Okay, with nothing better to do, I thought I would research the issues I think are causing my miscarriages. The two problems (that we've found at least) are MTHFR mutations and Protein S Deficiency. Maybe this can help someone else diagnosed with these. This stuff scares the crap out of me! Here it goes...
MTHFR (Methylene-Tetra-Hydro-Folate-Reductase) mutations- it is important that you find out which category of this mutation you fall under. This mutation could be either:
a) heterozygous (there are two parts to this gene, and each part has two parts, so there is a possiblity of 4 places for mutations. Heterozygous means you have one mutation on one part of the gene. This is the most common and impacts you the least),
b) compound heterozygous (this would be one mutation on each part for a total of two mutations. This would be a little more serious, but still fixable), and
c) homozygous (this is when you have both mutations on one part. This is the most serious of the mutations)
I did some more research and found an interesting site (which I lifted this info from).
"First, with MTHFR, there are two different kinds of mutations, as you've said, and it's possible to be "heterozygous," "compound heterozygous," or "homozygous."
The most severe MTHFR problems occur with homozygous C677T, meaning two copies of the "C" mutation. Next most serious is compound hetero, which means one copy of the "A" mutation and one copy of the "C" mutation. (LUCKY ME!) Next most serious is one "C" mutation. After that, it's two "A" mutations. The least serious is a single "A" mutation.
Any and all of these mutations can affect homocysteine levels, but there is much dispute as to whether elevated homocysteine levels are actually needed in order for MTHFR to cause trouble. Many other MTHFR patients have normal homocysteine levels, yet have had implantation problems and/or m/c's due to clotting problems. So it is important to find out your homocysteine levels (although again, normal doesn't necessarily mean all is well). This is a serious field and MTHFR is a serious condition, so consulting an expert is wise.
http://www3.fertilethoughts.com/forums/showthread.php?t=351238
Heterozygous MTHFR is fairly common in caucasion populations and is the "lesser" of the mutations. Compound heterozygous and homozygous MTHFR have definitely been linked to implantation failure, late term miscarriages and overall vascular health and also anything dealing with birth defects that lack of folic acid can cause. Which ever type of MTHFR you have, it should not be discounted.
Essentially what this means is that the genes that instruct MTHFR to convert homocysteine to Methionine are mutated and may not be capable of doing this important function. MTHFR is an enzyme that converts homocysteine to an essential amino acid (methionine). When the genes are mutated you may be lacking this enzyme. Your homocysteine levels can possibly climb making the blood clot. Some doctors don't check for the MTHFR mutations and rely only on homocysteine levels. This isn't as reliable as testing for the mutations because homocystein levels fluctuate (if you catch your level on a normal day, you may go undiagnosed).
Many doctors prescribe folgard which is high levels of folic acid, b12 and b6. These vitamins are what the body essentially needs to convert homocyteine to methionine. To put this into perspective, the average prenatal has 800mcgs of folic acid (200% of the normal daily value). I am compound heterozygous, and I am required to take 5mgs of folic acid/b vitamins (6 times more than the prenatals have in them plus the prenatal!) --compiled by "Sparkle"
Protein S is a vitamin K–dependent anticoagulant protein. It is apparently quite rare to have this deficiency (lucky me!). According to my protein s activity test, my levels are at 29% with the normal range above 60%.
Protein S deficiency also is associated with fetal loss in women, in the absence of VTE (venous thromboembolism which occurs when red blood cells, fibrin, and to a lesser extent platelets and leukocytes form a mass, clot, within an intact cardiovascular system). Some authors suggest that as many as 40% of women with obstetric complications other than VTE may carry some form of thrombophilia. Protein S deficiency is one of these factors along with several other more common genetic thrombophilic states.
Protein S deficiency was also associated with a 7-fold increase in fetal loss.
Many experts recommend that women with protein S deficiency and a history of fetal loss, and severe or recurrent eclampsia, receive low-dose aspirin and prophylactic dose LMW heparin during pregnancy, and the LMW heparin should extent for 6 weeks postpartum.
For women with heterozygous protein S deficiency some recommend prophylaxis for the entire pregnancy and 6 weeks postpartum.
For women with no prior history of VTE and protein S deficiency plus any other thrombophilic defect, active prophylaxis with LMW heparin should be given during pregnancy and for 6 weeks postpartum.
I think that is it for now. Here is a link of where I found the protein s info
http://www.emedicine.com/med/topic1924.htm
My husband took my first belly shot last night. I still have quite the bloat from all of the IVF stuff (or maybe it's all that food?), so I don't know if it is from the meds or the babies exactly. Surely something that is only 7-9mm couldn't make me that big, right? Even if it is times two? It should be interesting to see how I grow as I get further along. Wow. That sounds so strange as I write it. All this is still a little surreal...
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