Another set of interesting bits from the World Congress on Endometriosis 2011, so let’s get started with...
S. Banerjee from St Peter’s Hospital, Chertsey, UK (S#2-5) presented their work entitled
Identification of non-invasive markers of peritoneal deep infiltrating endometriosis in women with chronic pelvic pain.
The aim of this study was to record the symptoms and clinical observations of a group of 401 women with chronic pelvic pain. These women would then go for diagnostic laparoscopy to find the cause of their pain, then the results from the pain surveys and observations would be analysed to show if there is any difference between women with different diagnoses.
After the laparoscopies 167 women (42%) were diagnosed with deeply infiltrating endometriosis (DIE), 150 (37%) were diagnosed with superficial endometriosis and 84 women (21%) were found to not have endometriosis as the source of their symptoms. So, the focus of this study was to look at the difference in demographics and symptom profiles of women with DIE and compare it to women with superficial endometriosis to see if there were any significant differences that may help identify DIE before diagnostic surgery. This is how those factors broke down: women with DIE were on average 31 years old compared to 33 years old for those without. Dyschezia (painful bowel movements) throughout the month, a clinically immobile uterus, a palpable nodule, and the presence of an endometrioma (ovarian endometriotic cyst) were all more common in women with DIE. Interestingly, the authors then quantified the risk; so if all the above factors were present in one woman from this group, this raised their chance of being diagnosed with DIE from 42% to 82%. Conversely if all the above factors were absent it decreased the chance of them being diagnosed with DIE to 10%.
In conclusion this study will hopefully allow gynaecologists to identify women who have the highest chance of being diagnosed with DIE from the features of their pain symptoms and clinical observations, which in turn should make it easier for surgeons to know what they are looking for.
M.Takamura from University of Tokyo, Japan (S#4-1) resented the results of their study entitled
Probiotics inhibit the growth of endometriotic lesions in a murine model
You’re probably aware of some of the various commercial probiotic yoghurts and drinks available on the market at the moment, I must confess I have a probiotic drink myself with breakfast (it’s an acquired taste, I’ll tell you that much). Basically these products contain live bacteria that are supposedly beneficial to ones digestive system, if the marketing is to be believed. According to the authors of this study, these probiotics are recently gaining attention due to their ability to modulate the immune system in a favourable manner. This got the authors thinking that, due to the many immune system abnormalities associated with endometriosis, perhaps these probiotics may illicit some beneficial effects against the disease.
The way in which they studied this was to use a murine (mouse) model of endometriosis. Basically this involves surgically inducing endometriosis in a mouse. Now, although I’ll not go into detail about the positives and negatives of animal models, I will say though that despite the fact mice make excellent animals in which to model diseases and have a large amount of similarities to humans in more ways than you’d expect, in terms of modelling reproductive diseases, mice don’t have a menstrual cycle and have a distinctly different reproductive systems to humans so the true value of using mouse models may be someone questionable. Nevertheless it is one of the best tools we have, so until better comes along, we’re stuck with mice.
The authors then administered various doses of probiotics (containing such inventively named bacteria as L.acidophilus, L.casei, Bifidobacterium bifidium and Streptococcus thermophilus) to different groups of mice and noted any effects they had on the size or number of endometriotic lesions. Overall, the results of the study showed that mice receiving oral doses of the aforementioned probiotics suppressed the development of endometriotic lesions, reducing the size/growth, but not the number, of lesions. The authors note that, if this treatment works in a similar manner in humans, that fact that it causes no alteration to hormone levels may be beneficial for women.
G.M. Buck Louis from National Institute of Health, Rockville, USA (S#4-5) presented work from their collaborative research group entitled
Persistent organic pollutants and endometriosis: importance of biologic media for defining exposure – the endo study.
Now, talking about the relationship between endometriosis and environmental pollutants is opening a rather large can of worms because there are arguments both for and against the involvement of environmental pollutants in endometriosis. The arguments ‘for’ work on the premise that the mode of action of a lot of pollutants should increase the likelihood of developing endometriosis due to their ability to mimic estrogen and negatively affect the immune system in the human body. The arguments against rightly point out that the evidence supporting the role of pollutants in endometriosis is sketchy at best and, at present, does not prove any links between pollutant exposure and increase endometriosis risk in humans.
This study has obviously aimed to address some of the issues surrounding previous studies and provided a study with, from what I can see, is an extremely comprehensive methodology (which I’ll not go into here as it will take up too much space and may induce sedative effects). The study took women from 14 clinical centres undergoing laparoscopy or MRI for the diagnosis of endometriosis, then gave them questionnaires and took samples of blood, urine and fat and analysed the levels of various pollutants in these samples. The important difference to this study was the inclusion of analysing fat samples from women. Previous studies frequently use blood for analysis, but the problem with that is pollutants are transferred from the blood and accumulate in fatty tissue around the body, so sampling fat would be a much better indicator of pollutant exposure.
The results showed that the levels of several polychlorinated biphenyls (PCBs) and hexachlorobenzene were significantly higher in the fatty tissue (but not blood or urine) of women with endometriosis. This further highlights the importance of selecting the correct biological sample when looking for relationships between environmental pollutants and endometriosis. It also adds weight to the argument supporting the role of environmental pollutants in the development of endometriosis, how exactly these pollutants elicit their effects remains to be conclusively proven.