Comorbidities
Those suffering
from IC frequently present with multiple other maladies, creating an even more
challenging set of symptoms to manage. In a population-based study of 9,269 IC
patients and 46,345 randomly selected comparison subjects, researchers examined
the prevalence of 32 comorbidities ranging from cardiovascular, pulmonary and neurological
conditions to rheumatological, gastrointestinal and psychological conditions.9
Results displayed a significantly higher prevalence of all comorbidities
when compared to the control group, with the exception of metastatic cancer.9
A small
cross-sectional study of 132 subjects was studied in regard to interstitial
cystitis and comorbidities.10 Researchers determined that multiple
comorbidities existed in physician and questionnaire diagnosed patients.10
Findings coincided with previous outcomes that showed comorbidities with
conditions such as migraines, irritable bowel syndrome, and overall bodily
pain.10 However, results also showed several new apparent
comorbidities such as symptoms related to dyspepsia as well as orthostatic
intolerance (disorders with symptoms emerging during periods of standing
upright that are alleviated when reclining).10
Etiology
It is widely
accepted that the specific cause of IC is still unknown, though several factors
appear to be influential. Some researchers state that furtherance of knowledge
in regard to the causes of IC may be limited due to the central focus on the
bladder and lower urinary tract as the genesis of symptoms without examining
other pelvic influences and systemic factors.11 Research has also
shown the possible influence of other illnesses on the contraction of IC (rather
than simply a comorbidity as discussed above) such as fibromyalgia, irritable
bowel syndrome and chronic fatigue syndrome, suggesting that IC may entail
systemic pathophysiology.11 Therefore, researchers hypothesize that
a plethora of causes and contributing factors are likely involved in IC symptoms
which in turn lead to many sub-types of the disease.11 Likewise,
additional sources infer that multiple components are involved in the
development of IC such as an autoimmune reaction, hereditary factors, infection
or allergies.3 However, these possible instigating factors have
remained unproven.3 Similarly,
in a review of the literature, researchers studied possible causes of IC and
came up with a multitude of potential contributing factors including the
suggestion of infection and autoimmune response.12 Certain studies
have shown a connection between bacterial infection in the bladder and IC as a
causal factor, but recent research contradicts this finding and no longer
assumes that infection is the main etiology from which IC stems.12, 13, 14
In regard to the autoimmune connection, results have been contradictory.
Researchers
evaluating lymphocyte populations in the blood and bladder tissue of IC
patients discovered that lymphocyte populations were normal and thus not
supportive of the theory that autoimmune disorders are an initiating factor.15
In a different review of the literature, researchers looked at the
intertwining of IC and systemic autoimmune disease and postulated that there is
a possible association between IC patients and autoimmune diseases.16
However, researchers stated “direct evidence clearly showing autoimmune
mechanisms is lacking”.16 A connection between IC and Sjogren’s
syndrome has shown a more significant connection, according to the researchers
involved, and may warrant additional studies.16 Questions still
remain as to the causal or reactionary effect of autoimmune response in regard
to the etiology of IC and further research is necessary in this area.15
Research in some
studies has pointed to the hereditary nature of IC as a causal variable.
Researchers looked at a small group of monozygotic and dizygotic twins to
determine incidence of interstitial cystitis within this population.17 Results showed that in the monozygotic
twin group, five out of eight monozygotic twin respondents had probable or
confirmed IC as compared to the group of 26 dizygotic twin respondents who
showed no signs of IC.17 Researchers concluded that based on this
finding, a genetic contribution is likely.17 It appears somewhat
obvious, however, that basing statements upon one finding is ill-advised.
A pilot study
examining the prevalence of IC within groups of first-degree relatives with an
IC diagnosis was performed with a total number of 2,581 respondents.18
Out of those who responded, 101 participants reported an incidence of 107
first-degree relatives with IC.18 Researchers reported more detailed
findings, stating that not only is there a genetic component involved but adult
female first-degree relatives of those diagnosed with IC may have as high as 17
times higher prevalence rate than that found within the general population.18
Concluding comments stated that, “This, together with previously reported
evidence showing a greater concordance of IC among monozygotic than dizygotic
twins, suggests, but does not prove, a genetic susceptibility to IC”.18
The connection
between allergies and IC has been examined and some studies indicate that
40-80% of patients experience allergies.19 The nature of causation
versus correlation is not clear, however, and could be a comorbidity as easily
as it could be a predictive element.
Several popular,
but weakly referenced, IC blogs and websites suggest that leaky gut may be a
causal component of IC.20, 21 However, finding credible research
that points to causation, correlation or comorbidity does not appear easily
accessible. Due to the fact that there seems to be a possible connection
between IC and autoimmune disorders, it would make sense if leaky gut showed up
in IC patients (due to the role leaky gut plays in autoimmune disorders).
Despite this fact, little formal research has been done in this area.
Several risk
variables have been suggested that may contribute to the contraction of the
illness. Some articles state that risk factors range from heightened stress,
sex of the individual, fair skin, red hair, or having an existing chronic pain
disorder.3 However, most of the research in these areas is, at best,
lacking. One report on the epidemiology, risk factors, and impact of
interstitial cystitis clearly stated that the only decisive risk factor for IC
is female gender.22
Many other
hypotheses for the causal factors of IC have been postulated, but the bottom
line to the question of causation is the frustrating yet simple conclusion that
the cause of IC is still unknown.3 Though this does not provide
concrete data on what initiates the disorder, it may provide patients with a
clear understanding of the fact that a specific cause is not known, suggesting
time would be better spent on the prevention and treatment of IC.
References
9. Keller
JJ1, Chen YK, Lin HC. Comorbidities of bladder pain syndrome/interstitial
cystitis: a population-based study. BJU International. 2012;
110(11): 903-909.
10. Chelimsky G, Heller
E, Buffington CAT, Rackley R, Zhang D, Chelimsky T. Co-morbidities of interstitial
cystitis. Frontiers in Neuroscience. 2012; 6: 1-6.
11. Mullins C, Bavendam
T, Kirkali Z, Kusek JW. Novel research approaches for interstitial
cystitis/bladder pain syndrome: thinking beyond the bladder. Translational
Andrology and Urology. 2015; 4(5): 524-533.
12. Grover S, Srivastava
A, Lee R, Tewari AK, Te AE. Role of inflammation in bladder function and
interstitial cystitis. Therapeutic Advances in Urology. 2011;3 (1):
19-33.
13. Domingue GJ1,
Ghoniem GM, Bost KL, Fermin C, Human LG. Dormant microbes in interstitial
cystitis. The Journal of Urology. 1995; 153(4): 1321-1326.
14. Wilkins EG1, Payne
SR, Pead PJ, Moss ST, Maskell RM. Interstitial cystitis and the urethral
syndrome: a possible answer. British Journal of Urology. 1989;
64(1): 39-44.
15. MacDermott JP1,
Miller CH, Levy N, Stone AR. Cellular immunity in interstitial cystitis. The
Journal of Urology. 1991; 145(2): 274-278.
16. Van de Merwe JP.
Interstitial cystitis and systemic autoimmune diseases. Nature Clinical
Practice – Urology. 2007; 4(9): 484-91.
17. Warren JW, Keay SK,
Meyers D, Xu J. Concordance of interstitial cystitis in monozygotic and
dizygotic twin pairs. Urology. 2001; 57(6): 22-25.
18. Warren JW, Jackson
TL, Langenberg P, Meyers DJ, Xu J. Prevalence of interstitial cystitis in
first-degree relatives of patients with interstitial cystitis. Urology.
2004; 63(1): 17-21.
19. Van de Merwe JP,
Yamada T, Sakamoto Y. Systemic aspects of interstitial cystitis, immunology and
linkage with autoimmune disorders. International Journal of Urology.
2003; 10: S35–S38.
20. Stop UTI Forever.
Can a leaky gut cause IC (Interstitial Cystitis)? Available at: https://www.stoputiforever.com/interview/leaky-gut-and-ic/.
Accessibility verified July 13, 2018.
21. Eat Beautiful. How I
healed my interstitial cystitis. Available at: https://eatbeautiful.net/2015/10/04/how-i-healed-my-interstitial-cystitis/.
Accessibility verified July 13, 2018.
22. Association of
Reproductive Health Professionals. Screening, Treatment, and Management of
IC/PBS. Available at: http://www.arhp.org/Publications-and-Resources/Clinical-Proceedings/Screening-Treatment-and-Management-of-ICPBS/Epidemiology.
Accessibility verified July 13, 2018.
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