Interstitial cystitis: understanding the syndrome

Alternative Medicine Review,  Nov, 2003  by Keri Marshall

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Abstract

Interstitial cystitis (IC) is a chronic pain syndrome that affects close to a million people in the United States. The syndrome presents differently in many individuals, with the unifying factor being chronic pelvic pain and disruption of daily life activities. Many etiologies have been proposed as causative factors for IC, although it is likely triggered by more than one process. Treatment for many individuals revolves around symptom management and improving quality of life; however, it is imperative to remove aggravating factors such as food and daily stressors. Treatment will vary for individuals, as symptoms and etiology will differ. This article discusses nutritional and other non-toxic approaches to treating IC. (Altern Med Rev 2003;8(4):426-437)

Introduction

Interstitial cystitis is a chronic, debilitating, multifactorial syndrome characterized by pelvic and/or perineal pain, urinary urgency and frequency, and nocturia. This symptom complex has also been called painful bladder syndrome, leaky bladder syndrome, and irritative bladder syndrome. Individuals diagnosed with this syndrome typically fit no other pathologic picture, including urinary tract infections, carcinoma, or cystitis induced by radiation or medication. (1)

Interstitial cystitis was first described by Hunner in 1915, in patients who presented with fibrotic, contracted bladders and the presence of distinctive ulcers of the bladder epithelium. (2,3) At the time, IC was considered extremely rare. Today, epidemiological studies reveal quite different numbers. In a Finnish study in 1990, the annual incidence of new cases was estimated at 1.2 per 100,000 and the prevalence at 10-11 per 100,000. (4) By 2002, a similar Finnish study revealed the prevalence jumped to 450 per 100,000. (5) In 1997, Jones and Nyberg reported an incidence of 500,000-1,000,000 cases of IC in the United States. (6) A more recent population-based study revealed the incidence of IC to be as high as 52-67 per 100,000 cases, more than 50-percent greater than previously reported. (7)

IC has no single, definable presentation, but is best viewed as a continuum extending across decades of an individual's life, beginning with mild, intermittent symptoms. Ultimately, after years of remissions and relapses, symptoms become more severe and more constant. Most IC patients suffer from urgency and frequency in the early stages of disease. As the disease progresses, pain increases in severity and becomes the most dominating and debilitating symptom. For many, the pain becomes so severe it significantly impacts their personal and professional life.

Levels of pain not only correlate to stage of disease, but also vary with fluctuating factors that can provoke symptom flare-up, such as allergies and hormonal cycles. Although not well documented, it has been observed by many clinicians that IC symptoms are exacerbated the week before menses. In addition, both women and men with this condition may experience the most severe pain during or following sexual intercourse. This can be extremely psychologically damaging, as it places significant burden on relationships and often results in severe depression.

Pathophysiology

Several etiologic factors have been proposed for IC, involving structural, neurological, autoimmune, lymphatic, infectious, and psychological factors. These etiologies remain largely hypothetical, as insufficient data is available to definitively establish their roles in the pathology of IC. However, in any given patient, a combination of factors likely plays a role in causing insult to the bladder epithelium.

Normal bladder epithelium possesses an anionic, hydrophilic, sulfated glycosaminoglycan (GAG) surface layer that, when healthy, protects the bladder from noxious elements including microorganisms, toxins, carcinogens, and hyperosmolar, acidic and potassium-rich urine. Through the resulting formation of a water barrier of ionic hydrogen-sulfate bonds, the GAG layer has been found experimentally to prevent proteins, ionic substances, and non-ionic entities from contacting the luminal surface of the bladder (Figure 1). (8,9) Parsons et al have suggested breakdown of this "bladder protective layer" leads to changes in permeability, stimulation of pain receptors, and inflammatory/hyperalgesic symptoms. (10) Further investigations by Parsons using the potassium sensitivity test confirmed this theory.

[FIGURE 1 OMITTED]

Neurological up-regulation is likely an important component in the pathogenesis of IC. Neurogenic inflammation is a process by which sensory nerves may secrete inflammatory mediators, resulting in hyperalgesia and inflammation. Substance P, a short chain peptide, is a central component of this process. Substance P is an inflammatory mediator that functions as a nociceptive neurotransmitter in the central and peripheral nervous system. When released by peripheral nerves, substance P causes an inflammatory cascade to occur, resulting in such processes as mast cell degranulation and activation of nearby nerve terminals. Several studies support this theory, having found increased numbers of substance P-containing nerves in patients with IC. (11,12) In addition, substance P has been found in the urine of women with IC, with increased concentrations dependent on the severity of pain. (13) One recent study revealed no significant increase in substance P in women with IC when compared to a control group; (14) however, the control group consisted of women who suffered from symptoms of stress incontinence.