This condition is rarely compatible with life

I am making this public. Because, I am hoping someone has suffered the same thing, or understands where I am coming from, or might have some more insight for me…. Please, if you do, reach out to me. I need to know, esp right now more then anything, that I am not alone in this.

It has nearly been a yr since I was diagnoised with AT III.

And we know no more now, then we did then. Today has rendered me a mess. Mainly, thanks to the fact I dont feel well, and my INR is still low… which is scary enough. But, words like my title… make me think. To this date, we have decided I do not have the inheritated form of AT III. I possibly have the rare, less compatible with life form.If that is the case, I have beat the odds this far. Most babies with AT III dont live into adult hood. So, Im would be a rare breed, obviously.

There is also a possiblity its DIC. DIC is Disseminated Intravascular disorder. You want to know what they say about this one? "Disseminated intravascular coagulation (DIC) is not a specific diagnosis, and its presence always indicates another underlying disease. There are many diseases that may lead to the occurrence of disseminated intravascular coagulation (DIC)."

The listed causes:

• Bacterial infection, in particular septicemia, is commonly associated with disseminated intravascular coagulation (DIC). No difference exists in the incidence of disseminated intravascular coagulation (DIC) in patients with gram-negative sepsis or gram-positive sepsis. In addition, systemic infections with other microorganisms, such as viruses and parasites, may lead to disseminated intravascular coagulation (DIC) as well.
• Factors involved in the development of disseminated intravascular coagulation (DIC) in patients with infections may be specific cell membrane components of the microorganism (lipopolysaccharide or endotoxin) or bacterial exotoxins (eg, staphylococcal alpha toxin). These components cause a generalized inflammatory response, characterized by the systemic occurrence of proinflammatory cytokines.
• Severe trauma is another clinical condition frequently associated with disseminated intravascular coagulation (DIC). A combination of mechanisms—including release of tissue material (fat, phospholipids) into the circulation, hemolysis, and endothelial damage—may contribute to the systemic activation of coagulation. In addition, solid evidence indicates that cytokines play a pivotal role in the occurrence of disseminated intravascular coagulation (DIC) in trauma patients as well. In fact, systemic cytokine patterns have been shown to be virtually identical in trauma patients and septic patients.
• Both solid tumors and hematologic malignancies may be complicated by disseminated intravascular coagulation (DIC). The mechanism of the derangement of the coagulation system in this situation is poorly understood. Solid tumor cells can express different procoagulant molecules, including tissue factor and a cancer procoagulant, a cysteine protease with factor X–activating properties. Cancer procoagulant is found in extracts of neoplastic cells and in the plasma of patients with solid tumors.
• Some tumors are associated with a form of disseminated intravascular coagulation (DIC) that is characterized by severe hyperfibrinolysis on top of an activated coagulation system. For example, this is the case in acute promyelocytic leukemia and some forms of prostatic cancer. Although clinically bleeding predominates in this situation, disseminated thrombosis is found in a considerable number of patients at autopsy.
• Acute disseminated intravascular coagulation (DIC) occurs in obstetric calamities such as placental abruption and amniotic fluid emboli. Amniotic fluid has been shown to be able to activate coagulation in vitro, and the degree of placental separation correlates with the extent of the disseminated intravascular coagulation (DIC), suggesting that leakage of thromboplastinlike material from the placental system is responsible for the occurrence of disseminated intravascular coagulation (DIC).
• Although the coagulation system may be activated in patients with preeclampsia, and HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome, clinically significant disseminated intravascular coagulation (DIC) only occurs in a small percentage of patients, usually with secondary complications.
• Vascular disorders, such as large aortic aneurysms or giant hemangiomas (Kasabach-Merritt syndrome), may result in local activation of coagulation. Activated coagulation factors can ultimately "overflow" to the systemic circulation and cause disseminated intravascular coagulation (DIC) but more common is the systemic depletion of coagulation factors and platelets as a result of local consumption.
• Other causes of disseminated intravascular coagulation (DIC) include severe toxic or immunologic reactions (eg, transfusion reactions) or severe inflammation (eg, acute pancreatitis).

So, there is that possiblity, as well.

At this point>? I would welcome death. I will be writing up a will, very soon, to dictate where James would go in the event of my death. As much as I love my mom, I cannot send him to her. For one, my own child rasing seems to leave me lacking… and for two… I have a fear she will be dead in the next few yrs. I am already surrounded by death, unnaturally. I do not want him growing up in the same enviroment.

*sighs* I wish these drs would figure it out, so I could stop worrying.

I have had 7 strokes in the last yr. Mostly subtile, but some, not so much, like the most recent one, which has left me feeling awfully disconected.

Please note, if something is to happen to me? My sister will have access to this diary, and anything else I have, with instructions to post of my death, and within two weeks of that post, to delete EVERYTHING. (Aside from myspace and facebook, which will be turned into a memorial like I have done with Felix.)

Also, I found this: Women of childbearing age are of special concern. Antithrombin III deficiency, like other congenital procoagulant defects, may contribute to an increased risk of spontaneous abortions. Particularly in cases of fetal or umbilical thrombosis as the cause of the miscarriage, consider antithrombin III deficiency, along with protein C or protein S deficiency and AP antibody syndrome.

After my last hospitalization, they decided I had protein S and C deficienies. Heh. Both, resolved. The only thing left is the AT III which will never go away.

*SIghs* Its all starting to make sense. Its pretty damn sad when the patient knows more then the drs.