ENDO Messages for August, 1998: Other Autoimmune diseases

Other Autoimmune diseases

From: Melissa (anonymous@obgyn.net)
Mon Aug 31 16:48:50 1998

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Hi all:

I was wondering if any one else had been diagnosed with an auto-immune disease. I was diagnosed with Juvenile Rheumatoid Arthritis when I was 12 (about the time my period started). I went into remission when I was 18 and immediately started showing symptoms of endo. In my mind this has to be related since most research points to endo being some sort of auto-immune disease.

-----Original Message----- From: Paul Brother [SMTP:brother@stlnet.com] Sent: Monday, August 31, 1998 2:44 PM To: Multiple recipients of list Subject: Hello

Hi all. I have been working a lot lately so I have not had much time to read or respond to any of the posts. The little that I did read is somewhat concerning to me. At first people were wondering if tampon use was invovled in the cause of endo and then I saw a few posts about sex during your period causing endo. I am concerned that some of you are blaming yourselves for this illness. I don't believe there is any way any of us could have prevented this disease. I think genetic and environmental exposures are most likely the cause. There is much more research needed in what causes endo and we need better treatments. Lupron worked very well for me but I know it does not help everyone. I can only hope that with more research we can find better treatments.

For those of you interested in the immune system and how it relates to endo I have attached my post from a few months ago. Take care.

Michele

Hi all! Awhile back there was some discussion about endo and the immune system. I decided to search medline and see what the latest research showed. I found one review from 1995 that I think is pretty good. The reference is Dmowski, W.P. Immunological aspects of endometriosis. Internal J. Gyn Obs. 50. Suppl 1 (1995) S3-S10. You can get this from any med school library or I have copies I can mail if you want. Here's my assessment of the article:

How does endo develop? Endo is characterized by the proliferation and function of misplaced endometrial cells. There is retrograde transport of endometrial cells into the peritoneal cavity. This has been found to occur in most all women who menstruate, but endo only develops in 10-15% of women. What else is going on here?

Immune System Humoral immunity is the part of the immune system that forms antibodies against foreign things such as bacteria and cells. The antibodies are formed by the B cells. The purpose of antibodies is to destroy the foreign material; they help activate the immune system causing inflammation. In autoimmune disorders for some reason the body makes antibodies against its own tissue(these are called autoantibodies). There is a high frequency of autoantibodies found in women with endo. Increased B cell fundtion has also been seen. Autoantibodies against endometrial and ovarian tissue have been found in the blood, cervical and vaginal secretions, and peritoneal fluid(fluid in the abdominal cavity) of women with endo. This all suggests polyclonal B cell activation. Conclusion: Inpts with endo autoantibodies are formed against endometrial and ovarian tissue. Cell Mediated immunity involves the activation of white blood cells against foreign tissue. When the body is invaded by foreign tissue such as bacteria certain cells are activated mainly T cell and complement to kill the bacteria. In endo, cell mediated immunity is altered but they do not think that this affects the general immune system. In other words the changes in cell mediated immunity don't affect one's ability to fight off infections. There is a modification in the interaction between immune cells and endometrial cells. The immune cells proliferate when they come in contact with endometrial cells in a normal woman. In a woman with endo this response is reduced suggesting decreased regconition of endometrial cells. This means that if the immune system does not recognize endometrial cells in the abdomen it can not kill them. There is decrease destruction of misplaced endometrial cells. There is also some evidence that the endometrial cells themselves are altered. There is resistence to destruction of endometrial cells by an immune cell called a natural killer cell. The natural killer cells are regulated by other cells called monocytes and macrophages (also part of the immune system). In women with endo there seems to be increased activation of monocytes in the blood and increased numbers of macrophages in the abdominal cavity. Monocytes in the blood can cause proliferation of endometrial cells. Monocytes work by secreting different substance called cytokines and these cytokines are secreted differently in pts with endo and normal women. There is high levels of TNF alpha in pts with endo. This cytokine is responsible for proliferation of endometrial cells in pts with endo and causes induction of inflammation in endo lesions. IL 6 is also secreted in higher amounts in pts with endo. It is involved in the development of autoantibodies. Conclusion: In endo, there is decreased recognition of endometrial cells and these cells are resistant to killing by the immune system. This means when the cells flow back through the tubes into the abdomen the are not as effectively destroyed by the immune system as they are in normal women. Endo has many characteristics similar to other autoimmune diseases. These include: Female preponderance, familial occurance, tissue damage and multi organ involvement. It has been shown that women with autoantibodies have lower pregnancy rates than those who are autoantibody negative. Pts who are autoantibody positive and are treated with corticosteroids have higher pregnancy rates than those not treated. Steroids have no effect on autoantibody negative pts. Danazol, a medication used to treat endo has shown to inhibit auto- antibody production.

Sorry so long but this is a rather complicated topic. I tried to used plain english instead of doctor talk as much as possible. Please write to me if any of this is not clear. Take care, Michele

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