ICS 2016 Meeting in Tokyo Japan

September 13, 2016

Christopher Payne

The past 30 years of research about, and clinical care of patients with IC/BPS has been misguided, and thus largely ineffective. It is clear that ulcerative interstitial cystitis (UIC) is a distinct disorder that is linked to BPS only through common symptoms. In fact, they have little more in common than do meningitis and tension headaches as causes of head pain.

Dr. Payne presented an invited lecture entitled, "Patient phenotyping in BP/IC" Bio-Psycho-Social Model to Patients with Interstitial Cystitis / Bladder Pain Syndrome

Although there is no pathognomonic histology nor a clear understanding of the initiating pathophysiology, ulcerative IC patients have clear evidence of bladder pathology--Hunner lesions often associated with diminished bladder capacity during cystoscopic hydrodistention under anesthesia. In contrast BPS patients have little or no inflammation in bladder biopsy and have normal capacity at hydrodistention. These populations are distinct and separate; they do not represent a spectrum or continuum. More than 35 years after Messing and Stamey first proposed glomerulations as a pathognomonic finding indicating early IC we have to acknowledge that there is not a single case report of progression from non-ulcer to ulcer disease nor any defined diagnostic value to the presence of glomerulations.. Most patients diagnosed with IC/BPS actually have Bladder Pain Syndrome. The key word is SYNDROME. There is an underlying assumption that this is a disorder of the bladder and is due to chronic inflammation. Both assumptions are generally false and bladder-centric treatments have poor response. It is certainly reasonable to hypothesize that a “bladder phenotype” of BPS can be defined. Such patients respond to bladder instillations, GAG layer therapy, urinary analgesics, bladder training, etc. It is possible that we may one day find that glomerulations may be useful in defining this group. However, it is abundantly clear BPS (without Hunner’s lesion) is most commonly a complex phenotype of neuromuscular-psychosocial disorder. Other BPS phenotypes that may be explored include neuropathies (pudendal and other), allergy driven BPS, and systemic pain.

BPS patients reported express of the overlapping functional somatic syndrome including fibromyalgia, irritable bowel syndrome, chronic fatigue syndrome, chronic headache, and allergies. Moreover, a twin study demonstrated that 127 patients with chronic fatigue syndrome showed significantly higher prevalence of other functional somatic syndrome including IC/BPS compared to nonfatigued co-twin. Identifying and addressing these functional somatic syndromes should be emphasized rather than a blind focus on bladder symptoms. Only by properly categorizing the patient can we maximize the opportunity of recovering social function, such as ability to work, exercise, or sexual function.

In summary, a BioPsychoSocial model of patient care as proposed is meaningless unless it starts with a clear diagnosis (or at least a differential diagnosis). Algorithms of care are worth little for heterogeneous patient populations. Treatment must be individualized to the particular patient’s disease.

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