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Results for “Cystitis, Interstitial”

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PubMed1999

Bladder microvasculature in women with interstitial cystitis.

PURPOSE: A cardinal cystoscopic finding in women with interstitial cystitis is mucosal small vessel hemorrhage or glomerulations after hydrodistention. We quantified and compared microvascular density and endothelial proliferation in the bladder biopsies of women with interstitial cystitis and a control group of women who were undergoing incontinence or prolapse surgery. MATERIALS AND METHODS: We performed computer assisted image analysis and immunohistochemical studies to compare differences in the blood vessel count, and proportional area in the bladder suburothelium and deeper submucosa of bladder biopsies of 52 women, including 26 with interstitial cystitis. Routine light microscopy features were examined and correlated with microvascular density. RESULTS: In the bladder biopsies of women with interstitial cystitis there was a lower blood vessel count (p = 0.01), and a lower proportion of the total image consisted of blood vessel wall (p = 0.03) in the suburothelium than in control biopsies. We noted no difference in the blood vessel count of the deeper submucosa or in the degree of endothelial cell proliferation. Suburothelial blood vessel differences correlated with the degree of histological change, such as edema, inflammatory infiltrate and vascular congestion. CONCLUSIONS: We found decreased microvascular density in the suburothelium but not in the deeper submucosa in bladder biopsies of women with interstitial cystitis.

Cystitis, Interstitial↗

PubMed2003

Pregnancy outcomes following the diagnosis of interstitial cystitis.

OBJECTIVE: To describe the outcome of pregnancy in patients treated for interstitial cystitis. METHODS: Over a 4-year period, 12 patients with interstitial cystitis who had one course of intravesical dimethyl sulphoxide (DMSO) therapy for interstitial cystitis were studied. Information on the effects of the treatment-to-conception interval, symptom control during pregnancy and immediately post partum, other pregnancy events and pregnancy outcome were collected. RESULTS: The mean age was 32 years (SD = 5.4), and 6 (50%) were nulliparous. Fifty-eight percent of the women presented with combined urinary and pain symptoms, 25% with a pain symptom only and 17% with a urinary symptom only. Eleven women had 1 course (6 doses) of DMSO therapy. Symptom relief was maintained during pregnancy in almost all the women. The mean interval from diagnosis of interstitial cystitis to the first day of the last menstrual cycle preceding all pregnancies beyond 28 weeks was 19.3 months (SD = 14.7). This interval was 6 months or less for 2 pregnancies that were terminated on account of symptoms attributable to interstitial cystitis. Thirteen healthy babies were delivered. CONCLUSION: Pregnancy outcomes appear good following treatment for interstitial cystitis with 1 course of intravesical DMSO.

Adult↗

PubMed1999

Comparison of bladder blood flow in patients with and without interstitial cystitis.

PURPOSE: We compared bladder blood flow during filling and emptying in patients with and without interstitial cystitis, and correlated blood flow with symptoms in those with interstitial cystitis. MATERIALS AND METHODS: Bladder perfusion was measured using a dual channel endoscopic laser Doppler flow probe. Measurements were obtained in superficial and deeper vascular beds from the bladder mucosa at the trigone and back wall at baseline, at the volume of awake capacity, during 80 cm. water hydrodistention and after bladder drainage. American Urological Association symptom score was obtained preoperatively in interstitial cystitis patients. RESULTS: In all areas bladder perfusion decreased with filling in interstitial cystitis patients and increased in those without interstitial cystitis. There were no significant differences in response to emptying the bladder, as perfusion tended to increase in both groups. There was no correlation between bladder perfusion at baseline, or in response to filling or emptying with overall symptom score. CONCLUSIONS: Bladder perfusion decreases with bladder filling in patients with but increases in those without interstitial cystitis. The inability of the interstitial cystitis bladder to increase bladder blood flow with filling may be a reflection of other pathological processes in the bladder mucosa. The lack of correlation between blood flow and symptoms suggests that bladder ischemia alone cannot account for the symptoms in interstitial cystitis.

Adult↗

PubMed1993

Interstitial cystitis in minority women.

A bladder disorder of unknown etiology, interstitial cystitis affects mainly women, and its prevalence may be increasing. Little information is available on the demographic, clinical, diagnostic, and treatment aspects of interstitial cystitis in the minority population. This retrospective review of the patient database at the Interstitial Cystitis Center, New England Medical Center, identified 17 minority women among a total of 201 patients who satisfied the criteria of the National Institutes of Health's National Institute of Diabetes and Digestive and Kidney Diseases for diagnosis of interstitial cystitis. Minority women accounted for 8.5% of the patients, with 3% being African American; 3.5%, Hispanic American; and 2.0%, Asian American. The clinical and endoscopic findings as well as responses to treatment were similar in both the minority and nonminority populations. However, the average duration of symptoms prior to diagnosis was 2.9 years in the minority group, compared with an average of 13 months in the nonminority group. Minority women with interstitial cystitis appear to be symptomatic for longer periods before a definitive diagnosis is made. Their response to treatment parallels that of the nonminority population. Further studies are needed to address the natural history, urologic referral patterns, and treatment outcomes in minority women who have interstitial cystitis.

Adult↗

PubMed1995

[Interstitial cystitis: new concepts on etiology and diagnosis].

Interstitial cystitis is a common disease with non objective diagnostic criteria. In 1989 the National Institute of Health (NIH) defined symptoms and cystocopic findings in order to select patients to include in research programs on pathophysiology of interstitial cystitis. While there is no lack of theories, the etiology of interstitial cystitis remains obscure. Today, the general opinion is that the etiology is multifactorial and that we may be dealing with a syndrome rather than with a specific disease.

Biomarkers↗

PubMed2002

In vivo models of interstitial cystitis.

PURPOSE: We systematically identified and evaluated various animal models that have been studied to help identify the underlying mechanisms of and possible treatment options for interstitial cystitis. MATERIALS AND METHODS: Models of interstitial cystitis published between 1983 and 2001 were obtained by searching MEDLINE and other Internet databases using cystitis and model as the primary key words. Models with characteristics of interstitial cystitis similar to those defined by National Institutes of Arthritis, Diabetes, Digestive and Kidney Diseases criteria were reviewed. Some articles describing animal models with similar pathological conditions in other organs were also included to enlarge the base of potentially relevant material. RESULTS: We identified and evaluated some 16 animal models of interstitial cystitis, which we categorized as bladder inflammation induced by intravesical administration of an irritant or immune stimulant, systemic and environmentally induced inflammation, and a naturally occurring model of interstitial cystitis that occurs in cats. Some abnormalities identified in humans and cats with interstitial cystitis can be reproduced in healthy animals using luminal, systemic or environmental stimuli. At the level of the bladder the source of stimulation cannot be discriminated. Variability in the extent of bladder distention complicated the interpretation of some studies. In addition, the noxious stimuli used can affect many epithelial surfaces as well as the urothelium, suggesting they are nonspecific responses to injury rather than specific to interstitial cystitis. CONCLUSIONS: No model in bladder injury in healthy animals currently reproduces as many features of interstitial cystitis as the naturally occurring disease in cats. While induced models of relative injury may help to provide insight into the bladder response to injury, feline interstitial cystitis follows a similar chronic waxing and waning time course as does interstitial cystitis in humans, which may be more suitable for studying the effects of stressors on the severity of clinical signs as well as newly proposed therapies.

Animals↗

PubMed1991

Mast cell infiltration in intestine used for bladder augmentation in interstitial cystitis.

Two patients with histologically confirmed interstitial cystitis underwent bladder augmentation procedures (clam cystoplasty and Mainz pouch cystoplasty) because of therapy resistant low abdominal pain and decreased functional bladder capacity. However, symptoms of low abdominal pain and urinary retention (1 patient) persisted, and cystectomy was performed in both patients after 14 and 20 months, respectively. Histological examination of the specimens showed changes in the intestinal areas of the augmented bladder, resembling interstitial cystitis. The etiology of this phenomenon and the possible role of intestinal interstitial cystitis in augmentation failures are discussed.

Adult↗

PubMed1990

Interstitial cystitis: bladder mucosa lymphocyte immunophenotyping and peripheral blood flow cytometry analysis.

Interstitial cystitis is a chronic bladder disorder of unknown etiology that primarily afflicts women and is characterized by urgency and pain. Although immune mechanisms have been implicated in the disease process, little is known about the local or peripheral blood immune responses. Cryostat sections of snap-frozen bladder biopsies obtained by transurethral resection from 43 patients (24 with classical and 9 with nonulcerative or early interstitial cystitis, and 10 controls) were analyzed using a panel of monoclonal antibodies with an avidin-biotin immunoperoxidase technique to characterize the local immune response of bladder mucosa. Simultaneously obtained heparinized peripheral blood (10 cc) was analyzed by flow cytometry in 24 patients (9 with classical and 5 with nonulcerative early interstitial cystitis, and 10 controls) using the same panel of antibodies. The control group biopsies (median age 44 years, range 27 to 52 years) had no ulcers, few lymphoid cells (predominately T-helper cells), rare T cell nodules and no B cells. The nonulcer group (median age 39 years, range 29 to 44 years) had rare mucosal ruptures but no ulcers, slightly increased lymphoid cells (predominately T-helper), occasional T cell aggregates, no B cell nodules and rare plasma cells. No statistically significant difference between control and nonulcerative interstitial cystitis patients was identified. In contrast, the classical interstitial cystitis group (median age 68 years, range 47 to 73 years) had ulcers, intense inflammation with focal sheets of plasma cells, aggregates of T cells, B cell nodules including germinal centers, a decreased or normal helper-to-suppressor cell ratio and suppressor cytotoxic cells in germinal centers. Flow cytometry analysis of peripheral blood lymphocyte subsets showed normal patterns in controls, increased numbers of secretory Ig positive B cells and activated lymphocytes in the nonulcerative group, and increased numbers of secretory Ig positive B cells with mildly abnormal kappa-to-lambda ratios and activated lymphocytes in the classical group. We conclude that an immune mechanism has at least a partial role in the pathophysiology of interstitial cystitis. A parallel between interstitial cystitis and inflammatory bowel disease is evident. Further studies are indicated.

Adult↗

PubMed1999

Activation of the kallikrein kinin system in interstitial cystitis.

PURPOSE: We investigated whether the kallikrein kinin system is activated in interstitial cystitis by measuring urinary excretion rates of kinin peptides, active and total kallikrein, and the kininase neutral endopeptidase in women with interstitial cystitis. We compared these excretion rates to a control group of women with stress incontinence and normal bladder function. MATERIALS AND METHODS: Catheter urine was collected from subjects during a water diuresis (approximately 10 ml. per minute) before and after distention of the bladder with 100 ml. water. The contribution of the bladder wall to urinary kinins was assessed by measuring the change in kinin levels after 2 minutes of bladder stasis before and after distention. RESULTS: Absolute bradykinin and kallidin excretion rates were similar in women with interstitial cystitis and control subjects. Two minutes of bladder stasis after bladder distention increased urinary bradykinin (p = 0.02) but not kallidin excretion rates. Active and total kallikrein excretion rates were similar in patients with interstitial cystitis and control subjects. Neutral endopeptidase excretion rates were reduced in the initial urine collection from subjects with interstitial cystitis but were similar in both groups during later collection periods. CONCLUSIONS: These data provide evidence for increased bradykinin levels in the bladder wall of subjects with interstitial cystitis, which may be due in part to reduced neutral endopeptidase levels. These increased bradykinin levels may participate in the pathogenesis and symptomatology of interstitial cystitis.

Adult↗

PubMed2002

Toward a precise definition of interstitial cystitis: further evidence of differences in classic and nonulcer disease.

PURPOSE: Interstitial cystitis is a bothersome condition in urological practice. There is continuous discussion on the extent and demarcation of this syndrome. Accumulated evidence indicates that interstitial cystitis is a heterogeneous syndrome. Today it is often divided into classic and nonulcer disease. Compared with classic interstitial cystitis the nonulcer type appears different in terms of demographic, endoscopic and histological findings as well as in the response to various types of treatment. However, in clinical series subdivision is not always performed, which makes it difficult to draw conclusions. We determined whether there are additional dissimilarities in clinical presentation in the 2 subtypes of interstitial cystitis. MATERIALS AND METHODS: We evaluated 130 patients with classic and 101 with nonulcer interstitial cystitis diagnosed according to National Institute for Diabetes and Digestive and Kidney Diseases criteria by surveying the clinical records, including voiding diaries. RESULTS: Patients with nonulcer disease were younger at diagnosis (p <0.0001) and at symptom onset. Furthermore, there was a marked and significant difference in bladder capacity while patients were under general anesthesia (p <0.0001). CONCLUSIONS: The current findings together with previous findings clearly demonstrate that the 2 subtypes of interstitial cystitis represent separate entities. We suggest refining the National Institutes of Health-National Institute for Diabetes and Digestive and Kidney Diseases criteria, so that subtyping scientific materials is considered mandatory, hence, ensuring that the 2 subtypes are evaluated separately in clinical studies.

Adult↗

PubMed1996

Increased urinary levels of Tamm-Horsfall glycoprotein suggest a systemic etiology of interstitial cystitis.

PURPOSE: We investigated the role of Tamm-Horsfall protein in interstitial cystitis. MATERIALS AND METHODS: Urinary Tamm-Horsfall protein excretion was analyzed in interstitial cystitis patients and controls, and bladder biopsy specimens were stained immunohistochemically for Tamm-Horsfall protein. RESULTS: Urinary Tamm-Horsfall protein levels in 28 women with interstitial cystitis were statistically significantly greater than those in 25 female controls. No positive staining for Tamm-Horsfall protein was demonstrated in the bladder tissue from 10 interstitial cystitis cases. CONCLUSIONS: The results support the notion that interstitial cystitis may have a systemic etiology. In addition, this assay might have clinical value in the diagnosis of interstitial cystitis.

Adult↗

PubMedDate not supplied

[Physiopathologic relationship between interstitial cystitis and rheumatic, autoimmune, and chronic inflammatory diseases].

OBJECTIVES: To evaluate the current knowledge about interstitial cystitis pathophysiology and its relationship with rheumatic, autoimmune and chronic inflammatory diseases. METHODS: Literature search under "interstitial cystitis pathophysiology" either clinical or experimental trials and reports, in Medline, PubMed, Digital Urology Journal and Doctor's Guide, in addition to our own clinical research experience results. RESULTS: Both human and experimental trials show resemblances between interstitial cystitis and rheumatic, autoimmune, and chronic inflammatory diseases on clinical presentations, pathophysiology. Some interstitial cystitis patients show the bladder infiltrated with specific mononuclear cells, high incidence of circulating antinuclear antibodies, good response to anti-inflammatory and/or immunosuppressive therapies. Interstitial cystitis in association with rheumatic, autoimmune and chronic inflammatory diseases is very common. Many patients with systemic lupus erythematosus, Sjögren syndrome and fibromyalgia syndrome show antibodies against urothelium and/or muscle cells and/or other connective tissue components of urinary bladder. Systemic lupus erythematosus and Sjögren syndrome are the autoimmune diseases which bear strongest similarity with interstitial cystitis. Moreover, rheumatoid arthritis, chronic pelvic pain syndrome, irritable bowel syndrome, fibromyalgia, chronic fatigue syndrome, Evan's syndrome and atopic dermatitis share some pathogenic characteristics. CONCLUSIONS: Nowadays, interstitial cystitis pathophysiology is unknown. Based on clinical presentations, epidemiology, pathology and laboratory findings and treatment response, there is an important correlation among interstitial cystitis and rheumatic, autoimmune and chronic inflammatory diseases. These disorders may share some pathophysiologic mechanisms. Rigorous studies of pathophysiology of these group of diseases are needed to confirm consistently this approach for such conditions.

Autoimmune Diseases↗

PubMed1999

An assessment of the use of intravesical potassium in the diagnosis of interstitial cystitis.

PURPOSE: We evaluated the use of intravesical potassium in the diagnosis of interstitial cystitis. MATERIALS AND METHODS: A blinded test assessment on 39 consecutive subjects attending our urology clinic for the evaluation of symptoms consistent with interstitial cystitis was performed. The pain response to intravesical potassium and water as a control was measured. The response rate was compared to the results of cystoscopy using standard outcome measures associated with diagnostic test assessment. RESULTS: The probability of having interstitial cystitis given a positive intravesical potassium test was 66%. This finding added no new useful information and would not be helpful with clinical decisions as the probability of having interstitial cystitis in this population was already 56% before the test. Similarly, if the test was negative then 46% or nearly half of the subjects were still likely to have interstitial cystitis. Therefore, a negative test would have no ability to rule out disease nor would it be useful in making clinical decisions about how to proceed with evaluation or therapy. Test characteristics were considered poor with a sensitivity of 69.5% and a specificity of 50%. Likelihood ratios (positive 1.39, negative 0.61) also indicated poor inclusion and exclusion capabilities. CONCLUSIONS: The general use of intravesical potassium as a diagnostic test for interstitial cystitis is not validated. The diagnosis of interstitial cystitis must depend on the clinical presentation and endoscopic findings based on National Institutes of Health criteria.

Administration, Intravesical↗

PubMed2005

Intravesical resiniferatoxin for the treatment of interstitial cystitis: a randomized, double-blind, placebo controlled trial.

PURPOSE: Interstitial cystitis is a painful bladder condition of unknown etiology and poorly understood pathophysiology. Current therapies have met with limited success. Vanilloid receptor agonists such as resiniferatoxin (RTX) desensitize C-fibers that transmit pain; it is hypothesized that such drugs will be effective in the treatment of interstitial cystitis and painful bladder syndrome by decreasing the pain that leads to urinary frequency and urgency. MATERIALS AND METHODS: A randomized, double-blind, placebo controlled study was conducted in 163 patients with interstitial cystitis. Participants were randomly assigned to receive a single intravesical dose of 50 ml of either RTX 0.01 microM, 0.05 microM, 0.10 microM, or placebo. Safety and efficacy was evaluated over 12 weeks. The primary efficacy endpoint was the Global Response Assessment, a 7-point scale rating overall change in symptoms of interstitial cystitis after 4 weeks. Secondary efficacy endpoints included reduction in pain, urgency, frequency, nocturia, average void volume, and the O'Leary-Sant Symptom and Problem Indexes. RESULTS: RTX did not improve overall symptoms, pain, urgency, frequency, nocturia, or average void volume during 12 weeks followup. RTX resulted in a dose-dependent increase in the incidence of instillation pain, but was otherwise generally well tolerated. CONCLUSIONS: In the largest prospective, randomized clinical trial reported to date with intravesical vanilloid therapy, single administration of RTX at doses of 0.01 microM to 0.10 microM was not effective in patients with interstitial cystitis.

Administration, Intravesical↗

PubMed2007

Interstitial cystitis pathogenesis and treatment.

PURPOSE OF REVIEW: Interstitial cystitis remains an idiopathic illness characterized by urinary frequency, urgency and pelvic pain with substantial morbidity in those affected. There is significant variability in the presentation, severity of symptoms and response to therapy. This review focuses on recent findings on the possible pathogenesis and potential treatments for this disease. RECENT FINDINGS: Interstitial cystitis is manifested by sensory hypersensitivity. A small volume of urine will be associated with an exaggerated sensation of pain or pressure and urinary urgency. There is continued research regarding how this process is initiated and maintained and to what extent systemic dysfunction of the immune or autonomic nervous system may play a role. The urothelial lining has been demonstrated to be capable of secreting a large number of potential signaling molecules that may be significant factors in the disease. SUMMARY: The pathogenesis of interstitial cystitis remains uncertain and the illness has significant diversity. Additional research is needed to establish subtypes that share common processes that can be targeted for treatment as a single effective therapy for the condition remains elusive.

Cystitis, Interstitial↗

PubMed1997

Urinary chondroitin sulfates, heparan sulfate and total sulfated glycosaminoglycans in interstitial cystitis.

PURPOSE: We compared urinary glycosaminoglycan levels in patients with interstitial cystitis and healthy controls. MATERIALS AND METHODS: Total sulfated glycosaminoglycans assayed by dimethylmethylene blue binding and individual glycosaminoglycans analyzed by cellulose acetate electrophoresis were compared in patients with interstitial cystitis and healthy controls. Also, multiple urine samples were obtained from healthy female controls for 2 months to assess the relationship of urinary glycosaminoglycan and creatinine concentrations, and to determine whether glycosaminoglycan excretion changes during the menstrual cycle. RESULTS: Total sulfated glycosaminoglycan and creatinine concentrations correlated well in random voided samples. Menstrual cycle day did not affect total sulfated glycosaminoglycan levels. Cellulose acetate electrophoresis revealed 3 bands corresponding to chondroitin sulfates, heparan sulfate and acidic glycoprotein. Patients with interstitial cystitis had decreased urinary concentrations of each of these individual components and total sulfated glycosaminoglycans. However, glycosaminoglycan-to-creatinine ratios were similar in interstitial cystitis and control urine. CONCLUSIONS: Using these assays total and individual urinary glycosaminoglycan levels normalized to creatinine were not altered in interstitial cystitis.

Chondroitin Sulfates↗

PubMed2006

[Interstitial cystitis. An important differential diagnosis].

Interstitial cystitis (IC) is a chronic, debilitating inflammatory disease of the urinary bladder, characterized by chronic pelvic pain, urgency/frequency symptoms, and decrease of the functional bladder capacity. Both the etiology and pathogenesis of the condition that predominantly affects women are still not fully understood. Thus, a causal therapeutic approach still does not exist. IC remains a strict diagnosis of exclusion; distinct histopathological findings within the bladder wall are frequently found, although they are not pathognomonic. The diagnostic criteria elaborated by the NIH are helpful in clinical research; their dogmatic utilization will however lead to an underdiagnosis of IC in 60% of the patients. IC-specific symptom questionnaires and validated symptom scales help the physician to assess the therapeutic response during the follow-up of the patients.

Administration, Intravesical↗

PubMed2000

Interstitial cystitis: the painful bladder syndrome.

Interstitial cystitis (IC) is an enigmatic and frustrating condition to manage as a physician and to cope with as a patient. Many patients are declared as drug addicted and neurotic. Social status and number of sexual partners showed no correlation with incidence. Patients report moderate to excruciating pain in the suprapubic or vaginal area, urgency and frequency (up to 50 micturitions/d), and disruption of their social life. Diagnosis of IC is made by exclusion. Different pathophysiologic mechanisms have been proposed: changes in epithelial permeability, pelvic floor dysfunction, mastocytosis, activation of c-fibers, and increase of nerve growth factors and bradykinin. No single theory can explain IC.

Adaptation, Psychological↗