Pathophysiology of interstitial cystitis [review article], 2019, Birder

Andy

Retired committee member
Abstract
Interstitial cystitis/bladder pain syndrome is a chronic pain syndrome whose causes remains elusive with no generally accepted treatment. A hallmark of functional pain syndromes such as interstitial cystitis/bladder pain syndrome is pain in the absence of demonstrable pathology of the viscera or associated nerves. Patients with chronic pain experience a greater impairment in quality of life than healthy controls. In addition, interstitial cystitis/bladder pain syndrome symptoms can frequently overlap with other conditions including irritable bowel syndrome, fibromyalgia, chronic fatigue syndrome, anxiety disorders, and a number of other syndromes not directly related to the urinary bladder. Because of the complex pathophysiology, a number of animal models have been studied over the years to better understand mechanisms underlying patient symptoms. These models can include: bladder centric, complex mechanisms and psychological and physical stress models. Such animal models can aid in the investigation of aspects of interstitial cystitis/bladder pain syndrome that cannot be pursued in humans as well as to develop and test potential therapies. In addition, the search for urinary factors that may be a cause of interstitial cystitis/bladder pain syndrome has resulted in the discovery of a number of potential targets that could serve as predictive biomarkers which can aid in early diagnosis and treatment of this chronic disorder.
Open access, https://onlinelibrary.wiley.com/doi/full/10.1111/iju.13985
 
"the absence of demonstrable pathology of the viscera or associated nerves. "

It has now been found that demonstrable pathology is only missing because the bacteria that grow in the bladder do not grow on agar plates.

The most likely cause for interstitial cystitis is that it is the same as cystitis caused by bacteria that can grow on agar. Let's rule that out before we start looking for "complex mechanisms and psychological and physical stress models."
 
The most likely cause for interstitial cystitis is that it is the same as cystitis caused by bacteria that can grow on agar. Let's rule that out before we start looking for "complex mechanisms and psychological and physical stress models."
This.
I recently watched an online presentation about chronic/recurrent cystitis (and the association to vaginosis). These were my take-aways:


- Some pathogens are destroyed by oxygen, so the urine tests were you pee in a cup and the nurse later dips a test strip into it, might not detect the actual degree of the infection.

- Some pathogens are (as Mithriel said above) very hard to grow on media. The best test to detect those pathogens would be by PCR.

- The pathogenic type of E. coli can not only hide under a biofilm (where it is safe from antibiotics), it can also hide in the mucosa. In both cases the bacteria slow down their metabolism and are not detectable by common test methods. Still, symptoms can occur.

- If E. coli are the source of recurrent cystitis, it's most likely not a new infection caused by poor hygiene, but a flare-up of hidden, dormant bacteria.

- The bladder is not sterile, it has its own microbiome (urobiome). This might be harmed by frequent use of antibiotics or (through the close proximity) by a bad vaginal flora.

- One example: a bacterium called Gardnerella vaginalis, has been thought of as a normal part of the vaginal flora. But if they grow too much, they can damage the vaginal mucosa. If they wander into the bladder, and damage the mucosa there, they can release the former dormant E. coli. Gardnerella vaginalis is not detectable via urine dip sticks and very hard to grow on a medium. Best test would be a PCR.

- Men can be asymptomatic carriers of pathogens and re-infect through unprotected sex. The pathogens can hide in the seminal vesicles. To detect this one needs a PCR on a sperm sample.

- If infections are thoroughly ruled out, or the high susceptibility for new infections can not be explained otherwise, check for:
  • frequent Ibuprofen use (damages the mucosa)
  • oestrogen deficiency (in menopause or due to contraceptive pill) - estriol is a surface protector and feeds lactobacilli
  • food intolerances
- Therapy:
  • pathogen-specific antibiotics (co-treatment, if partner is carrier)
  • herbal medicine (for mild cases): Angocin (nasturtium, horeradish), Canephron (rosemary, centaury, lovage)
  • oral/vaginal pre- and probiotics to restore the microbiomes
  • estriol vaginal creme (if oestrogen deficient)
  • no tampons (dry up the mucosa), but pads or cups
  • autovaccines or urovaxom
 
"the absence of demonstrable pathology of the viscera or associated nerves. "

It has now been found that demonstrable pathology is only missing because the bacteria that grow in the bladder do not grow on agar plates.

The most likely cause for interstitial cystitis is that it is the same as cystitis caused by bacteria that can grow on agar. Let's rule that out before we start looking for "complex mechanisms and psychological and physical stress models."
I watched an interesting video last night about thermophilic bacteria growing in an abandoned coal town because of a runaway fire in the coal bed.

They mentioned how difficult it is to identify those because of that problem, too many bacteria not growing in a petri dish, and instead have to sequence DNA from a slurry. I wonder if that could be a method here. It's more expensive and slow but surely it's a better method than failing object permanence and assuming things you can't see cannot possibly exist.
 
I just remembered an article I read on UTIs and interstitial cystitis :

https://www.theguardian.com/society...ief-for-women-with-chronic-life-changing-utis

I was astonished by this paragraph :

He says the flaws in current methods for diagnosis date back to some of the earliest research on UTIs in the 1950s. It was thought, incorrectly, that the normal human bladder is completely sterile. So if bacteria grew in a cultured urine sample it was thought to signal an underlying infection. In an early paper, an arbitrary threshold was put forward as being indicative of a true infection rather than contamination. And despite this threshold never having been properly validated, it gradually became accepted.

I wonder how many other 70-year-old assumptions in the medical field are complete nonsense.
 
Back
Top Bottom