Sunday, June 7, 2009

Revisiting the diagnosis

Two years ago, when I was living on the Left Coast and first got the news that I sort-of had antiphopholipid syndrome (I'll explain that in a sec), my reproductive endocrinologist told me that, while she didn't expect me to exhibit any symptoms of APS outside of my tendency to miscarry, I should have annual blood checks to make sure my antibody levels didn't go through the roof. Also, I should make make sure I wasn't developing any of the antibodies associated with lupus, which sometimes exists concurrently with APS (though the relationship isn't thought to be causal).

So that was two years ago, and last year I was busy having Sam (yay!) and didn't get checked. But I went back a few weeks ago to meet with a rheumatologist here in my East Coast city.

If there's one thing your doctor likes to tell you when you show up with an autoimmune disease, it's that "there's still so much that we don't know." Here's a summary of what I've learned so far:

1) To get a diagnosis of APS, you have to meet both clinical and laboratory criteria. Clinical criteria include venous or arterial thrombosis and/or pregnancy losses (specifically, one or more miscarriages after 10th week of gestation, three or more miscarriages before 10th week of gestation, or one or more premature births before 34th week of gestation due eclampsia). To meet lab criteria, you have to test positive for anticardiolipin or lupus anticoagulant antibodies on 2 occasions of some weeks apart (6 to 12 weeks, depending on which antibodies they're looking for).

2) My particular problem antibody is of the anticardiolipin sort -- specifically, IgM (Immunoglobulin M). IgM and IgG antibodies are measured in the following way: fewer than 12 units = normal; 12 to 20 units= borderline; 20 to 80 units=moderate; more than 80 units=severe. My understanding is that lupus anticoagulant antibodies are a binary thing: either you have them, or you don't.

3) APS (also called Hughes Syndrome) can be quite a serious disease in some people, but there's a current line of thinking that there may be a population of women whose only symptoms are pregnancy-related. That is, they don't appear to be in danger of pulmonary embolism or thrombosis outside of pregnancy.

I've now had my IgM antibodies measured four times. After the miscarriages, they came in at 21.2 and 21.6, measured 7 weeks apart. During my pregnancy with Sam, while I was taking Lovenox, they were at 16. At my most recent visit, they were 19. It looks like I have a "mild" case. I've "only" had 2 miscarriages. No clots. docs on the left coast felt that while I was a borderline case, they should still treat me as if I definitely had APS. And so I went on Lovenox as soon as I knew I was pregnant with Sam. And it worked.

But the rheumatolgist here, who doesn't specialize in APS or miscarriage, wasn't as convinced. "Your levels are so low," she said. "Who knows if those first two miscarriages were just a matter of bad luck? And it's not like there aren't risks to being on blood thinners. I'm not sure if I'd even want you to be on Lovenox if you get pregnant again."

But, of course, if I get pregnant again (something Adam and I are discussing only in vague terms, with no final answer), I'll get right back on my vitamin L. Maybe it was just a matter of luck that this pregnancy worked. Maybe my ovaries are shaped like little roulette wheels. But I'm pretty convinced the drugs saved Sam's life, and in the matter of reproductive endocrinologist v. rheumatologist, I'm going to listen to the people with the better track record of bringing healthy babies into the world.