Interstitial Cystitis: Causes, Diagnosis, and CAM Treatment

Introduction to Interstitial Cystitis

Interstitial cystitis (IC), also called painful bladder syndrome, is an inflammatory disease of the bladder wall with typical ulceration of the urothelium. It is generally regarded as an elusive condition with inadequate therapeutic options. Critical to improving the prospects for therapy is early diagnosis, which may involve only careful history-taking and clinical examination. Complementary and alternative medicine (CAM) suggests multimodal treatment strategies in the early stage of the disease (Abrams, Cardozo, & Fall, 2002).

Due to definitional similarity, IC is often referred to as IC/PBS in the literature. It has been estimated that 1.2 million of 1.3 million Americans with IC are women (Payne, Joyce, Wise, & Clemens, 2007). Pain can originate in the urethra, lower back, abdomen, pelvis, or perineum. The pain experienced can be constant or intermittent, and its intensity may change as the bladder fills or empties. Men may experience pain in the scrotum, testicles, or penis, while women may feel pain in the vulva or vagina. Women may experience symptoms during vaginal intercourse, which often worsen during menstruation. Physical or mental stress, as well as certain foods and beverages, can cause symptoms to aggravate (Hall & Moldwin, 1995; Moldwin & Sant, 2002).

The objective of this literature review is to discuss the possible causes of IC, its diagnosis, prevalence, symptoms, and CAM treatment options. CAM is multimodal and individualized, and includes treatment methods such as neuromodulation, dietary modification, acupuncture, surgical methods, and medications.

Causes and Prevalence

It is likely that the disease process is multifactorial, with patients having one or more contributing factors. Among the hypothesized causes — none fully confirmed — are infections, allergic responses, autoimmune disease, and hereditary responses. One hypothesis holds that augmented permeability of the defensive glycosaminoglycan layer of the bladder epithelium results in the loss of potassium, contaminants, and other materials into the urinary interstitium, which activates mucosal mast cells and generates an automatic immune reaction. Mast cells generate immunoreactive chemicals that consequently cause generalized inflammation of the bladder and injury to the mucosa through the occurrence of tachykinins and cytokines. These cells then behave as mediators, releasing histamine, tumor necrosis factor, chymase, tryptase, and prostaglandins. Ultimately, the factors that cause inflammation sensitize neurons in the bladder, causing pelvic pain (Smeltzer, Bare, Hinkle, & Cheever, 2008).

The prevalence of IC varies according to geography, socioeconomic conditions, diagnostic capabilities, and physician and patient awareness of the disease. In the United States, it is estimated at 130 per 100,000 inhabitants; in Finland, at 250 per 100,000. Interestingly, the presumed prevalence in Asian and African-American populations is approximately 30 times lower (Smeltzer et al., 2008). Women are ten times more frequently affected than men. IC can manifest from youth to old age, but diagnosis is most often made between the ages of 40 and 50. It should be noted that it takes an average of four to seven years from first symptoms to diagnosis. The disturbed integrity of the urothelium plays a crucial role in the pathogenesis of IC.

Some patients experience aggravation of their symptoms after eating specific foods or drinks. A survey of people with IC — in which 90% responded — found that particular foods aggravated their signs and symptoms (Smeltzer et al., 2008). Patients were asked about 175 items that could worsen, improve, or have no effect on their symptoms. Cranberry, orange, pineapple, and other citrus-containing fruits and juices were found to aggravate IC symptoms. Coffee, decaffeinated coffee, tea, cola, soda, decaffeinated cola, diet cola, and certain alcoholic beverages also received considerably lower scores than other beverages, suggesting that caffeinated, alcoholic, and soft drinks aggravated the problem (Rothrock, 2007).

The pathology of interstitial cystitis is not fully known, although several theories have been proposed, including autoimmune disorder, genetic factors, allergy mechanisms, and neurologic mechanisms. Regardless of the cause, most people with BPS/IC are found to have a damaged bladder lining, often following several bladder infections, excess caffeine and soda intake, or past bladder injuries. This damage allows chemicals in the urine to penetrate the bladder muscle, causing swelling and pain.

Recently, it has been found that the FZD8 and PAND genes play a role in a small percentage of patients. The FZD8 gene causes production of a protein called antiproliferative factor, which slows the growth and repair of bladder lining cells. In patients carrying this gene, the bladder lining cannot form or repair itself normally.

Historically, diagnosis of IC is determined on the basis of multifaceted symptoms such as bladder-related soreness, urinary frequency, and urgency with no other definitive cause. Cystoscopy with hydrodistension under anesthesia (HUT) can provide information about bladder wall defects such as glomerulations, mucosal lacerations, low anesthetic bladder capacity, and the presence of painful lesions or "patches." One demonstrative study of 80 consecutive patients found that this procedure did not exceed the diagnostic value of careful history-taking and physical examination (Parsons & Parsons, 2004). Bladder biopsy is not routinely recommended unless gross abnormalities are present in the bladder wall (Moldwin & Sant, 2002).

Evaluation and Diagnosis

Before diagnosing IC, other treatable conditions must be ruled out. A detailed medical history and physical examination are a crucial part of the diagnostic workup. Diagnostic studies used to exclude other conditions include urine culture, urinalysis, cystoscopy, urodynamics, and hydrodistension. The patient with IC may have scarring, stiffening, or pinpoint hemorrhaging caused by recurrent irritation — referred to as glomerulation — which can often be appreciated during these studies. Hunner's ulcers are present in approximately 10% of IC patients (Kochakarn, Lertsithichai, & Pummangura, 2007). During urodynamic testing, patients with IC may display a small bladder capacity and experience pain with bladder filling.

No single treatment is effective for all patients; therefore, patients generally must try different treatments. Initial therapy includes adjustments in diet and lifestyle together with the use of oral medications. Recommended dietary adjustments include the exclusion of one or two foods from the individual's diet. Foods high in acid, potassium, caffeine, and alcohol should be avoided to determine whether IC symptoms improve. Hydrodistension can also be used as both a diagnostic measure and a treatment that may provide symptom relief for variable lengths of time (Graham, Glen, & Keane, 2004). CAM provides multimodal treatment options that help in treating patients with IC, and combinations of more than one treatment are often suggested by medical specialists.

The foundation of therapy begins with changing dietary habits to help patients avoid foods that further aggravate the injured layer of the urinary bladder. The type of food a patient consumes plays a vital role in increasing or decreasing IC symptoms. In fact, diet is considered one factor in triggering this syndrome. The most common dietary triggers include extremely spicy or acidic foods, alcohol, coffee, tea, sodas, fruit juices, chocolate, and potassium-rich foods such as bananas, tomatoes, citrus fruit, and cranberries. Because everyone's body reacts differently to various foods, dietary triggers differ from person to person. The easiest way to identify problematic foods is to use an elimination method. Lists of dietary options can be obtained from medical specialists. One study documented chronic pelvic pain caused by celiac disease in a woman who benefited from a gluten-free diet (Graham, Glen, & Keane, 2004).

Conclusion

Interstitial cystitis, described as an inflammatory disease of the bladder wall, is now a widespread condition. A reason for underdiagnosis is the widespread use of strict exclusion criteria. The disease can be identified through careful medical history and physical examination at an early stage, and then treated with multimodal therapeutic approaches. In addition to symptomatic oral therapy, instillation with local components that restore the protective glycosaminoglycan layer represents a common therapeutic approach, given that the integrity of this layer plays a key role in the pathogenesis of interstitial cystitis. There is no evidence that IC is hereditary. Over the last 15 years, knowledge regarding this disease has improved substantially.