Highlights from WCE 2014 - Part 2

Let’s continue our exploration through the World Congress on Endometriosis 2014 and we’re going to delve into some of the research about what makes women with endo different from those without and how this could give us clues as to what causes endo in the first place.

A team from Australia made an interesting discovery regarding stem cells and endometriosis. You have probably heard about stem cells before, but why would they be of interest in endometriosis? Stem cells are the precursors to the different types of cells in your body and are mostly of use during the very early part of your development when you were a foetus growing new organs. But they still have some use as an adult, for example, inside the uterus there are a population of stem cells that your body uses to regrow the endometrium after each menstruation, which are unsurprisingly referred to as endometrial stem cells. If these cells can grow endometrium and endometriosis is endometrium-like tissue, it becomes clear how these stem cells could play a role in endometriosis. Some researchers believe that genetic changes associated with endometriosis result in some endometrial stem cells becoming displaced during embryo development, which go on to produce endometriotic lesions as a girl approaches adolescence. Others believe these stem cells are shed into the pelvic cavity by retrograde menstruation (where the menstrual blood goes into the pelvic cavity) and implant around the pelvis and then develop into endometriotic lesions.

This investigation by the Australian team looked at the number of endometrial stem cells in the blood, menstrual blood and peritoneal fluid of women with and without endometriosis. What they found was that, although the amount of peritoneal fluid was similar between the two groups, the number of viable endometrial stem cells in the peritoneal fluid was massively higher in women with endo. So how did those cells get there? Retrograde menstruation is a likely explanation, but they found no difference in the amount of stem cells in the menstrual blood between women with and without endo.  It could be that the immune system of women with endo doesn’t clear the refluxed stem cells and they just accumulate or maybe there is some other way these cells are getting into the pelvic cavity, at this moment nobody knows for sure.

Speaking of peritoneal fluid, a group from the US and Brazil analysed the peritoneal fluid looking for inflammatory factors that are related to endometriosis associated pain. What they found was that dyspareunia (painful sex), non-cyclic pain and infertility were not related to the inflammatory factors they were studying. What they did find though was that certain inflammatory factors were associated with dysmenorrhea (excessively painful periods). This has some potentially very interesting implications, particularly as dysmenorrhea is the most common symptom of endometriosis. This suggests that dysmenorrhea is caused by areas of chronic inflammation around the sites of endometriosis regardless of stage or location. If it were possible to find out how these inflammatory factors are being produced and find a way to reduce the level of these factors, in the future this could be a new way of treating the pain associated with endo. 

More highlights on the way soon...

Highlights from the World Congress on Endometriosis 2014

It’s that time again, that time when the best and brightest in the field of endometriosis gather together in one place to share their collective experience and figure out where the future of endometriosis research and treatment is going; all whilst enjoying a caipirinha on the sunny beaches of Sao Paulo (us science types know how to multitask). Although I managed to go to the previous WCE in France, unfortunately I couldn’t make it this year, so instead of enjoying the glorious heat of the Brazilian south I was enjoying the drizzly rain of the English northwest, oh well. However, thanks to a friend, I did manage to get the book of abstracts (which is basically a summary of all the talks, presentations and posters at the conference) so I can give you a rundown of what’s been going on in the field of endometriosis research now and in the future.

Before I continue I must mention that the information I’ll be presenting here is taken only from the abstracts, which as basic summaries of the research and not in depth discussions and may or may not be taken from completed or peer-reviewed research. Also because these are conference papers I can’t provide links to source material as I normally would.

To start with, just looking at the book is encouraging, over 400 pages of research into all the many and varied aspects of endometriosis, which is broken down into different subject matters, so I’ll start with genetics and endometriosis.

Genetics is an important factor in endometriosis, mainly because we don’t really fully understand how genetic changes contribute to endometriosis risk. A team from Sweden aimed to examine indirectly the role genetics play, by looking at the rate of endometriosis in twins. There are two different types of twins: monozygotic (where both twins come from the same egg and are essentially genetically identical) and dizygotic twins (where each embryo comes from a different egg and can so each twin can be very different from the other). Of all the female twins this research looked at they found that there was a much higher risk of endometriosis if your monozygotic twin also had endometriosis. That certainly seems to suggest that genetics plays a role in the origin of the disease. Of course there are other factors at play too in determining endometriosis risk. This team, after doing some calculations, found that in the women they studied, genetics accounted for around half of the risk associated with endometriosis and environmental factors accounted for the other half. Finding out what the specific genetic and environmental factors are and how they increase or decrease the risk of endometriosis, is an ongoing challenge for the future.

Several other studies presented at the conference aimed to find out what these genetic factors are. Our genetic material (our DNA) is a funny thing, it can change in many different ways, some bits can swap, duplicate or be deleted all together and sometimes specific changes can be associated with specific diseases. Other research identified some of these specific changes associated with endometriosis which may, in the future, might allow us to identify women at risk of the disease with greater ease and hopefully give us to better understand the way in which the disease works.

Of course there are problems to consider, for example, are the genetic changes we see the same across all women? One of the presentations from an international team found that the genetic changes we know of so far are very similar between women of European and Japanese ancestry, but we still have no information on women of African, Chinese, Indian etc ancestry to compare them to. These types of studies though require a great deal of time and money invested in them, so it may be a while before we see a complete picture of the genetic risk associated with endometriosis for women across the world.

Another point to consider is the difference between types of endometriosis. One piece of research from a Danish team found genetic alterations specific to deeply infiltrating endometriosis. Therefore it could be that peritoneal, deeply infiltrating and ovarian endo all have different genetic alterations (and different genetic risks) associated with them. It’s good to know though there are people actually looking into this and one day, maybe soon, we’ll have that complete picture.

More to follow soon.