MCQp1a32

a.	is due to the presence of auto-antibodies	True
b.	affects phospholipid based coagulation tests	True
c.	anti-cardiolipin antibody should principally be sought	True
d.	is associated with recurrent miscarriage	True
e.	is associated with impaired fetal growth	True
f.	is associated with placental abruption	True
g.	is associated with an increased risk of thrombosis	True

This is a condition in which one finds auto-antibodies that predispose to serious disease, particularly vascular thrombosis.

They prolong phospholipid based coagulation tests such as the activated partial thromboplastin time (APTT) and kaolin clotting time (KCT).

The main culprit is anti-cardiolipin antibody (ACA), but lupus anticoagulant may also occur.

The condition may be primary or secondary.

Primary means that the anti-bodies are present without a specific auto-immune disease, such as systemic lupus erythematosis.

With secondary, there is obviously a recognised auto-immune disorder, usually systemic lupus erythematosis.

There is an overlap with Systemic Lupus Erythematosis.

Some patients with SLE will have Lupus Anticoagulant (LA), which, despite its name, is associated with thrombosis.

Patients with LA or ACA, or both, have an increased risk of miscarriage, mostly occurring in the first trimester.

So screening for LA and ACA should be done in all patients with recurrent miscarriage.

It is reckoned that about 15% of women with recurrent miscarriage will have APS.

Low dose aspirin and heparin have been shown to improve the prognosis in a couple of trials.

They are standard management at the time of writing .

As if the increased risk of miscarriage was not bad enough, pregnancies that get beyond that stage are at increased risk of:

abruption,

severe growth retardation

and premature delivery,

with consequent increased perinatal mortality rates.

The combination of heparin and aspirin appears to reduce the incidence of late pregnancy complications.

It has been thought that APS caused its mischief through increased placental thrombosi.

But, not every case with adverse outcome has been shown to have evidence of thrombosis within the placenta.

It is now believed that the adverse effects are more protean, with APS:

adversely affecting development of the decidua and trophoblast,

interfering with HCG production

and impairing the key phenomenon of trophoblastic invasion of the spiral arteries.