterial cystitis groups were significantly different (p <0.05) for IL-1beta, IL-1alpha, TNF alpha and IL-6, but not for IL-4. b) Except for IL-4, all cytokines were found to be significantly elevated in low count bacterial cystitis compared to normals. No statistically significant difference was observed between low and high count bacterial cystitis groups for any of the cytokines tested. CONCLUSIONS: a) Significant and similar inflammatory responses are present in both low and high count bacterial cystitis groups as compared with the normal group. b) IL-6 and TNF alpha are significantly elevated in patients with microhematuria compared to normals. c) The potential clinical utility of the assays lies in identifying the specific cytokines elevated, understanding the pathways that give rise to their production, and in defining potential virulence factors that may produce significant inflammation at low count bacterial infections.

Colony Count, Microbial↗
PubMed1998

Increased urinary hyaluronic acid and interstitial cystitis.

PURPOSE: We compared urinary levels of hyaluronic acid in patients who met the National Institute for Diabetes, and Digestive and Kidney Diseases criteria for interstitial cystitis and in age matched healthy female controls. MATERIALS AND METHODS: Urinary hyaluronic acid was measured by solid phase radiometric assay using hyaluronic acid binding protein. Hyaluronic acid and symptom scores were compared in interstitial cystitis patients who gave multiple urine samples during treatment. Since hyaluronic acid changed with treatment in some patients, 17 samples from untreated interstitial cystitis patients were selected and compared with 17 control samples. RESULTS: Mean plus or minus standard deviation urinary hyaluronic acid concentrations were similar in the 2 groups (interstitial cystitis group 574 +/- 496, controls 512 +/- 324 ng./ml., p = 0.77). When normalized to creatinine urinary hyaluronic acid was significantly higher in interstitial cystitis patients (interstitial cystitis group 674 +/- 220, controls 446 +/- 220 ng./mg. creatinine, p = 0.0019). Urinary creatinine concentrations did not differ significantly (interstitial cystitis group 842 +/- 715, controls 1,162 +/- 516 mg./l., p = 0.12). CONCLUSIONS: Urinary hyaluronic acid was higher in interstitial cystitis patients than healthy controls. Since bladder hyaluronic acid is below the epithelium, this finding may indicate leakage across the epithelium into the urine in interstitial cystitis patients.

Adult↗
PubMed1997

Cystitis associated with tiaprofenic acid: a survey of British and Irish urologists.

OBJECTIVE: To quantify the extent and natural history of cystitis in relation to treatment with the non-steroidal anti-inflammatory drug (NSAID) tiaprofenic acid. METHODS: Anonymous postal questionnaires were sent to all UK and Irish consultant urologists enquiring about their awareness of the association between tiaprofenic acid (Surgam) and cystitis, and the number, nature and clinical details of patients with the diagnosis. RESULTS: Of the 357 urologists, 45.7% replied; 37.4% of those who responded had had cases of NSAID-concurrent cystitis, 35.6% replied that they had no personal experience but were aware of the possibility of an adverse drug reaction and 27% were unaware of the possibility of NSAID-related interstitial cystitis. There were 108 reported cases of cystitis; 55 (51%) were women, 12 (11%) were men and gender was not stated in 41 (38%). The median duration of treatment was 59 weeks (range 6 weeks-4 years). Symptoms abated completely on stopping the drug in 86% of patients, resolving in a median of 14 weeks (range 7 days-2 years). In seven cases (10%), resolution was incomplete; 17 patients had undergone reconstructive urological surgery. CONCLUSION: Tiaprofenic acid has caused at least 108 cases of cystitis and several of these patients underwent extensive urological surgery based on the assumption that they were suffering from chronic interstitial cystitis. Most cases were reversible on withdrawal of tiaprofenic acid, but 10% of patients had residual symptoms. Tiaprofenic acid causes a higher incidence of cystitis than any other NSAID and its withdrawal from the market should be considered.

Adult↗
PubMed2004

Up-regulation of phosphorylated CREB but not c-Jun in bladder afferent neurons in dorsal root ganglia after cystitis.

We examined the changes of two transcription factors, CREB and c-Jun, in dorsal root ganglia (DRG) after acute (8 or 48 hours) or chronic (10 days) cyclophosphamide (CYP)-induced cystitis. Results showed an increase in the number of p-CREB-immunoreactive (-IR) cells in the L1 and L2 DRG (5-7-fold; P < or = 0.05) as well as L6 and S1 DRG (2-4-fold; P < or = 0.05) after acute and chronic cystitis. The number of p-CREB-IR cells in the L4-L5 DRG was not altered with cystitis. The number of c-Jun-IR cells increased in the L1-L2 DRG (L1: 10-fold; L2: 8-fold; P < or = 0.05) only with chronic cystitis, although it increased in the L6-S1 DRG with CYP-induced cystitis of acute (2-3-fold; P < or = 0.05) and chronic (6-10-fold; P < or = 0.05) duration. After CYP treatment, the percentage of bladder afferent cells expressing p-CREB immunoreactivity (3-7-fold; P < or = 0.05) increased in L1, L2, L6, and S1 DRG. The increase occurred 8 hours post-CYP injection and was maintained with chronic cystitis. There were few c-Jun-IR cells in the bladder afferent population. These results demonstrate that CYP induces p-CREB and c-Jun expression in DRG in a time-dependent manner. However, c-Jun expression is not associated with bladder afferent neurons. Resiniferatoxin reduced CYP-induced up-regulation of p-CREB in DRG, suggesting that cystitis can reveal an altered CREB phosphorylation that may be mediated by capsaicin-sensitive bladder afferents. Colocalization of p-CREB and Trk receptor(s) showed that a subpopulation of p-CREB-IR cells expressed p-Trk with cystitis. These results suggest that up-regulation of p-CREB may be mediated by a neurotrophin/Trk signaling pathway.

Animals↗
PubMed1994

Decreased expression of a glycoprotein component of bladder surface mucin (GP1) in interstitial cystitis.

Interstitial cystitis is a disease of unknown etiology characterized by unremitting urinary frequency, urgency and suprapubic pain. Recently, a change in urothelial permeability has been identified in interstitial cystitis patients that is presumably mediated by aberrations in bladder surface mucin. For this study we evaluated qualitative changes in a previously defined glycoprotein component of this layer (GP1) as it occurs in interstitial cystitis patients and normal controls. Paraffinized bladder biopsies were obtained from 23 interstitial cystitis patients (all meeting National Institutes of Health inclusion criteria) and 11 normal controls. All biopsy tissue was stained with hematoxylin and eosin, and periodic acid, Schiff reaction. The tissues were examined immunohistochemically for GP1 using an anti-GP1 serum. Periodic acid, Schiff staining clearly identified bladder surface proteoglycans in all specimens. Moderate GP1 reactivity was noted in all normal control specimens. Alternatively, GP1 expression was absent in 35% of the interstitial cystitis patient biopsies and decreased in 61%. These data demonstrate qualitative GP1 changes in a majority of interstitial cystitis patients. It is unknown whether these differences have an impact on the pathogenesis of interstitial cystitis. However, our findings suggest that the absence or decreased expression of GP1 in interstitial cystitis bladder biopsies may serve as a marker to characterize the disease further in conjunction with clinical findings.

Adult↗
PubMed1993

Evidence for urothelial cell activation in interstitial cystitis.

Bladder biopsy samples from 17 interstitial cystitis patients and 20 controls were evaluated for urothelial cell activation using a panel of monoclonal antibodies to HLA-DR, intercellular adhesion molecule 1, interleukin 1 alpha and tumor necrosis factor alpha. Urothelial cells in the majority (13 of 16, 81%) of the biopsies from patients with interstitial cystitis showed increased expression of HLA-DR, while fewer samples were positive for intercellular adhesion molecule 1 (3 of 16, 19%), interleukin 1 alpha (2 of 17, 12%) or tumor necrosis factor alpha (1 of 15, 7%). No urothelial cell expression of intercellular adhesion molecule 1, interleukin 1 alpha or tumor necrosis factor alpha was detected in the controls, and only 1 of 20 control samples contained HLA-DR positive urothelial cells. These results suggest that an unusual type of cellular activation is present in interstitial cystitis. In vitro studies with cultured normal urothelial cells indicated that cells activated with gamma interferon and tumor necrosis factor alpha expressed intercellular adhesion molecule 1 and HLA-DR, although increases in intercellular adhesion molecule 1 expression occurred earlier. Urothelial cells in interstitial cystitis patients may be defective in ability to express intercellular adhesion molecule 1. Alternatively, the differential expression of HLA-DR and intercellular adhesion molecule 1 in interstitial cystitis specimens may represent a functional subset of interstitial cystitis or reflect different stages of the disease. Urothelial cell activation in interstitial cystitis may result in aberrant immune responses and immune activation within the bladder. Because HLA-DR can be detected in paraffin-embedded tissues, evaluation of urothelial cell HLA-DR expression, although not specific for interstitial cystitis, may become a useful tool in the pathological evaluation of biopsy tissues from patients with this disease.

Adult↗
PubMed1994

Hemorrhagic cystitis in bone marrow transplantation.

OBJECTIVES: Patients undergoing bone marrow transplantation are at risk for hemorrhagic cystitis despite appropriate preventive measures. This complication could have an impact on patient survival and other outcome variables. METHODS: A retrospective study of patients subjected to bone marrow transplantation was conducted to determine risk factors for hemorrhagic cystitis and evaluate the impact of hemorrhagic cystitis on certain outcome variables. Patients who experienced hemorrhagic cystitis received various forms of therapy, at the discretion of the treating physician. RESULTS: Hemorrhagic cystitis occurred more frequently in younger patients and those undergoing allogeneic transplantation. The occurrence of hemorrhagic cystitis was associated with increased hospital costs, length of hospitalization, and mortality. Gender, race, type of malignancy, other pretransplantation comorbidity, and the occurrence of other peritransplantation complications were not associated with occurrence of hemorrhagic cystitis. CONCLUSIONS: Hemorrhagic cystitis is a significant complication of bone marrow transplantation, which influences economic and survival outcome. Since the number of bone marrow transplants being performed is increasing, urologists should be prepared to play an active role in treating patients who experience this complication.

Adolescent↗
PubMed1998

Effects of L-arginine treatment on symptoms and bladder nitric oxide levels in patients with interstitial cystitis.

OBJECTIVES: Nitric oxide (NO) is involved in host defense reactions, and NO production is elevated in various inflammatory disorders. We have found very high levels of luminal NO in the urinary bladder of patients with interstitial cystitis. Oral treatment with low doses of L-arginine, the substrate for NO production, has been reported to alleviate symptoms in patients with interstitial cystitis. The aim of our investigation was to evaluate the effect of higher doses of L-arginine in patients with interstitial cystitis and to study the effects of L-arginine on NO production in the bladder. METHODS: Nine women (age 69+/-3 years) with interstitial cystitis were treated daily with 3 or 10 g of L-arginine for 5 weeks. Symptoms were evaluated with an interstitial cystitis symptom score index, and NO production was measured. Patients with stress incontinence (n=18) were used as control subjects for measurement of NO levels. RESULTS: NO concentration in the urinary bladder was markedly elevated in the patients with interstitial cystitis (239+/-60 ppb) compared with the control patients (15+/-2 ppb). NO levels did not change in the patients with interstitial cystitis after oral treatment with L-arginine (189+/-72 ppb). There was no significant change in the symptom scores at either dose after 5 weeks of L-arginine treatment. CONCLUSIONS: L-arginine treatment in the doses used in this study did not change NO production in the urinary bladder in patients with interstitial cystitis. Furthermore, the patients in our study did not notice any relief of their symptoms.

Aged↗
PubMed1998

Potential role of rel/nuclear factor-kappaB in the pathogenesis of interstitial cystitis.

PURPOSE: Despite assertive investigation in the last 2 decades, interstitial cystitis remains an unresolved problem in clinical urology, and its etiology and the mechanisms involved in its pathogenesis are still a matter of conjecture. Recently nuclear factor (NF)-KB has been implicated in chronic inflammatory diseases, and is thought to be a key regulator of genes involved in response to infection, inflammation and stress. We document the presence, pattern and distribution of NF-kappaB in bladder biopsies from patients with interstitial cystitis. MATERIALS AND METHODS: Bladder biopsies from 7 women clinically diagnosed with interstitial cystitis according to National Institute for Diabetes and Digestive and Kidney Diseases criteria and 5 women diagnosed with urinary incontinence were used for immunohistochemical localization of p65, an NF-kappaB subunit. RESULTS: Our immunohistochemical localization experiments indicate that NF-kappaB was predominantly activated in bladder urothelial cells and cells of the submucosal layer in biopsies from patients with interstitial cystitis compared to controls. While activation was evident by intense nuclear localization of NF-kappaB in all interstitial cystitis specimens, diffuse and faint immunostaining was observed in control samples. The results also indicate that activation of NF-kappaB correlated with disease occurrence. CONCLUSIONS: The fact that NF-kappaB is capable of transactivating pro-inflammatory mediators, which in turn can amplify NF-kappaB activation by a positive regulatory loop, suggests that inflammatory and/or immune responses in interstitial cystitis can be exacerbated possibly by persistent activation of this nuclear factor. We believe that our study provides a novel basis for investigating the role of NF-kappaB activation in the pathophysiology of interstitial cystitis and further opens a frontier for the development of an innovative therapeutic approach to interstitial cystitis.

Biopsy↗