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Endometriosis is a condition whereby the lining of the uterus, known as the endometrium, grows outside of the uterus where it does not belong. There is no short word or nickname for endometriosis.
Women with endometriosis may have a variety of symptoms or, at times, may have no symptoms at all. The most common symptoms are menstrual cramps (dysmenorrhea), pelvic pain, deep pain with intercourse (dyspareunia) and pain with bowel movements especially during the menstrual period. A large percentage of women with endometriosis are infertile.
Over the years, there have been a variety of theories which attempt to explain how one gets endometriosis. Research has been difficult as endometriosis only occurs in the human so there are no animal models to study. The one theory that has survived and is generally accepted by most is Sampson’s Theory of Retrograde Menstruation. Instead of all the menstrual blood going through the cervix into the vagina, some of it backflows through the fallopian tubes into the pelvis carrying bits and pieces of the endometrium into the pelvic cavity. These microscopic pieces of endometrium may then attach to the pelvic organs and start to grow. These misplaced endometrial cells are now called endometriosis. It is generally believed that retrograde menstruation occurs in as many as 75% of all women from time to time, but certainly 75% of all women do not develop endometriosis. There are many theories offered to explain this discrepancy. We know there are cells in the fluid inside the pelvis and abdomen (peritoneal fluid) called peritoneal macrophages. These cells travel around and literally eat up impurities in the abdomen. Crudely, they can be thought of as the catfish of the abdominal cavity. There are other cells in the abdominal cavity known as killer T cells. They also immobilize foreign matter in the pelvis and abdomen. Some studies have shown or at least suggested that some women with endometriosis have decreased levels of peritoneal magrophages and killer T cells and this allows the endometrial cells to live long enough to attach and start to grow. Some women with normal levels of peritoneal macrophages and killer T cells may also get endometiosis if the amount of menstrual blood ‘dumped’ into the pelvis is so large that these normal levels of cells are simply overwhelmed with the amount of foreign endometrial cells.
At the present time there are no adequate methods of testing for levels of peritoneal macrophages and killer T cells so these theories cannot be clinically applied. In theory, if a patient is born with decreased levels of peritoneal macrophages and killer T cells she will probably never be cured of endometriosis. Even if her treatment completely eradicates the endometriosis, the next time she retrograde menstruates, she will get it again. However, if she has normal amounts of peritoneal macrophages and killer T cells, she may be able to be permanently cured of endometriosis providing she does not have an exceptionally large amount of menstrual blood ‘dumped’ into the pelvis again. This may explain why some women are cured of endometriosis and others are never cured. For many years we have told women that endometriosis was not inherited. However, we may have to re-think that if the inclination to have decreased numbers of peritoneal macrophages or killer T cells is inherited.
What is the natural history of endometriosis?
The concept of ‘the natural history’ of a condition is quite interesting. If we simply watch a condition without intervening, what happens? For example, let’s look at the common cold. A cold comes on in one to two days, lasts five to six days and leaves in another one to two days and there is nothing one can do to alter the course. Certainly, you might take an anti-histamine to make yourself feel better but it will not effect the natural history. The natural history of endometriosis is such that it always gets worse. It always spreads microscopically, cell by cell. Many times it invades into the tissues such as the ovaries, cul de sac (behind the uterus), or the bowel. Even though it spreads and invades it is not cancer and it is virtually unheard of that it becomes cancer. Even though endometriosis always spreads, it will spread at different rates in different women. Some will have very slow progression and some very rapid progression.
Why does endometriosis spread and grow?
The stimulus to make endometriosis grow is the same stimulus that causes the endometrium (lining of the uterus) to grow back after a menstrual period – estrogen. Estrogen secreted from the ovaries is the food supply or fuel supply for endometriosis. However, a combination of estrogen and progesterone present in the body continuously causes the growth to slow down or even stop but this combination does not make endometriosis go away. Situations in which the body is exposed to a combination of these hormones are pregnancy and taking combination birth control pills.
Why does endometriosis usually cause pain?
There are several possible reasons. Firstly, when the hormone levels in the body drop at the end of the ‘menstrual month’ the lining of the uterus starts to fall off with blood and that is the start of the menstrual period. We know that the lesions of endometriosis inside the pelvis may also bleed at that time and even small amounts of blood are highly irritating to the tissues in the pelvis and pain results.
Secondly, we know that the lesions of endometriosis secrete a grouping if chemicals know as prostaglandins. Prostaglandins act on certain types of muscle and cause those muscles to contract and go into spasm. The uterus is that kind of muscle and that is why menstrual cramps (dysmenorrhea) can be so severe. The highest level of prostaglandins in the abdominal fluid occurs just as the menses begins. It has also been shown that the amounts of prostaglandins secreted will vary as the predominate color of the endometriosis will vary. The classic blue-black color of endometriosis secretes the least amounts of prostaglandins, tan endometriosis a moderate amount and the red variety of endometriosis secretes the largest amounts. Therefore, the amount of endometriosis does not necessarily relate to the amount of pain. Small amounts of red endometriosis can cause as much or more pain than large amounts of blue-black endometriosis.
Thirdly, endometriosis may result in adhesions which may cause pain. The word adhesions is derived from the same Greek word derivative as is adhesive tape or adherent, meaning to stick. Endometriosis may cause so much irritation and inflammation that a sticky substance known as serum is secreted. Invision two pieces of flypaper being stuck together. That is similar to the dense adhesions we can find in the pelvis where ovaries can stick to the sidewall of the pelvis, the fallopian tubes, the back of the uterus, or even the bowel. Now invision trying to separate those two pieces flypaper and seeing ‘stringy’ material going from one piece to the other. This is what fine, filmy adhesions in the pelvis look like. As adhesions try to pull apart, pain may be initiated. Lastly, the endometrial lesions themselves may be quite tender. A common site for lesions to occur is in the cul de sac (behind the uterus, between the uterus and the lower bowel, at the top of the posterior vagina) and these tender lesions are a common cause of deep pain during intercourse.
How does endometriosis cause infertility?
We have already talked about the fact that endometrial lesions secrete prostaglandins. Prostaglandins can act on the muscle of the fallopian tubes and cause them to contract and to go into spasm. When ovulation occurs, the fallopian tube which is laying down in the pelvis, rises up out of the pelvis just like a charmed snake out of a basket and massages over the ovary. When the egg is picked up and is securely in the fallopian tube, the tube falls off of the ovary and goes back into the lower pelvis. We do not know what initiates this movement of the tube. When prostaglandins are present, the fallopian tube stays in the lower pelvis and simply quivers. All of this results in the failure of the tube to pick up the egg. Again, the amount of endometriosis is not necessarily related to the failure of egg pickup as the amount of prostaglandins are related to the color of the endometriosis. If significant adhesions are present they may prevent proper egg pickup especially if the fallopian tubes are involved.
How is endometriosis diagnosed?
Although a physician may suspect endometriosis from symptoms and pelvic exam, the only way it can be diagnosed is by direct visualization, usually by laparoscopy.
How do we treat endometriosis?
First of all, remember that there is no such thing as a “little bit of endometriosis”. Since endometriosis is a progressive, destructive condition which never goes away on its own and always gets worse, it should always be treated aggressively. We believe there are three main types of treatment.
Firstly, there is surgical treatment. If we could only surgically remove all of the endometriosis from the pelvis the treatment would be successful. We can remove the endometriotic tissue by excision, cautery or laser. A laser is a concentrated beam of light energy. However, we can only remove the areas that are visible and since endometriosis spreads microscopically, we cannot remove it all surgically. We certainly cannot laser the entire pelvis in an attempt to eradicate all of the endometriosis.
Secondly, there is medical treatment. In theory, if we could only take away the stimulus or food supply (estrogen) for endometriosis for a long enough period of time the implants would disappear. It has been my experience in over 20 years of treating endometriosis medically that we can eradicate the microscopic areas and the very small lesions with a six month course of medication but the larger lesions do not go away even though they will get smaller. Currently, the two most used medications are Depot-Lupron and Depot-Provera. They both work essentially the same way by suppressing pituitary FSH which is responsible for stimulating the ovary to produce estrogen. The estrogen is then not present for approximately six months and this should eradicate the small and microscopic lesions. I follow the patient frequently by obtaining blood estrogen levels to confirm we are getting the response we want. At the end of the treatment I also obtain a bone scan to determine if any bone loss has occurred. I find this very infrequently but bone loss, although replaceable, is a side effect of these medications. Another side effect is hot flashes. These can vary from mild to severe and occur mostly at night. Most patients learn to deal with them but for the small percentage of patients with severe hot flashes we can consider “add back therapy”. Add back therapy has been used for many years with Depot-Lupron. Until recently it consisted of giving enough oral estrogen to lessen the hot flashes. To me, this has never made good academic sense since estrogen is the stimulus to endometriosis and the purpose of Lupron is to lower the levels of estrogen in the body. Why give expensive injections to lower the estrogen only to give estrogen orally? We now know that some oral progestins (progesterone like medications) such as norithindrone acetate will help with severe hot flashes but will not act as a stimulus to the endometriosis.
The third method of treatment is a ‘sneaky’ third as is it a combination of #1 and #2. I believe that the very best approach to treating endometriosis is to treat the visible areas surgically and then follow up with medical treatment for six months to treat the microscopic endometriosis which almost certainly will be there if visible lesions are present. I also believe that the best overall surgical treatment is the KTP laser. The light energy put out by the KTP is absorbed by tissue that is pigmented and is in the red, tan, blue, black spectrum of color and all endometriosis is pigmented in that spectrum. Occasionally, open, major abdominal surgery is necessary to either laser or surgically excise lesions that are very deep. Even more rarely, resection of bowel lesions or resection of a portion of the bowel is required.
Does endometriosis “come back”?
Certainly if one is cured of all endometriotic lesions, both visible and microscopic, and significant retrograde menstruation occurs, one can ‘get’ endometriosis again. However, I believe that most of the time when a patient is told that her endometriosis has "come back", it really was never treated properly and never went away in the first place. This is not to say that if endometriosis “comes back” it was not treated properly. Sometimes the condition simply cannot be eradicated.
I hope this has not been too long or technical for you but I feel compelled to relate to you my ideas regarding endometriosis. Over the years, this condition has been the most misunderstood of any condition I treat.
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