Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677481 (urinary frequency)
 1,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of lupus interstitial cystitis in 17 year-old female. The patient presented with suprapubic pain, urinary frequency, dysuria, nocturia and no bacterial growth. Intravenous pyelography showed a low capacity bladder with thickwall, and a bilateral ureterohydronephrosis. Interstitial cystitis was confirmed on bladder biopsy specimen. Clinical symptoms remained eventhough after steroid treatment. Clinical signs of cystitis occurring in a patient with systemic lupus erythematous could be a manifestation of a lupus cystitis.
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PMID:[Lupus interstitial cystitis. Apropos of a case]. 963 53

Interstitial cystitis is a particular type of cystitis with clear urine, essentially observed in women. Persistent painful urinary frequency and bladder heaviness are suggestive of the diagnosis. Two different forms have been distinguished according to severity: Hunner's ulcer and small capacity bladder;-bladder distension to 800 ml, followed by haemorrhagic petechiae; with a whole series of intermediate forms. The bladder wall undergoes inflammatory reorganization, without infection, leading to fibrosis. The disease is improved by hydrocortisone instillations. Hunner's ulcer can be treated by partial resection. If the cystitis deteriorates, bladder replacement by detubulized intestinal graft may be required.
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PMID:[Interstitial cystitis]. 992 40

We examined the bladder function of cystitis models induced by intravesical acetone instillation in urethane-anesthetized rats. Acetone (0.35 ml) at 10, 30, or 50% concentration or deionized water (sham-treatment) was instilled into the bladder via the cannula which was inserted into the lumen. Acetone was withdrawn 90 sec after instillation and the bladder lumen was washed with saline after 15 min. One hour later, the cystometrogram induced by transvesical infusion of saline (3.3 ml/hr) was measured. During cystometrography of normal (non-treated) or sham-treated group, the time required to cause micturition, reflecting bladder capacity, was 9.6 +/- 0.9 (n = 7) or 10.0 +/- 0.8 min (n = 6), respectively. In the 10% acetone-treated group, the bladder capacity was similar to that in the normal or sham group. In the 30% acetone group, the time to micturition was 4.4 +/- 0.4 min (n = 7), indicating decreased bladder capacity, although the micturition pressure and the threshold pressure were not significantly different from those in the normal or sham group. However, in the 50% acetone group, the micturition reflex disappeared. In isolated rat bladder strips, contractile responses to carbachol or electrical field stimulation in the sham and 30% acetone group were similar. While, both responses in isolated strips from the 50% acetone group were reduced. The degree of damage from degeneration and desquamation of epithelium and hemorrhage in the bladder tissue from the 30% acetone group was less prominent than in the 50% acetone group. Additionally, some tissue from the 50% acetone group showed degeneration of muscle layer. The effects of three drugs were investigated in the 30% acetone group which showed increased urinary frequency. Baclofen (100 microg/kg, i.v.) and morphine (100 microg/kg, i.v.) increased significantly the bladder capacity and the threshold pressure. Atropine (10 microg/kg, i.v.) decreased the micturition pressure. These results suggest that cystitis models induced by intravesical instillation of 30% acetone may be valuable for evaluating drugs for the treatment of urinary frequency.
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PMID:Urodynamics in acetone-induced cystitis of anesthetized rats. 1008 51

Previously, we described an animal model for interstitial cystitis (IC), experimental autoimmune cystitis (EAC) [Luber-Narod et al. Urol Res 24:367]. Further characterization of animals with EAC indicates that peak and mean urinary frequency are elevated compared with sham-injected controls and that the disease progresses with at least two cycles of exacerbations and remissions. We had shown evidence suggesting EAC to be autoimmune in nature. In this paper, we identify serum autoantibodies from 9/10 EAC animals which bind to a protein specific to rat bladder with a relative molecular weight of 12-kDa. Such autoantibodies are absent in 12/13 normal and sham-injected animals as well as animals which fail to develop EAC despite disease induction. These findings suggest that EAC is a reproducible model of cyclical increases of urinary frequency, and that a 12-kDa antigen is the target of autoantibodies which correlate with those elevations. Identification of this target antigen may explain the pathogenesis of increased urinary frequency in these animals and potentially in IC as well.
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PMID:Experimental autoimmune cystitis: further characterization and serum autoantibodies. 1055 May 23

We investigated the effects of AH-9700 (1-[2-(3,4-dihydro-6,7-dimethyl-2-naphthalenyl)ethyl] pyrrolidine fumarate; a novel sigma receptor ligand), (+)-pentazocine and 1,3-di-o-tolylguanidine (DTG) (two typical sigma receptor ligands), and oxybutynin (a currently used anti-pollakiuria drug) on cystometrograms in anesthetized rats with 30% acetone-induced cystitis. Compared to sham-treated rats, acetone-treated cystitis models exhibited an increase in urinary frequency during continuous filling cystometry. Intravenous administration of AH-9700 (1-5 mg/kg), (+)-pentazocine or DTG to the rats with cystitis dose-dependently prolonged micturition intervals and increased the micturition threshold pressure. Oxybutynin (1 mg/kg. i.v.) also extended micturition intervals, but decreased the micturition pressure. These results indicate that AH-9700, (+)-pentazocine and DTG improve abnormal frequent urination caused by acetone-induced cystitis in a manner different from that of oxybutynin.
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PMID:Effects of AH-9700, (+)-pentazocine, DTG and oxybutynin on micturition in anesthetized rats with acetone-induced cystitis. 1158 9

A 4-year-old Jewish boy presented with dysuria, urinary dribbling, increased urinary frequency, and new onset of diurnal enuresis. An infiltrating solid mass involving the entire bladder wall was found. Biopsy revealed "tumor-forming" eosinophilic cystitis, a rare bladder lesion of unclear cause. Antitoxocariasis treatment was unsuccessful. High-dose corticosteroids failed. The child's clinical condition and bladder sonographic findings continued to deteriorate. Treatment with cyclosporin A was given for 8 months, with a complete clinical, radiologic, and histopathologic cure and no side effects. Two years of follow-up showed a complete recovery.
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PMID:Eosinophilic cystitis in a 4-year-old boy: successful long-term treatment with cyclosporin A. 1173 40

Interstitial cystitis (IC) is a chronic disorder of unknown etiology that affects the lower urinary tract of up to 500,000 women and men in the United States. It is characterized by bladder and pelvic pain that varies from moderate discomfort to severe, debilitating pain and related lower urinary tract symptoms including nocturia, diurnal urinary frequency, and urgency. Because the symptoms of IC superficially resemble a urinary tract infection, it is often misdiagnosed and may remain so for months or even years. This article discusses the clinical manifestations of IC, including its differentiation from acute or recurring bacterial cystitis. Options for managing this significant and often debilitating voiding dysfunction are also discussed.
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PMID:Interstitial cystitis: a guide to recognition, evaluation, and management for nurse practitioners. 1190 18

The involvement of C-fiber afferent pathways in urinary frequency and pain associated with painful bladder syndrome raises the possibility of multiple targets for the treatment of this disease. Using an in vivo measurement of bladder activity as well as whole-cell patch clamp recording techniques to examine the properties of bladder afferent neurons in animal models of chronic cystitis, we have documented that tetrodotoxin-resistant sodium channels encoded by the Na(v) 1.8 (PN3/SNS) gene and nitric oxide acting via a cyclic guanosine monophosphate (cGMP)-dependent mechanism are important in modulating bladder pain responses. Thus, suppression of C-fiber afferent nerve activity by blocking specific sodium channels, elevating nitric oxide levels, or activating cGMP-dependent pathways might represent novel strategies for the treatment of symptoms in patients with painful bladder syndrome. Another treatment strategy is suppression of release or activity of proinflammatory agents that can cause normally unexcitable C-fiber afferents to become hyperactive or hyperexcitable. This approach to management of bladder pain was tested in patients with painful bladder syndrome by examining the effectiveness of the antiallergic agent suplatast tosilate (IPD-1151T), which suppresses urinary frequency in a rat model of cystitis. IPD-1151T is an immunoregulator that suppresses cytokine production in T-helper 2 cells and inhibits immunoglobulin E antibody formation and antigen-induced histamine release from mast cells. Preliminary data from an open-label clinical trial showed that 16 of 23 (70%) patients responded to treatment with IPD-1151T (300 mg/day orally for 12 months). The finding that expression of platelet-derived endothelial cell growth factor, which can activate mast cells, was lower in the bladder of responders than nonresponders indicates that bladder levels of platelet-derived endothelial cell growth factor may be a useful marker for this disease.
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PMID:Targeting afferent hyperexcitability for therapy of the painful bladder syndrome. 1200 24

Interstitial cystitis (IC) is a chronic condition characterized by a constellation of symptoms such as urinary frequency, nocturia, urinary urgency, suprapubic pressure, and bladder and pelvic pain. Since its original description, the etiology of the disorder has remained unknown despite intense investigations. The International Cystitis Association (ICA) and the National Institutes of Arthritis, Diabetes, Digestive and Kidney Diseases (NIDDK) have been instrumental in supporting the United States Interstitial Database (ICDB) and foster research to study the disorder. The NIDDK developed criteria to ensure that all groups of patients treated would be relatively comparable. However, many patients who would be clinically considered to have IC do not fulfill all the NIDDK criteria. Many clinical criteria for the diagnosis of IC, such as the presence of glomerulations and the intravesical potassium chloride test, are being challenged. The epidemiology of the disorder is not well established, but there are an estimated 700,000 cases of IC in the United States. Numerous pathophysiologic mechanisms have been proposed, but none have been proven. There is no representative animal model of IC. Both the oral and intravesical treatments of IC are noncurative, and few are based on a plausible mechanism or scientific evidence. Surgical treatment should be considered with extreme caution; it is the last therapeutic option because failure rate can be substantial.
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PMID:Current investigations and treatment of interstitial cystitis. 1208 13

We document a case of 61-year-old woman with a 24 year history of rheumatoid arthritis (RA), who developed severe polyarthralgia, dry cough, paresthesia in the legs, frequent micturition, and severe macrohematuria. We diagnosed as severe RA with extraarticular manifestations based on interstitial pneumonia, mononeuritis multiplex, subcutaneous nodules, and high titer of rheumatoid factor. Ultrasonography demonstrated an intravesical mass lesion. A histological examination of the urinary bladder by endoscopic biopsy revealed marked deposition of AA amyloid. The diagnosis of secondary amyloidosis and bacterial cystitis were made based on histological findings and urine culture. At first, we administered antibiotics by intravenous infusion, which resulted in cure of cystitis and partial improvement of macrohematuria. Then combination therapy of corticosteroids and cyclophosphamide successfully reduced the disease activity of RA. There have only been a few reports published so far on the vesical amyloidosis in patients with RA. However, 5 of 10 patients (50%) in vesical amyloidosis died because of continuous massive hematuria, which induced disseminated intravascular coagulation and multiple organ failure. In conclusion, secondary amyloidosis of the urinary bladder should be considered as a possible cause of hematuria in patients with long-term RA and as an important prognosis factor of RA.
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PMID:[A case of rheumatoid arthritis with secondary amyloidosis in urinary bladder]. 1216 17


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