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Question answered:07/08/06 Warning! this question is over two years old.
eMedicine, an American online textbook, has a chapter on interstitial cystitis [1], which includes a section on etiology, which states:
“The etiology of IC remains unknown. Proposed etiologies include the following:
- Pathogenic role of mast cells in the detrusor and/or mucosal layers of the bladder
- Deficiency in the glycosaminoglycan layer on the luminal surface of the bladder, resulting in increased permeability of the underlying submucosal tissues to toxic substances in the urine
- Infection with a poorly characterized agent (eg, a slow-growing virus or extremely fastidious bacterium)
- Production of a toxic substance in the urine
- Neurogenic hypersensitivity or inflammation mediated locally at the bladder or spinal cord level
- Manifestation of pelvic floor muscle dysfunction or dysfunctional voiding
- Autoimmune disorder”
The article also discusses the problematic nature of interstitial cystitis, stating:
“Because IC is a poorly defined entity of unknown etiology, the clinical presentation often is not uniform and the symptoms are variable in severity and nature.”
With regard to treatment it states:
“Because no discrete pathognomonic pathologic criteria exist for assessing and monitoring disease severity, indications and goals for treatment are based on the degree of patient symptoms. Assessing patient response to treatment is also complicated because of the subjective nature of symptoms and the lack of objective serological, physical, or histopathological findings.”
“The therapy for interstitial cystitis (IC) begins with extensive patient education regarding the chronic nature of the disease and realistic assessments of the condition, prognosis, and potential responses to therapy. Ongoing reassurance and physical and emotional support are important as the diagnostic evaluation progresses and therapies are applied. Only rarely will patients with IC have an immediate, complete, and durable response to any particular therapy. They must be counseled at length regarding the lack of universally effective therapies. Often, referral to one of the local IC support groups, especially a local chapter of the Interstitial Cystitis Association, can be helpful in providing a continuing network of support for the patient.
Ideally, in clinical practice, the treatment of IC should be initiated with the least invasive, least expensive, and most reversible therapy. In general, this consists of a program of dietary and fluid management, time and stress management, and behavioral modification. Thereafter, treatments are applied in a progressively more invasive step-wise fashion until some degree of symptomatic relief is obtained.
Interventions might include various pharmacological agents (eg, Elmiron, antihistamines, tricyclic antidepressants, analgesics, anti-inflammatory agents), intravesical therapy (ie, medications intermittently instilled directly into the bladder via a catheter), electrical stimulation, and complementary therapies such as acupuncture and hypnosis.”
With regard to the specific question of mycoplasma involvement we found one paper in medline [2] whose abstract states:
“Antibodies to Mycoplasma hominis were detected by indirect hemagglutination in nine (56%) of 16 patients with chronic interstitial cystitis. In seven patients (44%), titers of greater than or equal to 160 were found. Antibodies to Ureaplasma urealyticum were detected in three (19%) of these patients; in only one patient was a high titer, i.e., greater than or equal to 160, found. M. hominis was isolated from voided urine of two patients, and U. urealyticum was recovered from the urine of three patients. A similar incidence of antibodies to M. hominis was found in 20 age- and sex-matched women treated transurethrally for bladder tumors. The high incidence of indirect hemagglutination antibodies to M. hominis found in these two groups of urologic patients who were subjected to repeated instrumentation of the urinary tract remains unexplained.”
We also looked for any clinical trials of antibiotics in interstitial cystitis and found one trial in medline [3]. In this trial 50 patients with interstitial cystitis were randomised to receive 18 weeks of placebo or antibiotics, including rifampin plus a sequence of doxycycline, erythromycin, metronidazole, clindamycin, amoxicillin and ciprofloxacin for 3 weeks each. Overall the authors concluded:
“Our findings suggest that these antibiotics alone or in combination may sometimes be associated with decreased symptoms in some patients but they do not represent a major advance in therapy for interstitial cystitis.”
References
1) eMedicine. Interstitial cystitis. 2005 (http://www.emedicine.com/med/topic2866.htm)
2) Hedelin HH et al. Mycoplasma hominis and interstitial cystitis. Sex Transm Dis. 1983 Oct-Dec;10(4 Suppl):327-30. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=6665676)
3) Warren JW et al. Pilot study of sequential oral antibiotics for the treatment of interstitial cystitis. J Urol. 2000 Jun;163(6):1685-8. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10799160)
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