Highlights from the WCE 2011: Part 2

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.

Highlights from WCE 2011: Part 1

As I mentioned briefly in my last post I attended the 11^th world congress on endometriosis in Montpellier a few weeks ago. It’s a tough life having to travel to beautifully picturesque Mediterranean cities, but hey, somehow I managed to cope. The main body of the conference was run over three days where experts from all over the world presented their latest research and shared up to date knowledge about endometriosis. If you would like to see the whole program for the conference you can download it here. All in all it was a very enlightening few days, but don’t worry if you couldn’t make it yourself because over the next few weeks I’ll be posting highlights from the conference. Unfortunately, I can’t post about everything that was discussed because it would probably take more years to write than I will live, so I’ve gone through the different talks and posters and picked out the ones that I hope you’ll find the more interesting. I’ll start off with the oral presentations that were given then move onto the posters that were presented. I’ll also give a bit of my own interpretation of the science, but I won’t be doing much critical appraisal. So without further ado, let’s jump straight in.

R.S. Bevan from the Brighton and Sussex Medical School, UK (S#1-3) presented their work entitled ‘Alcohol consumption and endometriosis: A multi-centre, case-control study’

This study took 1,418 women from 10 countries that were undergoing laparoscopic surgery for either suspected endometriosis or tubal ligation. After surgery the main group were divided into three groups: Those who were found to have endometriosis (745 women), those who had symptoms but no disease was found (565) and those women undergoing sterilisation who had neither symptoms nor endometriosis (86). These women were asked to complete a questionnaire which gave included questions about alcohol consumption.

The results of this study showed that alcohol consumption between the three groups of women did not significantly vary. Although there is still more analysis of this data to be done it is still interest to see these preliminary findings. I think there may have been some expectation that alcohol consumption may be increased in women with endometriosis, perhaps due to the fact alcohol can give pain relief, so the results are interesting from that pint of view. There was also some discussion as to whether alcohol consumption increases the risk of endometriosis. I’m not sure whether or not this is folly. Mainly because the symptoms of endometriosis tend to begin around adolescence, but alcohol consumption doesn’t even seriously start for most people until their late teens, so I’m sure whether there could really be any connection between the two.

S.A. Missmer from Havard Medical School in Boston, US (S#1-4) presented their work entitled ‘Vitamin A and endometriosis risk: A prospective cohort study’

This study analysed consumption of different micronutrients in 1382 women with laparoscopically diagnosed endometriosis. What this study found was that increased consumption of vitamin A seems to reduce the risk of endometriosis. Or rather, I should say, reduced the risk of being diagnosed with endometriosis. These investigators reported a 21% reduction in risk of diagnosis of endometriosis when comparing the highest consumers of vitamin A with the lowest, with the association most prominent in women with no history of infertility, who had a BMI below 25 and who had smoked during their lifetime. The investigations are still undergoing to find out why this reduction in diagnosis risk was observed.

M.Kvaskoff from The Gustave Roussy Institute, France (S#1-5) presented their work entitled

‘Early life events and the risk of endometriosis: The French E3N cohort’

This study analysed questionnaire data from a large group of women with health insurance in France. The purpose of this study was to see if women with endometriosis had exposure to different factors during childhood that made them more susceptible to endometriosis in later life. This study found that both exposure to cats or dogs at home and living on a farm for more than 3 months during childhood increased the risk of endometriosis in later life.

Girls who started their periods before the age of 12 or who had short menstrual cycles before the age of 17 (a short cycle being anything less than 24 days, were also found to be at a higher risk of endometriosis.

Whilst the level of out if school exercise was unrelated to endometriosis risk, more time spent walking (i.e. greater than 5 hours per week) between the ages of 8 and 15 appeared to increase the risk of endometriosis. Higher exposure to UV radiation at place of birth was found to decrease endometriosis. There were a number of early life factors that were found to have no influence over the risk of endometriosis including: birth height/weight, being born premature, breast feeding and maternal smoking.

So what do we make of this study? Well firstly it is important to distinguish causal factors from incidental factors. What do I mean by causal and incidental? Firstly I’ll stop asking rhetoric questions, then I’ll tell you that a causal factor is a factor that is likely to actually increase the risk of endometriosis, whereas a incidental factor is one that is associated with a causal factor so appears to be associated with endometriosis even though it could have no baring directly on the development of the disease.

Let me give you an example; this study found that young girls who undertook more walking exercise were at higher risk of endometriosis. Does this mean that we should stop all young girls from walking so much? No, because if we look at the rest of the results we can see that girls who lived on a farm were at higher risk; girls who lived on a farm are likely to do more walking, so we can see that walking isn’t directly linked to endometriosis risk, rather it is incidentally linked to endo via other factors (such as childhood environment).

More highlights coming soon!