But it can't be avoided now. The story of my "little visitor" has become too compelling, personally and scientifically, to make light of. So here goes:
For about three and a half years (from just before the time I developed psoriatic arthritis), I've had very heavy, and LONG, menstrual bleeding. My visitor was a terrible guest. Stayed too long (two weeks or more) and didn't clean up after herself.
Then came Remicade. I started Remicade (Infliximab) about 6 weeks ago, and missed my period a week later. Please note: I never miss a period (except when pregnant). Of course I ran off to RiteAid for a pregnancy test, which came back negative. So I waited.
About 4 weeks after my first Remicade treatment, I had a visit, finally, and she was an easier houseguest than I've had in years. Not heavy, not long, just...normal. She practically did the dishes for me.
Now, here's the kicker. The bleeding started again, 4 days ago, right when the second Remicade dose wore off and I started feeling the arthritic aches and fatigue again. This was just two weeks after my last, very late, period. Is it coincidence that Remicade delayed and then "normalized" my period, and the absence of Remicade made me bleed? I think not.
So, as always, I'm turning to the research journals. First, I must give credit to the KickAS website and support group, which had a bunch of useful information in this thread.
It turns out that TNF-alpha has been linked to endometriosis, and is probably involved in the development of ovarian follicles. A fascinating 2004 review article by Sakumoto and Okuda (Journal of Reproduction and Development) states (italic mine):
3. Although the physiological significance of TNF-alpha regulating CL (corpus luteum) function during gestation is still obscure, TNF-alpha may play physiological roles in regulating CL function in the gestation period as well as in the estrous cycle.Good golly I wish I was a research scientist and understood all of this better. But what I'm getting is: the corpus luteum is a little blister-like object that is formed when the ovary pops out an egg halfway through the menstrual cycle (here's a good diagram about the cycle). It produces hormones that support a potential pregnancy, and it decays towards the end of the cycle if the egg isn't fertilized. What these researchers believe is that the CL formation, and perhaps the entire estrous cycle, are partially regulated by TNF-alpha.
And of course, as we all know, TNF-Alpha is what the Remicade blocks. It's a lead factor in inflammatory arthritis, as well as other autoimmune diseases.
So by my reckoning, for the last three years my little visitor has arrived at the end of my menstrual cycle... she arrives early and dances in the front yard lightly for about a week, but then moves in and trashes the house at about the time I would normally be expecting guests. But possibly, the Remicade has shortened her stay.
(Translated, I think I bleed lightly for the last week of my cycle, when the CL is disintegrating, and then I bleed heavily when my period should start. But with remicade, somehow the TNF-alpha blocking is shortening dear Aunt Flo's visit).
I don't know what to think here, except to feel grateful for a better understanding of why I've had these nasty periods for so long. I don't really know why TNF-alpha affects me in so many ways, but at least I can blame it for my heavy bleeding. And I now have a new topic for reading and speculation about autoimmune illness. Just think...some researchers now think some endometriosis is caused by flaws in the immune system!
I'm also quite curious as to what Remicade has in store for me and my bad house guest - maybe I can close up the B&B for a while.