SLE and pregnancy?

Started by as90
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as90

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Hi,
Just had a weird question about the SLE and I'm still not understanding what is taking place. Apparently there are suppose to be anti-tpa antibodies in SLE, yet PTT is prolonged? The woman miscarriages the fetus. Apparently, there is a hypercoaguable state yet I thought you have lupus anticoagulant.

Sorry for the vagueness, but is there something similar to DIC that is observed with these individuals that predisposes them to not be able to carry to term?

Trying to reason through the clotting cascade to figure this out and don't quite see how PTT is long yet PT is normal. Was originally thinking some type of hemophilia but the answer was SLE.

Any advice appreciated.
 
Hi,
Just had a weird question about the SLE and I'm still not understanding what is taking place. Apparently there are suppose to be anti-tpa antibodies in SLE, yet PTT is prolonged? The woman miscarriages the fetus. Apparently, there is a hypercoaguable state yet I thought you have lupus anticoagulant.

Sorry for the vagueness, but is there something similar to DIC that is observed with these individuals that predisposes them to not be able to carry to term?

Trying to reason through the clotting cascade to figure this out and don't quite see how PTT is long yet PT is normal. Was originally thinking some type of hemophilia but the answer was SLE.

Any advice appreciated.

You'll never get tested on the mechanism for this. The only thing they want you to know is what you've said in bold: SLE increases the chance of miscarriage.
 
Hi,
Just had a weird question about the SLE and I'm still not understanding what is taking place. Apparently there are suppose to be anti-tpa antibodies in SLE, yet PTT is prolonged? The woman miscarriages the fetus. Apparently, there is a hypercoaguable state yet I thought you have lupus anticoagulant.

The term "lupus anticoagulant" is a misnomer in vivo. I don't know if you have Pathoma but Sattar explains it in the lupus section in there. Like Pholston said, just remember what happens and don't get thrown off by the "anticoagulant" in the name.
 
Per Goljan RR, SLE is associated with anti-phospholipid syndrome which consists of anti-cardiolipid antibodies, anti-B2-glycoprotein antibodies, and lupus anti-coagulant. As said, lupus anticoagulant is a misnomer because it only prevents coagulation in vitro, but causes coagulation in vivo. All 3 antibodies listed above are associated with SLE and cause thrombosis/coagulation. Thrombosis of any of the arterial supplies to the fetus (ie. umbilical veins) or the intra-fetal blood vessels will produce ischemia and subsequent death of fetus.

Another HY association between SLE and pregnancy is heart block following seepage of IgG anti-SS-A into the fetal blood supply.
 
Per Goljan RR, SLE is associated with anti-phospholipid syndrome which consists of anti-cardiolipid antibodies, anti-B2-glycoprotein antibodies, and lupus anti-coagulant. As said, lupus anticoagulant is a misnomer because it only prevents coagulation in vitro, but causes coagulation in vivo. All 3 antibodies listed above are associated with SLE and cause thrombosis/coagulation. Thrombosis of any of the arterial supplies to the fetus (ie. umbilical veins) or the intra-fetal blood vessels will produce ischemia and subsequent death of fetus.

Another HY association between SLE and pregnancy is heart block following seepage of IgG anti-SS-A into the fetal blood supply.

So I'm curious why this is the case in vitro? I too got the ame question as the OP, I was able to narrow it down to whether or not a 1:1 mixing study would fix this.

Of course there was no mechanism mentioned in the answer and all google returned was vague articles so I decided to go with the rote-memorization route, but I might actually be able to recall it if I can understand it.
 
So I'm curious why this is the case in vitro? I too got the ame question as the OP, I was able to narrow it down to whether or not a 1:1 mixing study would fix this.

Of course there was no mechanism mentioned in the answer and all google returned was vague articles so I decided to go with the rote-memorization route, but I might actually be able to recall it if I can understand it.

Understanding, he wants. Memorization, he needs. -Yoda.
 
Useful add-on to this is that if you do a PTT mix (add some normal subject's plasma to your pt w/ lupus anticoagulant plasma), the PTT prolongation will not correct in contrast to a PTT mix on a patient with factor VIII deficiency (normal sample provides coag factors).
 
Useful add-on to this is that if you do a PTT mix (add some normal subject's plasma to your pt w/ lupus anticoagulant plasma), the PTT prolongation will not correct in contrast to a PTT mix on a patient with factor VIII deficiency (normal sample provides coag factors).

This was very high-yield on the Immuno Pathophys test :naughty:
 
Useful add-on to this is that if you do a PTT mix (add some normal subject's plasma to your pt w/ lupus anticoagulant plasma), the PTT prolongation will not correct in contrast to a PTT mix on a patient with factor VIII deficiency (normal sample provides coag factors).

Someone with factor VIII deficiency isn't going to be worked up because he has a high PTT. He's gonna get worked up because he's bleeding like a mother****er. Totally opposite presentation than someone with lupus anticoagulant. No way it's in the differential diagnosis.

Cool trivia, but I can't see them writing a board question based on mixing results. "Man walks into your clinic with a lab paper saying high he has a PTT, what do you do next..." I doubt it. They're going to start from the basis of if he's clotting or bleeding.
 
Someone with factor VIII deficiency isn't going to be worked up because he has a high PTT. He's gonna get worked up because he's bleeding like a mother****er. Totally opposite presentation than someone with lupus anticoagulant. No way it's in the differential diagnosis.

Cool trivia, but I can't see them writing a board question based on mixing results. "Man walks into your clinic with a lab paper saying high he has a PTT, what do you do next..." I doubt it. They're going to start from the basis of if he's clotting or bleeding.

The way it can get presented though (slightly off topic but in pathoma) is when you have a factor VIII deficiency (Hemophilia A) vs acquired coagulation factor inhibition (anti-factor VIII usually). Same mechanism, exact same presentation except the mixing tests are different.

So yeah in that situation the right answer would probably be on there as acquired coag factor inhibition.
 
I definitely agree with that presentation. Anti-VIII autoantibodies versus Hemophilia A seems like a fair question for the use of mixing studies.