About all

Interstitial cystitis genetic: Genetic Studies in Interstitial Cystitis (IC) – Full Text View


Interstitial cystitis and panic disorder: a potential genetic syndrome


Evidence from a genetic linkage study had suggested a possible syndrome in some families with panic disorder (PD). This syndrome includes bladder problems (possibly urinary interstitial cystitis [IC]), thyroid disorders, chronic headaches/migraine, and/or mitral valve prolapse. In 19 multiplex families with PD, one marker (D13S779) on chromosome 13 gave a logarithm of odds score of more than 4 when individuals with any of the syndrome conditions were analyzed as affected. Families with the bladder problems yielded the highest logarithm of odds scores. These findings were replicated in an extended sample of 60 families. Whereas PD had been well characterized by direct interview, the urologic problems had been found only via medical history checklists and records. A case review by a board-certified urologist suggested they could be IC.


To determine whether patients diagnosed as having IC by urodynamics and/or cystoscopy and their first-degree relatives (FDRs) have increased rates of the syndrome conditions, thus validating that the bladder problems observed in the linkage study could be IC and providing further support for the panic syndrome.


Case-control and family history study.


Two metropolitan urology clinics.


One hundred forty-six probands (67 with IC and 79 with other urologic disorders) and 815 FDRs.

Main outcome measures:

Lifetime rates of syndrome conditions in probands and FDRs who were blind to urologic or psychiatric diagnoses in the proband.


Compared with patients without IC, patients with IC had a significantly higher lifetime prevalence of PD (controlling for age and sex) (odds ratio, 4.05; 95% confidence interval, 1.22-13.40; P =.02) and a higher lifetime prevalence of any of the syndrome disorders (controlling for age and sex) (odds ratio, 2.22; 95% confidence interval, 0.89-5.54; P =.09). First-degree relatives of probands with (vs without) IC were significantly more likely to have PD, thyroid disorder, urologic problems, and any of the syndrome disorders (controlling for age and sex of the relative and sex of the proband) (adjusted odds ratio, 1. 95; 95% confidence interval, 1.13-3.38; P =.02). These results in relatives were not influenced by PD in probands, and did not change substantially when controlling for the proband-relative relationship, modeling age as a categorical (vs continuous) variable, or excluding FDRs with PD. There were no interactions between proband IC status and sex of the relative.


The increased frequency of seemingly disparate disorders in patients with IC and their FDRs is consistent with the genetic linkage findings in families with PD. These findings suggest that the bladder problems observed in the linkage study may be IC. The hypothesis that there is a familial, possibly pleiotropic, syndrome that may include IC, PD, thyroid disorders, and other disorders of possible autonomic or neuromuscular control deserves further investigation.

Interstitial Cystitis | Johns Hopkins Medicine

What is interstitial cystitis?

Interstitial cystitis (IC) is an inflamed or irritated bladder wall. It can lead to scarring and stiffening of the bladder. The bladder can’t hold as much urine as it did in the past. It is a chronic disorder. IC may also be known as:

What causes interstitial cystitis?

The cause of interstitial cystitis (IC) is unknown. Researchers are looking at many theories to understand the causes of IC and find the best treatments.

Most people with IC find that certain foods make their symptoms worse. These include:

What are the symptoms of interstitial cystitis?

These are the most common symptoms of interstitial cystitis (IC):

  • Frequent urination

  • Urgency with urination

  • Feelings of pressure, pain, and tenderness around the bladder, pelvis, and the area between the anus and vagina or anus and scrotum (perineum)

  • Pain during sex

  • In men, discomfort or pain in the penis and scrotum

  • In women, symptoms may worsen around their period

Stress may also make symptoms worse, but stress does not cause symptoms.

The symptoms of IC may look like other conditions or medical problems. Always talk with a healthcare provider for a diagnosis.

How is interstitial cystitis diagnosed?

No single test can diagnose IC. And symptoms of IC are a lot like those of other urinary disorders. For these reasons, a variety of tests may be needed to rule out other problems. Your healthcare provider will start by reviewing your medical history and doing a physical exam. Other tests may include:

  • Urinalysis. Lab testing of urine to look for certain cells and chemicals. This includes red and white blood cells, germs, or too much protein.

  • Urine culture and cytology. Collecting and checking urine for white blood cells and bacteria. Also, if present, what kind of bacteria there are in the urine.

  • Cystoscopy. A thin, flexible tube and viewing device, is put in through the urethra to examine the bladder and other parts of the urinary tract. This checks for structural changes or blockages.

  • Bladder wall biopsy. A test in which tissue samples are removed from the bladder (with a needle or during surgery) and checked under a microscope to see if cancer or other abnormal cells are present.

  • Lab exam of prostate secretions (in men). This is done to look for inflammation and/or infection of the prostate.

How is interstitial cystitis treated?

There is no cure for IC and it can be hard to treat. Treatments are aimed at easing symptoms, and may include:

  • Bladder enlargement. This method increasing bladder capacity. It also interferes with pain signals being sent by the nerve cells in the bladder.

  • Bladder wash. The bladder is filled with a solution that is held for varying times, from a few seconds to 15 minutes. Then it is drained out through a catheter.

  • Medicine. Medicine may be taken by mouth or put right into the bladder. There are many different drugs that may be used.

  • Transcutaneous electrical nerve stimulation (TENS). Mild, electric pulses enter the body for minutes to hours, 2 or more times a day. The pulses are sent through wires placed on the lower back, or through special devices put into the vagina in women or into the rectum in men. For some people, TENS eases bladder pain and urinary frequency and urgency.

  • Bladder training. You urinate at specific times and use relaxation techniques and distractions to help keep to the schedule. Over time, you try to lengthen the time between the scheduled voids.

  • Surgery. Surgery to remove all or part of the bladder may be done in severe cases, if other treatments do not work.

Management of IC may also include:

  • Diet changes. No proof links diet to IC, but some believe that alcohol, tomatoes, spices, chocolate, caffeinated and citrus beverages, and high-acid foods may contribute to bladder inflammation. Removing these from the diet may help to decrease some symptoms.

  • Not smoking. Many people with IC find that smoking makes their symptoms worse.

  • Exercise. Exercise may help ease symptoms or make them stop for a while.

  • Reducing stress. There is no proof that stress causes IC. But, if a person has IC, stress can make the symptoms worse.

Talk with a healthcare provider with any questions of concerns you may have about this health problem.

Key points about interstitial cystitis

  • Interstitial cystitis (IC) is an inflamed or irritated bladder wall.

  • The cause of IC is unknown and it does not get better with antibiotics.

  • Symptoms of IC include changes in urination such as frequency and urgency; pressure, pain, and tenderness around the bladder, pelvis, and the area between the anus and vagina or anus and scrotum; and pain during sex.

  • There is no best way to diagnose IC. A variety of tests may be needed. Urine tests will be done and imaging tests may be used to look at the different parts of the urinary tract and make sure everything is normal. Tissue samples may be removed from the bladder (with a needle or during surgery) and examined under a microscope to see if cancer or other abnormal cells are present.

  • Treatments are aimed at easing symptoms. A variety of procedures, medicines, and lifestyle changes may be advised.

What evidence supports a genetic role in the etiology of interstitial cystitis/bladder pain syndrome (IC/BPS)?

  • Daniels AM, Schulte AR, Herndon CM. Interstitial Cystitis: An Update on the Disease Process and Treatment. J Pain Palliat Care Pharmacother. 2018 Mar. 32 (1):49-58. [Medline].

  • Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U, et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn. 2002. 21(2):167-78. [Medline].

  • [Guideline] Hanno PM, Erickson D, Moldwin R, Faraday MM, American Urological Association. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. J Urol. 2015 May. 193 (5):1545-53. [Medline]. [Full Text].

  • [Guideline] Cox A, Golda N, Nadeau G, Curtis Nickel J, Carr L, Corcos J, et al. CUA guideline: Diagnosis and treatment of interstitial cystitis/bladder pain syndrome. Can Urol Assoc J. 2016 May-Jun. 10 (5-6):E136-E155. [Medline]. [Full Text].

  • Hosseini A, Ehrén I, Wiklund NP. Nitric oxide as an objective marker for evaluation of treatment response in patients with classic interstitial cystitis. J Urol. 2004 Dec. 172(6 Pt 1):2261-5. [Medline].

  • Tyagi P, Killinger K, Tyagi V, Nirmal J, Chancellor M, Peters KM. Urinary chemokines as noninvasive predictors of ulcerative interstitial cystitis. J Urol. 2012 Jun. 187(6):2243-8. [Medline].

  • Blalock EM, Korrect GS, Stromberg AJ, Erickson DR. Gene expression analysis of urine sediment: evaluation for potential noninvasive markers of interstitial cystitis/bladder pain syndrome. J Urol. 2012 Feb. 187(2):725-32. [Medline].

  • Grigorescu B, Powers K, Lazarou G. Update on Urinary Tract Markers in Interstitial Cystitis/Bladder Pain Syndrome. Female Pelvic Med Reconstr Surg. 2016 Jan-Feb. 22 (1):16-23. [Medline].

  • Kim J, Freeman MR. Antiproliferative factor signaling and interstitial cystitis/painful bladder syndrome. Int Neurourol J. 2011 Dec. 15(4):184-91. [Medline]. [Full Text].

  • Kim J, Keay SK, Freeman MR. Heparin-binding epidermal growth factor-like growth factor functionally antagonizes interstitial cystitis antiproliferative factor via mitogen-activated protein kinase pathway activation. BJU Int. 2009 Feb. 103(4):541-6. [Medline].

  • Chai TC, Zhang CO, Shoenfelt JL, Johnson HW Jr, Warren JW, Keay S. Bladder stretch alters urinary heparin-binding epidermal growth factor and antiproliferative factor in patients with interstitial cystitis. J Urol. 2000 May. 163(5):1440-4. [Medline].

  • Hunner GL. A rare type of bladder ulcer in women: Report of cases. J Boston Med Surg. 1915. 172:660-5.

  • Dyer AJ, Twiss CO. Painful bladder syndrome: an update and review of current management strategies. Curr Urol Rep. 2014 Feb. 15(2):384. [Medline].

  • Hurst RE, Zebrowski R. Identification of proteoglycans present at high density on bovine and human bladder luminal surface. J Urol. 1994 Nov. 152(5 Pt 1):1641-5. [Medline].

  • Meares EM Jr. Interstitial cystitis–1987. Urology. 1987 Apr. 29(4 Suppl):46-8. [Medline].

  • Ford AP, Gever JR, Nunn PA, Zhong Y, Cefalu JS, Dillon MP, et al. Purinoceptors as therapeutic targets for lower urinary tract dysfunction. Br J Pharmacol. 2006 Feb. 147 Suppl 2:S132-43. [Medline]. [Full Text].

  • Mukerji G, Yiangou Y, Grogono J, Underwood J, Agarwal SK, Khullar V. Localization of M2 and M3 muscarinic receptors in human bladder disorders and their clinical correlations. J Urol. 2006 Jul. 176(1):367-73. [Medline].

  • Nazif O, Teichman JM, Gebhart GF. Neural upregulation in interstitial cystitis. Urology. 2007 Apr. 69(4 Suppl):24-33. [Medline].

  • Twiss C, Kilpatrick L, Craske M, Buffington CA, Ornitz E, Rodríguez LV. Increased startle responses in interstitial cystitis: evidence for central hyperresponsiveness to visceral related threat. J Urol. 2009 May. 181(5):2127-33. [Medline].

  • Peeker R, Fall M. Toward a precise definition of interstitial cystitis: further evidence of differences in classic and nonulcer disease. J Urol. 2002 Jun. 167(6):2470-2. [Medline].

  • Peters KM, Jaeger C, Killinger KA, Rosenberg B, Boura JA. Cystectomy for ulcerative interstitial cystitis: sequelae and patients’ perceptions of improvement. Urology. 2013 Oct. 82(4):829-33. [Medline].

  • Rofeim O, Hom D, Freid RM, Moldwin RM. Use of the neodymium: YAG laser for interstitial cystitis: a prospective study. J Urol. 2001 Jul. 166(1):134-6. [Medline].

  • Peeker R, Aldenborg F, Fall M. The treatment of interstitial cystitis with supratrigonal cystectomy and ileocystoplasty: difference in outcome between classic and nonulcer disease. J Urol. 1998 May. 159(5):1479-82. [Medline].

  • Hillelsohn JH, Rais-Bahrami S, Friedlander JI, Okhunov Z, Kashan M, Rosen L. Fulguration for Hunner ulcers: long-term clinical outcomes. J Urol. 2012 Dec. 188(6):2238-41. [Medline].

  • Fall M, Oberpenning F, Peeker R. Treatment of bladder pain syndrome/interstitial cystitis 2008: can we make evidence-based decisions?. Eur Urol. 2008 Jul. 54(1):65-75. [Medline].

  • Shie JH, Liu HT, Kuo HC. Increased cell apoptosis of urothelium mediated by inflammation in interstitial cystitis/painful bladder syndrome. Urology. 2012 Feb. 79(2):484.e7-484.e13. [Medline].

  • Nickel JC, Tripp DA, Pontari M, et al. Childhood sexual trauma in women with interstitial cystitis/bladder pain syndrome: a case control study. Can Urol Assoc J. 2011 Dec. 5(6):410-5. [Medline]. [Full Text].

  • Parsons CL, Boychuk D, Jones S, et al. Bladder surface glycosaminoglycans: an epithelial permeability barrier. J Urol. 1990 Jan. 143(1):139-42. [Medline].

  • Warren JW, Keay SK, Meyers D, Xu J. Concordance of interstitial cystitis in monozygotic and dizygotic twin pairs. Urology. 2001 Jun. 57(6 Suppl 1):22-5. [Medline].

  • Lorenzo Gómez MF, Gómez Castro S. [Physiopathologic relationship between interstitial cystitis and rheumatic, autoimmune, and chronic inflammatory diseases]. Arch Esp Urol. 2004 Jan-Feb. 57(1):25-34. [Medline].

  • Elliott CS, Payne CK. Interstitial cystitis and the overlap with overactive bladder. Curr Urol Rep. 2012 Oct. 13(5):319-26. [Medline].

  • Konkle KS, Berry SH, Elliott MN, Hilton L, Suttorp MJ, Clauw DJ, et al. Comparison of an interstitial cystitis/bladder pain syndrome clinical cohort with symptomatic community women from the RAND Interstitial Cystitis Epidemiology study. J Urol. 2012 Feb. 187(2):508-12. [Medline]. [Full Text].

  • Berry SH, Elliott MN, Suttorp M, Bogart LM, Stoto MA, Eggers P. Prevalence of symptoms of bladder pain syndrome/interstitial cystitis among adult females in the United States. J Urol. 2011 Aug. 186(2):540-4. [Medline].

  • Lifford KL, Curhan GC. Prevalence of painful bladder syndrome in older women. Urology. 2009 Mar. 73(3):494-8. [Medline].

  • Berry SH, Bogart LM, Pham C, Liu K, Nyberg L, Stoto M. Development, validation and testing of an epidemiological case definition of interstitial cystitis/painful bladder syndrome. J Urol. 2010 May. 183(5):1848-52. [Medline].

  • Suskind AM, Berry SH, Ewing BA, Elliott MN, Suttorp MJ, Clemens JQ. The prevalence and overlap of interstitial cystitis/bladder pain syndrome and chronic prostatitis/chronic pelvic pain syndrome in men: results of the RAND Interstitial Cystitis Epidemiology male study. J Urol. 2013 Jan. 189(1):141-5. [Medline].

  • Close CE, Carr MC, Burns MW, Miller JL, Bavendam TG, Mayo ME, et al. Interstitial cystitis in children. J Urol. 1996 Aug. 156(2 Pt 2):860-2. [Medline].

  • Konkle KS, Berry SH, Elliott MN, et al. Comparison of an interstitial cystitis/bladder pain syndrome clinical cohort with symptomatic community women from the RAND Interstitial Cystitis Epidemiology Study. J Urol. 2012 Feb. 187(2):508-12. [Medline].

  • Bogart LM, Suttorp MJ, Elliott MN, et al. Validation of a quality-of-life scale for women with bladder pain syndrome/interstitial cystitis. Qual Life Res. 2011 Dec 7. [Medline].

  • Bogart LM, Suttorp MJ, Elliott MN, Clemens JQ, Berry SH. Validation of a quality-of-life scale for women with bladder pain syndrome/interstitial cystitis. Qual Life Res. 2012 Nov. 21(9):1665-70. [Medline].

  • Quillin RB, Erickson DR. Management of interstitial cystitis/bladder pain syndrome: a urology perspective. Urol Clin North Am. 2012 Aug. 39(3):389-96. [Medline].

  • Hanno PM. Interstitial cystitis-epidemiology, diagnostic criteria, clinical markers. Rev Urol. 2002. 4 Suppl 1:S3-8. [Medline]. [Full Text].

  • Troxel WM, Booth M, Buysse DJ, Elliott MN, Suskind AM, Clemens JQ, et al. Sleep disturbances and nocturnal symptoms: relationships with quality of life in a population-based sample of women with interstitial cystitis/bladder pain syndrome. J Clin Sleep Med. 2014 Dec 15. 10 (12):1331-7. [Medline].

  • Keller ML, McCarthy DO, Neider RS. Measurement of symptoms of interstitial cystitis. A pilot study. Urol Clin North Am. 1994 Feb. 21(1):67-71. [Medline].

  • Goin JE, Olaleye D, Peters KM, Steinert B, Habicht K, Wynant G. Psychometric analysis of the University of Wisconsin Interstitial Cystitis Scale: implications for use in randomized clinical trials. J Urol. 1998 Mar. 159(3):1085-90. [Medline].

  • Sirinian E, Azevedo K, Payne CK. Correlation between 2 interstitial cystitis symptom instruments. J Urol. 2005 Mar. 173(3):835-40. [Medline].

  • O’Leary MP, Sant GR, Fowler FJ Jr, Whitmore KE, Spolarich-Kroll J. The interstitial cystitis symptom index and problem index. Urology. 1997 May. 49(5A Suppl):58-63. [Medline].

  • Lubeck DP, Whitmore K, Sant GR, Alvarez-Horine S, Lai C. Psychometric validation of the O’Leary-Sant interstitial cystitis symptom index in a clinical trial of pentosan polysulfate sodium. Urology. 2001 Jun. 57(6 Suppl 1):62-6. [Medline].

  • Gish BA. Interstitial cystitis/bladder pain syndrome: symptoms, screening and treatment. Nurs Womens Health. 2011 Dec. 15(6):496-507. [Medline].

  • Helwick C. Think Beyond the Bladder for Interstitial Cystitis Pain. Medscape Medical News. Available at https://www.medscape.com/viewarticle/887862. October 31, 2017; Accessed: November 2, 2017.

  • Hanno PM, Landis JR, Matthews-Cook Y, Kusek J, Nyberg L Jr. The diagnosis of interstitial cystitis revisited: lessons learned from the National Institutes of Health Interstitial Cystitis Database study. J Urol. 1999 Feb. 161(2):553-7. [Medline].

  • Ackerman AL, Lai HH, Parameshwar PS, Eilber KS, Anger JT. Symptomatic overlap in overactive bladder and interstitial cystitis/bladder pain syndrome: development of a new algorithm. BJU Int. 2018 Sep 25. [Medline].

  • Ackerman AL, Lee UJ, Jellison FC, Tan N, Patel M, Raman SS, et al. MRI suggests increased tonicity of the levator ani in women with interstitial cystitis/bladder pain syndrome. Int Urogynecol J. 2016 Jan. 27 (1):77-83. [Medline].

  • Ueda T, Nakagawa M, Okamura M, Tanoue H, Yoshida H, Yoshimura N. New cystoscopic diagnosis for interstitial cystitis/painful bladder syndrome using narrow-band imaging system. Int J Urol. 2008 Dec. 15(12):1039-43. [Medline].

  • Wennevik GE, Meijlink JM, Hanno P, Nordling J. The Role of Glomerulations in Bladder Pain Syndrome: A Review. J Urol. 2016 Jan. 195 (1):19-25. [Medline].

  • Aihara K, Hirayama A, Tanaka N, Fujimoto K, Yoshida K, Hirao Y. Hydrodistension under local anesthesia for patients with suspected painful bladder syndrome/interstitial cystitis: safety, diagnostic potential and therapeutic efficacy. Int J Urol. 2009 Dec. 16(12):947-52. [Medline].

  • Lee JD, Lee MH. Activation of extrinsic apoptotic pathway from bladder biopsy in patients with interstitial cystitis/painful bladder syndrome. Urology. 2013 Dec. 82(6):1451.e7-1451.e11. [Medline].

  • Clemens JQ, Calhoun EA, Litwin MS, Walker-Corkery E, Markossian T, Kusek JW, et al. A survey of primary care physician practices in the diagnosis and management of women with interstitial cystitis/painful bladder syndrome. Urology. 2010 Aug. 76(2):323-8. [Medline]. [Full Text].

  • FitzGerald MP, Payne CK, Lukacz ES, Yang CC, Peters KM, Chai TC. Randomized multicenter clinical trial of myofascial physical therapy in women with interstitial cystitis/painful bladder syndrome and pelvic floor tenderness. J Urol. 2012 Jun. 187(6):2113-8. [Medline].

  • Groutz A, Blaivas JG, Chaikin DC, Resnick NM, Engleman K, Anzalone D, et al. Noninvasive outcome measures of urinary incontinence and lower urinary tract symptoms: a multicenter study of micturition diary and pad tests. J Urol. 2000 Sep. 164(3 Pt 1):698-701. [Medline].

  • Han E, Nguyen L, Sirls L, Peters K. Current best practice management of interstitial cystitis/bladder pain syndrome. Ther Adv Urol. 2018 Jul. 10 (7):197-211. [Medline]. [Full Text].

  • Gordon B, Shorter B, Sarcona A, Moldwin RM. Nutritional considerations for patients with interstitial cystitis/bladder pain syndrome. J Acad Nutr Diet. 2015 Sep. 115 (9):1372-9. [Medline].

  • Shorter B, Lesser M, Moldwin RM, Kushner L. Effect of comestibles on symptoms of interstitial cystitis. J Urol. 2007 Jul. 178(1):145-52. [Medline].

  • Bassaly R, Downes K, Hart S. Dietary consumption triggers in interstitial cystitis/bladder pain syndrome patients. Female Pelvic Med Reconstr Surg. 2011 Jan. 17(1):36-9. [Medline].

  • Friedlander JI, Shorter B, Moldwin RM. Diet and its role in interstitial cystitis/bladder pain syndrome (IC/BPS) and comorbid conditions. BJU Int. 2012 Jun. 109(11):1584-91. [Medline].

  • Sant GR, Propert KJ, Hanno PM, et al. A pilot clinical trial of oral pentosan polysulfate and oral hydroxyzine in patients with interstitial cystitis. J Urol. 2003 Sep. 170(3):810-5. [Medline].

  • van Ophoven A, Pokupic S, Heinecke A, Hertle L. A prospective, randomized, placebo controlled, double-blind study of amitriptyline for the treatment of interstitial cystitis. J Urol. 2004 Aug. 172(2):533-6. [Medline].

  • Foster HE Jr, Hanno PM, Nickel JC, Payne CK, Mayer RD, Burks DA, et al. Effect of amitriptyline on symptoms in treatment naïve patients with interstitial cystitis/painful bladder syndrome. J Urol. 2010 May. 183(5):1853-8. [Medline]. [Full Text].

  • Sairanen J, Tammela TL, Leppilahti M, et al. Cyclosporine A and pentosan polysulfate sodium for the treatment of interstitial cystitis: a randomized comparative study. J Urol. 2005 Dec. 174(6):2235-8. [Medline].

  • Forrest JB, Payne CK, Erickson DR. Cyclosporine A for refractory interstitial cystitis/bladder pain syndrome: experience of 3 tertiary centers. J Urol. 2012 Oct. 188(4):1186-91. [Medline].

  • Nickel JC, Mills IW, Crook TJ, Jorga A, Smith MD, Atkinson G, et al. Tanezumab Reduces Pain in Women with Interstitial Cystitis/Bladder Pain Syndrome and Patients with Nonurological Associated Somatic Syndromes. J Urol. 2016 Apr. 195 (4 Pt 1):942-8. [Medline].

  • Bosch PC. A Randomized, Double-blind, Placebo-controlled Trial of Certolizumab Pegol in Women with Refractory Interstitial Cystitis/Bladder Pain Syndrome. Eur Urol. 2018 Nov. 74 (5):623-630. [Medline].

  • Yang CC, Burks DA, Propert KJ, Mayer RD, Peters KM, Nickel JC. Early termination of a trial of mycophenolate mofetil for treatment of interstitial cystitis/painful bladder syndrome: lessons learned. J Urol. 2011 Mar. 185(3):901-6. [Medline].

  • Jain N, Li AL, Yu Y, VanderBeek BL. Association of macular disease with long-term use of pentosan polysulfate sodium: findings from a US cohort. Br J Ophthalmol. 2020 Aug. 104 (8):1093-1097. [Medline].

  • Lyons RJ, Ahmad S, Ansari S, Foote JE, Jain N. Pentosan Polysulfate-Associated Macular Disease in Patients With Interstitial Cystitis. Obstet Gynecol. 2020 May. 135 (5):1091-1094. [Medline].

  • Lai HH, Gardner V, Ness TJ, Gereau RW 4th. Segmental Hyperalgesia to Mechanical Stimulus in Interstitial Cystitis/Bladder Pain Syndrome – Evidence of Central Sensitization. J Urol. 2013 Dec 5. [Medline].

  • Charrua A, Pinto R, Taylor A, Canelas A, Ribeiro-da-Silva A, Cruz CD, et al. Can the adrenergic system be implicated in the pathophysiology of bladder pain syndrome/interstitial cystitis? A clinical and experimental study. Neurourol Urodyn. 2013 Dec 24. [Medline].

  • Payne CK, Mosbaugh PG, Forrest JB, et al. Intravesical resiniferatoxin for the treatment of interstitial cystitis: a randomized, double-blind, placebo controlled trial. J Urol. 2005 May. 173(5):1590-4. [Medline].

  • Guo C, Yang B, Gu W, Peng B, Xia S, Yang F. Intravesical resiniferatoxin for the treatment of storage lower urinary tract symptoms in patients with either interstitial cystitis or detrusor overactivity: a meta-analysis. PLoS One. 2013. 8(12):e82591. [Medline].

  • Colaco MA, Evans RJ. Current recommendations for bladder instillation therapy in the treatment of interstitial cystitis/bladder pain syndrome. Curr Urol Rep. 2013 Oct. 14(5):442-7. [Medline].

  • Riedl CR, Engelhardt PF, Daha KL, Morakis N, Pflüger H. Hyaluronan treatment of interstitial cystitis/painful bladder syndrome. Int Urogynecol J Pelvic Floor Dysfunct. 2008 May. 19(5):717-21. [Medline].

  • Chintea CL, Belal M. Is there enough evidence for the use of intravesical instillations of glycosaminoglycan analogues in interstitial cystitis?. BJU Int. 2013 Feb. 111(2):192-3. [Medline].

  • Shao Y, Shen ZJ, Rui WB, Zhou WL. Intravesical instillation of hyaluronic acid prolonged the effect of bladder hydrodistention in patients with severe interstitial cystitis. Urology. 2010 Mar. 75(3):547-50. [Medline].

  • Cervigni M, Natale F, Nasta L, Mako A. Intravesical hyaluronic acid and chondroitin sulphate for bladder pain syndrome/interstitial cystitis: long-term treatment results. Int Urogynecol J. 2012 Sep. 23(9):1187-92. [Medline].

  • Nickel JC, Hanno P, Kumar K, Thomas H. Second multicenter, randomized, double-blind, parallel-group evaluation of effectiveness and safety of intravesical sodium chondroitin sulfate compared with inactive vehicle control in subjects with interstitial cystitis/bladder pain syndrome. Urology. 2012 Jun. 79(6):1220-4. [Medline].

  • Mayer R, Propert KJ, Peters KM, et al. A randomized controlled trial of intravesical bacillus Calmette-Guerin for treatment refractory interstitial cystitis. J Urol. 2005 Apr. 173(4):1186-91. [Medline].

  • Reimer K, Fleischer W, Brögmann B, Schreier H, Burkhard P, Lanzendörfer A, et al. Povidone-iodine liposomes–an overview. Dermatology. 1997. 195 Suppl 2:93-9. [Medline].

  • Fraser MO, Chuang YC, Tyagi P, Yokoyama T, Yoshimura N, Huang L. Intravesical liposome administration–a novel treatment for hyperactive bladder in the rat. Urology. 2003 Mar. 61(3):656-63. [Medline].

  • Chuang YC, Lee WC, Lee WC, Chiang PH. Intravesical liposome versus oral pentosan polysulfate for interstitial cystitis/painful bladder syndrome. J Urol. 2009 Oct. 182(4):1393-400. [Medline].

  • Dayem AA, Kim K, Lee SB, Kim A, Cho SG. Application of Adult and Pluripotent Stem Cells in Interstitial Cystitis/Bladder Pain Syndrome Therapy: Methods and Perspectives. J Clin Med. 2020 Mar 12. 9 (3):[Medline]. [Full Text].

  • Tanaka T, Nitta Y, Morimoto K, Nishikawa N, Nishihara C, Tamada S, et al. Hyperbaric oxygen therapy for painful bladder syndrome/interstitial cystitis resistant to conventional treatments: long-term results of a case series in Japan. BMC Urol. 2011 May 24. 11:11. [Medline]. [Full Text].

  • Gallego-Vilar D, García-Fadrique G, Povo-Martin I, Salvador-Marin M, Gallego-Gomez J. Maintenance of the response to dimethyl sulfoxide treatment using hyperbaric oxygen in interstitial cystitis/painful bladder syndrome: a prospective, randomized, comparative study. Urol Int. 2013. 90(4):411-6. [Medline].

  • Evans RJ. Sacral neuromodulation is an effective treatment for interstitial cystitis/bladder pain syndrome: con. J Urol. 2012 Dec. 188(6):2044-5. [Medline].

  • Marcelissen T, Jacobs R, van Kerrebroeck P, de Wachter S. Sacral neuromodulation as a treatment for chronic pelvic pain. J Urol. 2011 Aug. 186(2):387-93. [Medline].

  • Gajewski JB, Al-Zahrani AA. The long-term efficacy of sacral neuromodulation in the management of intractable cases of bladder pain syndrome: 14 years of experience in one centre. BJU Int. 2011 Apr. 107(8):1258-64. [Medline].

  • Chai TC, Zhang C, Warren JW, Keay S. Percutaneous sacral third nerve root neurostimulation improves symptoms and normalizes urinary HB-EGF levels and antiproliferative activity in patients with interstitial cystitis. Urology. 2000 May. 55(5):643-6. [Medline].

  • Comiter CV. Sacral neuromodulation for the symptomatic treatment of refractory interstitial cystitis: a prospective study. J Urol. 2003 Apr. 169(4):1369-73. [Medline].

  • Peters KM, Konstandt D. Sacral neuromodulation decreases narcotic requirements in refractory interstitial cystitis. BJU Int. 2004 Apr. 93(6):777-9. [Medline].

  • Rajkumar GN, Conn IG. Botulinum toxin: a new dimension in the treatment of lower urinary tract dysfunction. Urology. 2004 Jul. 64(1):2-8. [Medline].

  • Flynn MK, Webster GD, Amundsen CL. The effect of botulinum-A toxin on patients with severe urge urinary incontinence. J Urol. 2004 Dec. 172(6 Pt 1):2316-20. [Medline].

  • Lee HY, Doo SW, Yang WJ, Song YS, Sun HY, Nho EJ, et al. Efficacy and Safety of Noninvasive Intravesical Instillation of Onabotulinum Toxin-A for Overactive Bladder and Interstitial Cystitis/Bladder Pain Syndrome: Systematic Review and Meta-analysis. Urology. 2019 Mar. 125:50-57. [Medline].

  • Kuo HC, Jiang YH, Tsai YC, Kuo YC. Intravesical botulinum toxin-A injections reduce bladder pain of interstitial cystitis/bladder pain syndrome refractory to conventional treatment – A prospective, multicenter, randomized, double-blind, placebo-controlled clinical trial. Neurourol Urodyn. 2015 Apr 24. [Medline].

  • Pinto R, Lopes T, Silva J, Silva C, Dinis P, Cruz F. Persistent therapeutic effect of repeated injections of onabotulinum toxin a in refractory bladder pain syndrome/interstitial cystitis. J Urol. 2013 Feb. 189(2):548-53. [Medline].

  • Gottsch HP, Miller JL, Yang CC, Berger RE. A pilot study of botulinum toxin for interstitial cystitis/painful bladder syndrome. Neurourol Urodyn. 2011 Jan. 30(1):93-6. [Medline].

  • Tirumuru S, Al-Kurdi D, Latthe P. Intravesical botulinum toxin A injections in the treatment of painful bladder syndrome/interstitial cystitis: a systematic review. Int Urogynecol J. 2010 Oct. 21(10):1285-300. [Medline].

  • Peng CH, Jhang JF, Shie JH, Kuo HC. Down regulation of vascular endothelial growth factor is associated with decreased inflammation after intravesical OnabotulinumtoxinA injections combined with hydrodistention for patients with interstitial cystitis–clinical results and immunohistochemistry analysis. Urology. 2013 Dec. 82(6):1452.e1-6. [Medline].

  • Norus T, Fode M, Nordling J. Ileal conduit without cystectomy may be an appropriate option in the treatment of intractable bladder pain syndrome/interstitial cystitis. Scand J Urol. 2013 Sep 27. [Medline].

  • Nordling J, Blaivas JG. Should urinary diversion for bladder pain syndrome/interstitial cystitis include cystectomy?. J Urol. 2014 Feb. 191(2):293-5. [Medline].

  • Evans RJ, Moldwin RM, Cossons N, Darekar A, Mills IW, Scholfield D. Proof of concept trial of tanezumab for the treatment of symptoms associated with interstitial cystitis. J Urol. 2011 May. 185(5):1716-21. [Medline].

  • Manning J, Dwyer P, Rosamilia A, Colyvas K, Murray C, Fitzgerald E. A multicentre, prospective, randomised, double-blind study to measure the treatment effectiveness of abobotulinum A (AboBTXA) among women with refractory interstitial cystitis/bladder pain syndrome. Int Urogynecol J. 2013 Nov 26. [Medline].

  • Downregulation of WNT11 is associated with bladder tissue fibrosis in patients with interstitial cystitis/bladder pain syndrome without Hunner lesion

    Here, we observed that downregulation of WNT11 is associated with bladder tissue fibrosis in NHIC patients than in HIC patients. Moreover, silencing of WNT family genes in bladder epithelial cells induced fibrotic changes. Higher WNT2B and WNT5A expression was observed in HIC patients than in NHIC patients. WNT11 expression was characteristically down-regulated in NHIC patients. To our knowledge, this is the first study to investigate the relationship between the WNT signalling pathway and bladder tissue fibrosis in IC/BPS patients.

    IC is classified into HIC and NHIC. However, whether they belong to the same disease entity is still controversial. In practice, the phenotypes of both types of IC differ. A diagnosis of HIC can be established based on the presence of Hunner’s lesions. However, such lesions are absent in NHIC patients. Therefore, urine or tissue biomarkers may be helpful for the diagnosis of IC. Previously, we observed that NHIC is characterised by severe fibrosis11. Thus, we attempted to identify genes that are associated with fibrosis in NHIC patients.

    The WNT gene functions in embryonic development, and acts as an oncogene when aberrantly triggered20. In our previous study, we revealed that WNT signalling genes were downregulated in the IC rat model13. The WNT signalling pathway is known to modulate tissue fibrosis and associated EMT processes21. Thus, we further investigated the association of fibrosis with WNT signalling cascades in IC/BPS patients.

    In this study, WNT11 expression was remarkably repressed in NHIC patients. In our previous study, we observed that NHIC was characterised by severe fibrosis and increased mast cell infiltration, while HIC was characterised by severe inflammation and urothelial denudation in the whole bladder11. These results indicate that the downregulation of WNT11 enhances EMT activation and bladder tissue fibrosis, which is mainly observed in an NHIC bladder. Thus, we propose that inhibition of the WNT11 would be novel pathogenesis and differential diagnosis of NHIC.

    In our functional study using HBlEpC, we selected WNT2B, WNT5A, and WNT11, as their expression is lower in NHIC patients, and selected WNT10A as its expression is lower in the NHIC group than in the HIC group, although there was no clinical significance. HB-EGF, a growth factor responsible for urothelial integrity is a potential biomarker for the diagnosis of IC/BPS. Further, its expression is higher in NHIC patients than in HIC and non-IC patients. Hence, it was selected for comparison22. The knockdown of all selected WNT genes induced fibrotic changes in EMT-related morphology and activated the TGF-β pathway (Figs 4–8). However, these fibrotic changes were barely observed in HB-EGF-silenced HBlEpCs. These in vitro functional studies support our hypothesis that downregulation of WNT genes triggers fibrotic changes in bladder epithelial cells, thus playing a pivotal role in the pathogenesis of NHIC.

    Studies on IC/BPS have been published for a century, but pathophysiology of IC/BPS is still complex and multifactorial. Numerous reports have implicated mast cell activation, GAG layer defects, developmental defects in the Tamm-Horsfall protein, and the autoimmune theory in the pathophysiology of IC/BPS. However, consensus is lacking2,3,4,7,23. Studies have proposed antiproliferative factor, epidermal growth factor, GAGs, bladder nitric oxide, and multiple urine proteins and serum cytokines as potential biomarkers of IC/BPS24. However, no definite biomarker has been identified for the differential diagnosis of IC/BPS. Furthermore, to our knowledge few studies on biomarkers of NHIC have been conducted, whereas urinary CXCL10 has been recently reported as a promising biomarker and the Bladder Permeability Defect Risk Score (BP-RS) using crowdsourcing has been developed (IP4IC study) in HIC patients25,26. Of note, no study has reported that downregulation of WNT pathway leads to fibrotic changes of HBlEpCs, and severe fibrosis observed in NHIC is strongly associated with decreased levels of WNT-related gene expression.

    In this study, HIC patients had significantly more episodes of urinary frequency (16.1 versus 8.5 times/day, p = 0.006) and lower maximal bladder capacity (208.6 ml versus 361.4 ml, p = 0.006) than NHIC patients. Duration of symptom was significantly shorter (30.9 vs 70.8 months, p = 0.046) in HIC patients. This is probably due to the severity in symptoms, which might have provoked patients to seek earlier medical treatment leading to earlier diagnosis. Conversely, as the symptoms are less severe in NHIC, diagnosis and treatment could be delayed. Therefore, it is important to identify biomarkers that can help diagnose NHIC quickly.

    Patients can be easily diagnosed with HIC owing to characteristic symptoms, such as bladder pain and/or urinary urgency/frequency, and Hunner’s lesions observed on cystoscopy. However, if Hunner’s lesions is not observed on cystoscopy and obvious glomerulation or submucosal haemorrhage is not observed during hydrodistention, a diagnosis of NHIC will be difficult to establish. Thus, histopathologic and gene expression studies of a bladder mucosal biopsy sample can aid in the differential diagnosis of IC/BPS by identifying fibrotic changes and WNT-related gene expression levels. Fibrotic changes could be a potential therapeutic target for NHIC. Indeed, in the rat models in our previous study, direct administration of MSCs into the submucosal layer of the bladder significantly restored voiding function and ameliorated tissue fibrosis12,13. These preclinical results indicate that fibrosis of the bladder epithelium may be treatable and require additional clinical trials using stem cells for confirmation. The use of antifibrotic agents, such as NAC, which was effective in an IC rat model, may be helpful for treating fibrosis in NHIC patients27.

    This study has several limitations. First, the biopsy specimens in this study were confined to the mucosa and submucosa layer of the bladder and in vitro functional assays of WNT genes were investigated using only primary bladder epithelial cells. In this regard, the results represent the pathogenesis, which could be responsible mainly for the urothelium, but not the whole bladder. Further studies employing the animal models with the alternation of the WNT genes in entire bladder tissues could be required to understand the precise role of these WNT genes on the pathogenesis of IC/BPS. Second, this study involves a tissue biomarker and not a urine biomarker, and although urine-based studies are difficult, a urine biomarker is ideal because urine collection is more convenient and noninvasive than a bladder mucosal biopsy. Third, the sample size of each group was heterogeneous. The number of patients was relatively smaller in the NHIC and control groups than in the HIC group; hence, it was difficult to obtain significant differences between each group. A prospective study involving a higher number of participants is required in the future. Nevertheless, novel findings have been obtained here via the WNT signalling pathway, which have not been shown in previous IC/BPS studies.

    In conclusion, downregulated WNT genes resulted in fibrotic changes in bladder epithelial cells and is significantly associated with the pathogenesis and differential diagnosis of NHIC. Decreased expression WNT genes could have diagnostic value as a biomarker for predicting NHIC. Additional clinical trials using stem cells or antifibrotic agents could be helpful for treating IC/BPS patients.

    Correlation of Gene Expression with Bladder Capacity in Interstitial Cystitis/Bladder Pain Syndrome

    https://doi.org/10.1016/j.juro.2014.05.047Get rights and content


    Interstitial cystitis and bladder pain syndrome are terms used to describe a heterogeneous chronic pelvic and bladder pain disorder. Despite its significant prevalence, our understanding of disease etiology is poor. We molecularly characterized interstitial cystitis/bladder pain syndrome and determined whether there are clinical factors that correlate with gene expression.

    Materials and Methods

    Bladder biopsies from female subjects with interstitial cystitis/bladder pain syndrome and female controls without signs of the disease were collected and divided into those with normal and low anesthetized bladder capacity, respectively. Samples then underwent RNA extraction and microarray assay. Data generated by these assays were analyzed using Omics Explorer (Qlucore, Lund, Sweden), GeneSifter® Analysis Edition 4.0 and Ingenuity® Pathway Analysis to determine similarity among samples within and between groups, and measure differentially expressed transcripts unique to each phenotype.


    A total of 16 subjects were included in study. Principal component analysis and unsupervised hierarchical clustering showed clear separation between gene expression in tissues from subjects with low compared to normal bladder capacity. Gene expression in tissue from patients with interstitial cystitis/bladder pain syndrome who had normal bladder capacity did not significantly differ from that in controls without interstitial cystitis/bladder pain syndrome. Pairwise analysis revealed that pathways related to inflammatory and immune response were most involved.


    Microarray analysis provides insight into the potential pathological condition underlying interstitial cystitis/bladder pain syndrome. This pilot study shows that patients with this disorder who have low compared to normal bladder capacity have significantly different molecular characteristics, which may reflect a difference in disease pathophysiology.

    Key Words

    urinary bladder



    gene expression


    microarray analysis

    Abbreviations and Acronyms


    differentially expressed transcript


    principal component analysis


    Pelvic Pain and Urinary Frequency patient symptom scale

    Recommended articlesCiting articles (0)

    View full text

    Copyright © 2014 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.

    Recommended articles

    Citing articles

    Analysis of key genes and micro-RNA-mRNA regulatory networks in women with ulcerative interstitial cystitis/pain bladder syndrome

  • 1.

    McLennan MT. Interstitial cystitis: epidemiology, pathophysiology, and clinical presentation. Obstet Gynecol Clin N Am. 2014;41(3):385–95.


    Google Scholar 

  • 2.

    Vasudevan V, Moldwin R. Addressing quality of life in the patient with interstitial cystitis/bladder pain syndrome. Asian J Urol. 2017;4(1):50–4.


    Google Scholar 

  • 3.

    Patnaik SS, Lagana AS, Vitale SG, Buttice S, Noventa M, Gizzo S, et al. Etiology, pathophysiology and biomarkers of interstitial cystitis/painful bladder syndrome. Arch Gynecol Obstet. 2017;295(6):1341–59. d.


    Google Scholar 

  • 4.

    Peeker R, Fall M. Toward a precise definition of interstitial cystitis: further evidence of differences in classic and nonulcer disease. J Urol. 2002;167(6):2470–2.


    Google Scholar 

  • 5.

    Erickson DR, Tomaszewski JE, Kunselman AR, Stetter CM, Peters KM, Rovner ES, et al. Urine markers do not predict biopsy findings or presence of bladder ulcers in interstitial cystitis/painful bladder syndrome. J Urol. 2008;179(5):1850–6.


    Google Scholar 

  • 6.

    Schaeffer AJ, Freeman M, Giambarresi L. Introduction to the national urology research agenda: a roadmap for priorities in urological disease research. J Urol. 2010;184(3):823–4.


    Google Scholar 

  • 7.

    Hanno PM, Landis JR, Matthews-Cook Y, Kusek J, Nyberg L Jr. The diagnosis of interstitial cystitis revisited: lessons learned from the national institutes of health interstitial cystitis database study. J Urol. 1999;161(2):553–7.


    Google Scholar 

  • 8.

    Hanno P, Nordling J, van Ophoven A. What is new in bladder pain syndrome/interstitial cystitis? Curr Opin Urol. 2008;18(4):353–8.


    Google Scholar 

  • 9.

    Bogart LM, Berry SH, Clemens JQ. Symptoms of interstitial cystitis, painful bladder syndrome and similar diseases in women: a systematic review. J Urol. 2007;177(2):450–6.


    Google Scholar 

  • 10.

    Keay SK, Szekely Z, Conrads TP, Veenstra TD, Barchi JJ Jr, Zhang CO, et al. An antiproliferative factor from interstitial cystitis patients is a frizzled 8 protein-related sialoglycopeptide. Proc Natl Acad Sci U S A. 2004;101:11803–8.


    Google Scholar 

  • 11.

    Gamper M, Viereck V, Geissbühler V, Eberhard J, et al. Gene expression profile of bladder tissue of patients with ulcerative interstitial cystitis. BMC Genomics. 2009;10:199.


    Google Scholar 

  • 12.

    Erickson DR, Tomaszewski JE, Kunselman AR, Bentley CM, Peters KM, Rovner ES, et al. Do the National Institute of Diabetes and Digestive and Kidney Diseases cystoscopic criteria associate with other clinical and objective features of interstitial cystitis? J Urol. 2005;173(1):93–7.


    Google Scholar 

  • 13.

    Denson MA, Griebling TL, Cohen MB, Kreder KJ. Comparison of cystoscopic and histological findings in patients with suspected interstitial cystitis. J Urol. 2000;164(6):1908–11.


    Google Scholar 

  • 14.

    Meunier JC, Mollereau C, Toll L, Suaudeau C, Moisand C, Alvinerie P, et al. Isolation and structure of the endogenous agonist of opioid receptor-like ORL1 receptor. Nature. 1995;377(6549):532–5.


    Google Scholar 

  • 15.

    Witkin JM, Statnick MA, Rorick-Kehn LM, Pintar JE, Ansonoff M, Chen Y, et al. The biology of Nociceptin/Orphanin FQ (N/OFQ) related to obesity, stress, anxiety, mood, and drug dependence. Pharmacol Ther. 2014;141(3):283–99.


    Google Scholar 

  • 16.

    Wachman EM, Hayes MJ, Sherva R, Brown MS, Shrestha H, Logan BA, et al. Association of maternal and infant variants in PNOC and COMT genes with neonatal abstinence syndrome severity. Am J Addict. 2017;26(1):42–9.


    Google Scholar 

  • 17.

    Lutz PE, Zhou Y, Labbe A, Mechawar N, Turecki G. Decreased expression of nociceptin/orphanin FQ in the dorsal anterior cingulate cortex of suicides. Eur Neuropsychopharmacol. 2015;25(11):2008–14.


    Google Scholar 

  • 18.

    Yamada Y, Stoffel M, Espinosa R 3rd, Xiang KS, Seino M, Seino S, et al. Human somatostatin receptor genes: localization to human chromosomes 14, 17, and 22 and identification of simple tandem repeat polymorphisms. Genomics. 1993;15(2):449–52.


    Google Scholar 

  • 19.

    Ha HS, Huh JW, Gim JA, Han K, Kim HS. Transcriptional variations mediated by an alternative promoter of the FPR3 gene. Mamm Genome. 2011;22(9-10):621–33.


    Google Scholar 

  • 20.

    Migeotte I, Communi D, Parmentier M. Formyl peptide receptors: a promiscuous subfamily of G protein-coupled receptors controlling immune responses. Cytokine Growth Factor Rev. 2006;17(6):501–19.


    Google Scholar 

  • 21.

    MacFarlane LA, Murphy PR. MicroRNA: biogenesis, function and role in cancer. Curr Genomics. 2010;11(7):537–61.


    Google Scholar 

  • 22.

    Liu W, Mao SY, Zhu WY. Impact of tiny miRNAs on cancers. World J Gastroenterol. 2007;13(4):497–502.


    Google Scholar 

  • 23.

    Rajewsky N. L(ou)sy miRNA targets? Nat Struct Mol Biol. 2006;13(9):754–5.


    Google Scholar 

  • 24.

    Fulci V, Chiaretti S, Goldoni M, Azzalin G, Carucci N, Tavolaro S, et al. Quantitative technologies establish a novel microRNA profile of chronic lymphocytic leukemia. Blood. 2007;109(11):4944–51.


    Google Scholar 

  • 25.

    Jongen-Lavrencic M, Sun SM, Dijkstra MK, Valk PJ, Lowenberg B. MicroRNA expression profiling in relation to the genetic heterogeneity of acute myeloid leukemia. Blood. 2008;111(10):5078–85.


    Google Scholar 

  • 26.

    Li X, Xin S, He Z, Che X, Wang J, Xiao X, et al. MicroRNA-21 (miR-21) post-transcriptionally downregulates tumor suppressor PDCD4 and promotes cell transformation, proliferation, and metastasis in renal cell carcinoma. Cell Physiol Biochem. 2014;33(6):1631–42.


    Google Scholar 

  • 27.

    Frankel LB, Christoffersen NR, Jacobsen A, Lindow M, Krogh A, Lund AH. Programmed cell death 4 (PDCD4) is an important functional target of the microRNA miR-21 in breast cancer cells. J Biol Chem. 2008;283(2):1026–33.


    Google Scholar 

  • 28.

    Bai J, Zhu X, Ma J, Wang W. miR-205 regulates A549 cells proliferation by targeting PTEN. Int J Clin Exp Pathol. 2015;8(2):1175–83.

    PubMed Central 

    Google Scholar 

  • 29.

    Sempere LF, Christensen M, Silahtaroglu A, Bak M, Heath CV, Schwartz G, et al. Altered MicroRNA expression confined to specific epithelial cell subpopulations in breast cancer. Cancer Res. 2007;67(24):11612–20.


    Google Scholar 

  • 30.

    Yamada Y, Nishikawa R, Kato M, Okato A, Arai T, Kojima S, et al. Regulation of HMGB3 by antitumor miR-205-5p inhibits cancer cell aggressiveness and is involved in prostate cancer pathogenesis. J Hum Genet. 2017;63(2):195–205.


    Google Scholar 

  • Conditions that mimic interstitial cystitis (IC)

    Overactive bladder (OAB)

    IC symptoms can mimic the symptoms of unresolved overactive bladder (OAB)

    Consider IC in patients who present with

    • Urinary urgency and frequency (≥8 voids/day)2
    • Urgency associated with bladder pain2
    • Pelvic pain relieved upon urination2
    • Pain during sexual intercourse2
    • Symptoms unresponsive to anticholinergic therapy for presumed OAB3

    Pain is a characteristic symptom of IC, but not OAB, and may help differentiate between the 2 conditions4

    • In patients with OAB, urgency is associated with fear of leakage, whereas in patients with IC, urgency is associated with bladder pain2

    Findings suggest a high prevalence of IC in patients with OAB symptoms refractory to anticholinergic therapy3

    • A study showed that 25 of 47 patients with detrusor overactivity did not respond to therapy with 1 anticholinergic medication3

      • 96% (24 of 25) of those patients were diagnosed with IC*

    *Based on a positive Potassium Sensitivity Test (PST).

    90,000 Interstitial Cystitis – Elizabethan Hospital

    Interstitial cystitis is a special form of chronic nonspecific inflammation of the bladder with cicatricial degeneration of its wall and the development of microcystis. Diagnosis of the disease: It is characterized by sterile urine cultures and no effect of antibiotic therapy. Diagnosis is based on ultrasound, which determines the small capacity of the bladder, deformation and thickening of its walls, expansion of the distal ureters.The prognosis for interstitial cystitis in terms of bladder preservation is poor. A long course of interstitial cystitis leads to microcystis and requires surgical treatment – its replacement with a section of the ileum on the mesentery.


    IS URINE RETENTION COMMON? WITHDRAWAL OF URINE IN WOMEN. According to the studies conducted, about 39% of women in Russia over 40 suffer from urinary incontinence, and only 4% do not consider this phenomenon to be natural, which was the reason for seeking help from a specialist.WITHDRAWAL OF URINE IN MEN. In men, urinary incontinence is much less common and, as a rule, appears after surgical interventions on the prostate gland (transvesical adenomectomy, transurethral resection of the prostate, radical prostatectomy). WHAT IS THE MECHANISM OF RETENTION OF URINE IN NORMALITY? Normal urinary retention is carried out through the interaction of four main mechanisms: 1. correct position in the body of the bladder 2. immobility of the urethra 3. adequate innervation of the pelvic floor muscles and the muscular membrane of the bladder 4.anatomical and functional integrity of the closure apparatus of the bladder and urethra URINE CONTENT – A DISEASE OR A NORMAL OPTION? Urinary incontinence is a pathological condition in which there is an involuntary discharge of urine as a result of a violation of the adequate innervation of the muscular sheath of the bladder and the muscles of the pelvic floor; pathological mobility of the urethra; failure of the closure apparatus of the bladder and urethra; instability of the bladder.WHAT ARE THE KINDS OF URINE CONTENT? According to the International Society for Urinary Continence, there are six types of urinary incontinence: 1. Urgent urinary incontinence – involuntary discharge of urine with a sudden, strong and intolerable urge to urinate 2. Stress urinary incontinence (stress urinary incontinence) – involuntary discharge of urine during physical exertion, coughing, sneezing, etc., i.e. in cases of a sharp increase in intra-abdominal pressure. 3. Reflex urinary incontinence 4. Involuntary leakage of urine 5.Nocturnal urinary incontinence (enuresis) 6. Leakage of urine after urination is complete Urgent urinary incontinence and stress urinary incontinence are the most common and common. WHAT ARE THE RISK FACTORS FOR DEVELOPING URINE CONTENT ?? Sex of the patient – more common in females? Is the patient’s age more common after 40 years? The increased weight of the patient? Is the hereditary factor a genetic predisposition to the development of urinary incontinence? Neurological factor – the presence of various diseases of the nervous system? Anatomical factor – anatomical abnormalities of the pelvic floor muscles and pelvic organs? Surgery – Pelvic Nerve Damage or Muscle Damage? Pregnancy, childbirth


    Involuntary discharge of urine on exertion, coughing, sneezing, etc.etc.? Episodes of involuntary urination with a strong, sudden urge to urinate? Frequent urination? Nighttime urination? Episodes of incontinence during intercourse? Episodes of incontinence while lying down? Increase in incontinence episodes when drinking alcohol


    Urinary incontinence is a disease that never leads to serious impairment of the functional activity of the body and to death.This problem, as it progresses, leads to a gradual deterioration in the quality of life, and sometimes to complete isolation of the patient. That is why it is important to know that URINE INTAKE CAN BE CURED. To do this, first of all, you need to seek help from a qualified specialist who will help you choose the most effective and appropriate treatment method for a particular case. It is not worth living with this problem, traumatizing the psyche and refusing to live a full life! REMEMBER: URINE RETENTION IS A DISEASE THAT IS NEVER HEALED BY ITSELF WITHOUT THE HELP OF A QUALIFIED SPECIALIST!

    Recurrence of cystitis: why it occurs, treatment and prevention

    Relapses are caused by various infections, including fungi of the genus Candida, the simplest viruses.Sometimes the causes of exacerbation can be associated with insufficient hygiene, hypothermia. 63

    Recurrent cystitis: causes and symptoms

    Not everyone understands why cystitis recurs after treatment. Causes of frequent relapses include 63 :

    • Anatomical and physiological features of the body (in women), suggesting a wide and short urethra, its close location to the reservoirs of infection;
    • bacteria (including E. coli) that provoke infections and have the ability to attach to epithelial cells;
    • hormonal disorders and inflammation, as a result of which the microflora of the vagina changes;
    • genetic predisposition;
    • active sex life, frequent change of partners;
    • use of contraceptives with spermicides.

    Recurrent cystitis can occur with insufficient treatment of the previous episode of the disease, with non-observance of personal hygiene, hypothermia, a decrease in the protective functions of the body, and various autoimmune diseases. 4

    Symptoms of chronic cystitis

    The symptoms of recurrent cystitis are 63 :

    • painful urination;
    • false urge to urinate, most often occurring at night;
    • removal of small portions of urine;
    • weakness and malaise;
    • increased body temperature;
    • 90,033 chills;

    • pulling or sharp pain in the lower abdomen.

    Treatment is prescribed depending on the cause of the exacerbation, the severity of the symptoms, and the degree of damage to the cells of the bladder.

    What to do in case of recurrent cystitis?

    The treatment of recurrent cystitis must be given special attention, because inadequate therapy leads to chronic inflammation, reactive changes, tissue hypoxia, incomplete regeneration of the epithelium and to the next exacerbation.There are several directions in the treatment of the disease 63 :

    • Etiological. In this case, the specialist prescribes antibacterial drugs, depending on the causative agent of inflammation.
    • Pathogenetic. In this case, correction of immune and anatomical disorders, treatment of venereal and gynecological diseases is carried out.
    • Prophylactic. Your doctor may prescribe herbal diuretics, antibacterials, and anti-inflammatory drugs.

    To reduce the risk of relapse, it is recommended to observe personal hygiene, adhere to a special diet, avoid hypothermia and physical exertion. 7, 63

    In addition to antibiotics, Fitolizin® can be used – a paste for preparing a special suspension for oral administration. This medicinal product contains extracts of nine plants. 6.7

    Fitolysin® paste helps to relieve pain caused by spasms and inflammation 6 .Before taking, the paste must be dissolved in water to obtain a suspension. Suspensions are quickly absorbed and deliver active substances to the inflammation focus better than tablet preparations 2 .

    Fitolizin® paste has antispasmodic, anti-inflammatory, diuretic effects. 6

    Urinary Bladder Distention Evoked Visceromotor Responses as a Model for Bladder Pain in Mice

    An illustration of a general UBD-VMR setup can be seen in of FIG.1A. Steps Increasing pressure cause an increase in raw VMR (i.e. EMG) (Figure 1B). The crude VMR, pressure, and stimulus marker signal that should be observed during recording using the digitizer software can be seen in Figure 2. Upper channel seen in Figure 2 is the EMG trace (at V). The background signal of the EMG trail should be stable and low in amplitude (<0.2 V). If hum is high or contains sporadic large spikes (> 0.5V) the wires and amplifier settings may need to be adjusted.In some cases, wrapping wires (from mouse to amplifier and / or amplifier to digitizer) in foil can reduce noise. The middle of the channel at Figure 2 shows the pressure signal as quantified by the pressure regulator in mmHg. It should be noted that the start signal is a curve. This is because a full bladder is not immediately distended. After the pressure signal reaches the maximum value for this trial (e.g. 75 mmHg)Art. Figure 2), the pressure should remain at this maximum value. Occasionally, air may escape from the urethra around the catheter. This occurs most often at high pressures (eg> 60 mmHg), can be observed by changing the amplitude of the pressure signal, and can be reduced by adding a small amount of lubricant around the surgical opening of the urethra. The final channel (bottom of Figure 2) shows the stimulus marker channel.The stimulus channel marker shows two separate signals. At the beginning of the prepressure interval, there is an instantaneous marker 2 V. This signal can be used to automate the data analysis process for a given experiment. Specifically, the data analysis system can be programmed to scan through the data file in search of stimulus markers that rise above 1.5 V. This allows the data analysis system to quickly find every complete trial. The second component of the canal stimulus is the V 1 signal that occurs during the entire process of stretching the uterine cavity pressure.Again, the presence of this second signal can be used to facilitate data analysis.

    Representative data from one experimental animal can be seen in Fig. 3 and in Table 1 the animal was stretched three times at each of the following pressure. (Fig. 3A; Table 1) 15, 30, 45, 60, and 75 mm Hg. the three Puffs are averaged and presented as a single data point on the graph. Note that the normalized signal increases gradually with increasing bladder pressure in the abdomen.After this first set of abdomen, this animal received two additional sets of graded bladder abdomen. As seen in Figure 3B, second and third sets of Swell produced similar VMRs (at each pressure.) These three sets of Swell occurred over 2.5 hours periodically demonstrating the stability of the recording setup and the reproducibility of the UBD stimulus and VMR response in one animal. It is important to note that the long term stability of this prep occurs only when the anesthetic isoflurane is gradually released down over 1 hour.In short, the anesthesia procedure can result in a progressive loss in the UBD VMR signal with each set of Bulge (unpublished observations, Sadler and Kolber.) Another important factor in the stability of the UBD VMR system is maintaining a stable body temperature. As seen in Figure 4, UBD VMR (in response to 60 mm Hg abdomen) is significantly lower at 33.5 ° C in body temperature compared to 37.5 ° C.

    Figure 1. Visceromotor responses (VMR) from UBD. (A) schematically from a UBD setup.The compressed air enters the bladder through the urethral catheter. During distensions, electrodes in the abdomen record EMG muscles. Throughout the procedure, the temperature is maintained using a battery operated heating pad and overhead lamps. (AT) An example of an EMG trace in UBD. As the pressure increases, the electrical power from the abdominal muscles increases congruently.

    Figure 2. Screen shot showing data during UBD trial. Three channels are shown.The upper channel shows a crude EMG trace (in V.) The middle channel shows the pressure (in mm Hg) that is being delivered to the bladder. The bottom line shows the channel of the stimulus marker, which indicates the beginning of the prepressure interval and the entire process of stretching the uterine cavity pressure. Image for a 40 sec full trial (20 sec prepressure interval plus 20 sec abdominal pressure trial.)

    Figure 3. Representative data showing differentiated VMR.(A) Normalized VMR increases gradually with increasing pressure (15-75 mm Hg) delivered to the mouse bladder. (B) Subsequent sets of Bladder expansion (15-75 mmHg = 1 set) show similar VMRs compared to the first set of Bladder expansion.

    . Figure 4 Body temperature decreases UBD VMR A decrease in body temperature from 37.5 ° C to 33.5 ° C leads to a significant decrease in UBD VMR. (P = 6; Pare T-test * P <0.05)

    Table 1.Typical data for a complete set of Swelling. The table shows data including distension of the uterine cavity pressure AUC, prepressure interval AUC, background corrected abdominal pressure AUC and normalized abdominal pressure AUC. For each pressure, the animal received three belly tests. The average value of the normalized stretching of the uterine cavity pressure AUC at each pressure is given in Figure 3A.

    Subscription Required. Please recommend JoVE to your librarian.

    Types of urinary incontinence

    What is urinary incontinence?

    According to the official definition, this name is a condition in which there is an involuntary flow of urine that cannot be controlled by the patient.Most often, this condition does not pose a threat to the patient’s life, but it is a very significant social problem for a person.

    What are the types of urinary incontinence?

    There are many classifications of these violations, to varying degrees reflecting the characteristics of each case. But one of the most complete, covering all types of pathologies, is the classification developed by the International Continence Society – the Standards Committee of the International Society for Urinary Continence.At the moment, it is she who is the most popular among doctors. This classification includes the following types:

    1. Urgent urinary incontinence.

    Imperative, or urgent, urinary incontinence is characterized by the fact that the patient is not able to keep urine at the peak of the expressed urge to urinate. The reason for this form of incontinence lies in the increased activity of the muscles in the bladder wall. Urgent urinary incontinence can be caused by pathologies of the brain or spinal cord, hormonal disorders, inflammation, or damage to the bladder wall.

    2. Stress urinary incontinence.

    This type of incontinence is associated with involuntary loss of urine with a sharp increase in pressure in the abdominal cavity. Stress urinary incontinence can be caused by laughing, lifting weights, coughing, sneezing, etc. In addition, in this case, the contractility of the sphincters that retain urine decreases due to hormonal disorders, anatomical disorders of the muscles and organs of the small pelvis, or a violation of nerve conduction in this area.

    Stress urinary incontinence in women often develops after complicated childbirth, and in men it sometimes occurs after surgery to remove the prostate.The age factor also plays an important role.

    3. Unconscious urinary incontinence.

    Unconscious, or reflex, urinary incontinence is caused by a violation of the conduction of nerve impulses from the brain structures to the bladder. As a result, the patient does not feel the need to urinate even with a full bladder. Sooner or later, the bladder empties reflexively.

    4. Continuous urine leakage.

    Uncontrolled constant flow of urine is caused by both a violation of nerve conduction and the failure of the blocking sphincters.In addition, the loss of the ability of the muscles of the bladder to contract leads to the fact that more fluid accumulates in it than it can hold, and urine gradually begins to leak.

    5. Nocturnal urinary incontinence.

    The term “enuresis” often refers to any type of urinary incontinence. But in the medical world, this word only defines urinary incontinence during sleep. Enuresis as a disease is diagnosed only if there are episodes of bedwetting at the age of more than 5 years. It can be primary, that is, it develops from birth, or secondary, that is, it arises at a later date after the formation of the urinary retention reflex.

    The cause of bedwetting can be:

    • Immaturity of the urinary system;
    • pathology of the brain and spinal cord;
    • genetic predisposition;
    • mental trauma;
    • infectious and inflammatory diseases;
    • endocrine pathologies, etc.
    6. Leakage of urine after the completion of urination.

    This disorder is caused by a failure of the muscles that release urine.In such a situation, after the natural emptying of the bladder, there is still some fluid in it. The force of contraction of the muscle walls of the bladder is insufficient, and this is what leads to such delays. Then the residual urine begins to gradually flow outward under the influence of gravity, and the weakened muscular apparatus is not able to resist this.

    Leakage of urine after the end of natural urination may result from:

    • tumors or narrowing of the urethra;
    • 90,033 urinary tract infections;

    • weakness of the pelvic muscles;
    • prostatitis and prostate adenoma;
    • increased body weight;
    • 90,033 spinal hernias and spinal cord injuries;

    • violation of the blood supply to the brain;
    • 90,033 operations on the pelvic organs.


    All articles

    Features of diagnosis and treatment of interstitial cystitis

    Interstitial cystitis (IC) is a severe chronic disease of the bladder wall, manifested by frequent, urgent urination and pain in the pelvic area, perineum, bladder, urethra, and external genital organs [1-3]. This symptom complex is included in the concept of “painful bladder” or “chronic pelvic pain syndrome”.

    Interstitial cystitis affects mainly women, the ratio of sick women and men, according to many studies, is 9–10: 1 [1, 3]. Patients with interstitial cystitis usually complain of a significant decrease in quality of life and limitation of daily activity. Without timely and correct treatment, IC can lead to bladder atrophy with a sharp decrease in capacity and the formation of a microcyst. Unfortunately, sometimes only surgical removal of the bladder is the only way to restore the quality of life [4, 5].

    Despite numerous hypotheses, the cause of IC remains unknown, and the number of people suffering from this disease is increasing every year.

    IC symptoms resemble those of bladder infections, but numerous studies have not identified a specific pathogen. The absence of the effect of antibiotic therapy also testifies in favor of the non-infectious genesis of the disease.

    In the USA, according to G.C. Curhan, there are 60–70 cases of IC per 100,000 women, while in Western Europe – only 18 per 100,000 women and only 3-4 cases per 100,000 women in Japan [5, 6].Such a difference in statistics may arise due to differences in diagnostic approaches and examination technologies, but may also be due to differences in lifestyle, nutrition, etc.

    In recent studies, a new substance was isolated from the urine of patients with IC, which the researchers called antiproliferative factor (APF), and which, as it turned out, blocks the growth of cells lining the inner wall of the bladder. Perhaps, in the future, with an in-depth study of this substance, light will be shed on the mechanism of development of this unclear disease [5, 7].

    Other possible causes of IC include a defect in the protective layer of the bladder wall (glycosaminoglycan layer), activation of inflammatory cells (mast cells) in the bladder wall, autoimmune process, infectious pathogens, toxic substances in the urine, lack of sex hormone production, bladder outlet obstruction, disorders blood circulation and lymph circulation in the wall of the bladder (increased sympathetic activity, operations on the pelvic organs, etc.). However, according to many experts, the occurrence of IC is most likely polyetiological and associated with the involvement of several pathogenetic links [3, 4, 8].

    Despite numerous studies, it is still not clear whether IC is an independent disease or a symptom complex in other autoimmune diseases (fibromyalgia, Sjogren’s syndrome, irritable bowel syndrome, systemic lupus erythematosus – SLE). Taking into account the results of a number of studies, it can be concluded that IC has some properties of an autoimmune disease, namely: the presence of autoantibodies in the blood in combination with chronic inflammation, alternation of periods of increase and regression of symptoms, a positive effect from the use of anti-inflammatory drugs and glucocorticoids in some cases.Various injuries to the bladder can cause cell destruction or alter antigens, leading to the production of antibodies and further organ damage. In addition, it is possible that antigens of the normal bladder or some antigens of extravesical origin as a result of an unusual immune response can stimulate the production of antibodies that cause the onset of IC symptoms [2, 4, 9]. Thus, there are similarities between IC and SLE – the same histological changes in the bladder wall and the coexistence of these diseases in individual patients, that is, SLE can cause bladder damage and induce cystitis similar to IC [8, 9].In addition, clinical associations of IC with thyroid dysfunction and systemic autoimmune diseases such as Sjogren’s syndrome and arthritis have been described. In addition, recent studies have shown a 100-fold increase in the risk of inflammatory bowel disease (Crohn’s disease and ulcerative colitis) in patients with IC [7, 8].

    Diagnosis of IC is mainly based on the clinical manifestations of pain in the bladder in conjunction with frequent and urgent, painful urination in the absence of other diseases of the pelvic organs that can give similar symptoms.

    The mandatory list of examination of patients includes a clinical analysis of urine, a culture of urine, cystoscopic examination with biopsy of suspicious areas of the mucous membrane, hydraulic distension of the bladder, urine cytology and laboratory examination of prostate secretion [4, 5, 8].

    Urinalysis in patients with IC is usually not useful. A pathognomonic sign is the detection of a bladder ulcer (the so-called Gunner’s ulcer) or characteristic multiple submucosal hemorrhages of the bladder wall after hydraulic stretching during cystoscopy.Urine culture is usually negative or saprophytic flora is excreted on urine culture. Histological examination of the layers of the bladder wall is characterized by the presence of many mast cells in the process of degranulation, neutrophils and macrophages [4, 6, 7].

    Thus, the diagnosis of IC is more of a diagnosis of exclusion.

    It is very important not to confuse Gunner’s ulcer with carcinoma in situ and remember that classic ulcerative IC occurs infrequently, in approximately every tenth patient.

    In the countries of Western Europe, the potassium test is widespread, when 40.0 ml of 3% KCl solution is injected into the bladder cavity, after which the pain in the bladder area sharply increases, and its capacity decreases by about a third. All this also indicates the presence of IC [5, 8].

    Given that IC belongs to inflammatory diseases of unclear etiology, its treatment is aimed mainly at relieving symptoms that cause suffering to patients.

    Various methods of treatment are used:
    – intravesical instillation of medicinal substances;
    – hydraulic expansion of the bladder under anesthesia;
    – oral treatment;
    – physiotherapy;
    – non-drug methods;
    – surgical treatment.

    According to some reports, 90% success is achieved with the combined use of several therapies.

    According to many clinics, instillations of 50% dimethyl sulfoxide solution, cocktails with an antibiotic, hydrocortisone and lidocaine, heparin instillations, as well as instillations of chondroitin sulfate, pentosan sulfate or hyaluronic acid in order to restore the integrity of the glycosaminoglycan layer [8– 10, 12].

    Hydraulic stretching of the bladder is both diagnostic and therapeutic, because after stretching, patients suffering from IC report a significant improvement in well-being, which can last for many months or even years.

    One should also not forget about the long-used urothelium-destroying agents, which, according to some experts, contribute to the desquamation of defective defective urothelium and the rapid restoration of normal (dimethyl sulfoxide, chloropactin) [4, 8, 11].

    Preparations for additional oral therapy:
    – analgesics / morphine derivatives / type 2 cyclooxygenase inhibitors (COX-2): diclofenac, metamizole, buprenorphine, levomethadone, meloxicam, celecoxib;
    – antihistamines and corticosteroids: suprastin, loratadine, prednisolone;
    – antagonists of H 2 -histamine receptors: cimetidine, ranitidine, famotidine;
    – antidepressants: amitriptyline, doxepin;
    – nitric oxide donors: L-arginine;
    – muscarinic receptor blockers – oxybutynin, tolteradine, which have a pronounced positive effect both for IC and for symptoms of an overactive bladder.

    Recently, more and more reports have appeared in the literature on the positive results of IC treatment with botulinum toxin, which is injected under the bladder mucosa, and the BCG vaccine, administered intravesically [4, 8, 12].

    Antibiotics for IC are rarely used, and generally not so much as the main treatment, but rather to prevent the addition of urinary infections [4, 6, 8].

    According to literature data, endovesical iontophoresis, laser photoirradiation of the bladder, UHF, inductotherapy, balneotherapy have a positive effect in the subacute period of IC [3, 5, 7].

    Thus, we can conclude that IC, apparently, is a multifactorial disease, possibly occurring in people with a genetic predisposition. Despite the long period of study of this disease, it remains unclear whether IC is a homogeneous disease or a combination of various diseases of the bladder. Perhaps IC is a manifestation of some kind of autoimmune syndrome. And although the significance of an infectious factor in the development of the disease has not been proven, it cannot be ruled out that it is a chronic persistent infection that causes such changes – at least in part.

    One of the urgent tasks of modern urology is the development of new diagnostic criteria and methods, as well as the systematization of the existing criteria for the selection of patients with IC. To understand the pathogenesis of this unexplored disease, it is also important to identify new disease markers. Treatment regimens for the disease are not systematized and, unfortunately, at this stage require further research.


    1. Darenkov A.F., Balchiy-Ool D.K. Reflexology of cystalgia // Urology and Nephrology.- 1982. – No. 1. – S. 32-37.

    2. Kan D.V. Guide to obstetric and gynecological urology. – 2nd ed., Rev. and add. – M .: Medicine, 1986 .– 488 p.

    3. Laurent O.B., Zaitsev A.V., Lipsky V.S. Diagnosis and treatment of interstitial cystitis in women. – Saratov: Privolzhskoe book publishing house, 2001 .– 190 p.

    4. Laurent O.B. Chronic cystitis in women // Doctor. – 1996. – No. 8. – S. 6-9.

    5. Curhan G.C., Speizer F.E., Hunter D.J. Epidemiology of interstitial cystitis: a population based study / // The journal of urology. – 1999. – Vol. 161. – P. 549-552.

    6. Bereznyakov I.G. Infections and antibiotics. – Kharkov: Constanta, 2004 .– 447 p.

    7. Elbadawi A.E., Light J.K. Distinctive ultrastructural pathology of nonulcerative interstitial cystitis: new observations and their potential significance in pathogenesis A.E. Elbadawi, // Urol. Int. – 1996 – Vol.56. – P. 137-162.

    8. Epithelial dysfunction in nonbacterial cystitis (Interstitial Cystitis) / C.L. Parsons, J.D. Lilly, P. Stein // J. Urol. – 1991. – Vol. 145. – P. 732-735.

    9. Intragranular activation of bladder mast cells and their association with nerve processes in interstitial cystitis / R. Letourneau, X. Pang, G.R. Sant, T.C. Theoharides // Br. J. Urol. – 1996. – Vol. 77. – P. 41-54.

    10. Intravesical hyaluronic acid in the treatment of refractory interstitial cystitis / A.Morales, L. Emerson, J.C. Nickel, M. Lundie // J. Urol. – 1996. – Vol. 156 .– 45 p.

    11. Nigro D.A. Interstitial cystitis: clinical and endoscopic features // Interstitial Cystitis / D.A. Nigro, J. Wein. – Philadelphia: Lippincott-Raven, 1997. – P. 137-142.

    12. Randomized, double-blind, dose-ranging study of pentosan polysulfate sodium (PPS) for interstitial cystitis / J.C. Nickel, J. Barkin, J. Forrest et al. // J. Urol. – 2001. – Vol. 165 (5) – P.67-72.

    Page not found |

    Page not found |

    404. Page not found

    Monthly archive













































    for visually impaired

    Department of Andrology and Urology | FSBI “National Medical Research Center of Endocrinology” of the Ministry of Health of Russia

    I.O. Head of the Department of Andrology and Urology

    Oncologist, Urologist

    Candidate of Medical Sciences

    Make an appointment

    The Department of Andrology and Urology of the Federal State Budgetary Institution “NMIC of Endocrinology” of the Ministry of Health of the Russian Federation was organized to provide specialized consultative, diagnostic and therapeutic assistance to patients with andrological and urological pathology.

    Quick help
    Examinations and treatment in the Department of Andrology and Urology are carried out using the latest generation of laser and endoscopic technology.

    Full range of services
    We carry out the whole range of examinations, outpatient and inpatient treatment of urological diseases. Qualified specialists The staff of the Department consists of professors, doctors and candidates of sciences, specialists in the field of reproductive endocrinology, conservative and surgical uroandrology.

    Affordable treatment
    Citizens of the Russian Federation, regardless of the region of residence, residents of the near and far abroad can undergo examination and treatment using the best medical equipment in our clinic.

    Diagnostic equipment and modern approaches make it possible to establish a diagnosis in the shortest possible time.

    The clinic uses modern equipment for treatment. Up to 90% of operations are performed by endoscopic and laparoscopic methods, which allows you to return to your usual way of life in the shortest possible time.

    At FSBI “NMIC Endocrinology” doctors of urological and oncourological profile, performing a wide range of surgical interventions, are receiving appointments.

    Polyclinic and inpatient care:

    Diagnostics and treatment of diseases of the prostate gland:

    • Chronic prostatitis
    • Benign prostatic hyperplasia (prostate adenoma)
    • Prostate cancer (using minimally invasive techniques)

    Diagnosis and treatment of urological diseases in women:

    • Cystitis (inflammation of the bladder)
      • Interstitial cystitis
      • Postcoital cystitis
    • Urinary incontinence
    • Pyelonephritis
    • Genitourinary fistula (involuntary discharge of urine in the vagina)

    Oncourological diseases:

    • Kidney tumor
    • Bladder tumor
    • Prostate tumor
    • Penile tumor
    • Testicular tumor

    Urologist-andrologist, Endocrinologist

    Candidate of Medical Sciences, doctor of the highest qualification category

    Doctor of Medical Sciences, Chief Researcher, Professor of the Department of Endocrinology-Diabetology