I note that pre eclampsia is caused by damage to the placenta.

When you have LOCAH, because you can make a good percent of cortisol, but never quite enough, you in fact are always in effect "short" on cortisol, no matter what time of day or level of stress, activity or whatever.  In pregnancy, stress on the body steps up and especially in the last trimester.  Cortisol levels are usually elevated in fact in late pregnancy.  What I feel happens for LOCAH is that the adrenals never let up and are constantly being agitated to make more cortisol --and because they never really make the grade where the pituitary gland is concerned, you get this situation where the cortisol levels can quite rightly seem to appear in the normal ranges.  however, this is only because of continuous over stimulation of the adrenals.  That in itself is not normal really--adrenals are supposed to have resting phases not be active all the time.  So taking the cortisol or ACTH levels do not really give one the picture of what is truly happening.  Of course elevated cortisol levels means elevated blood sugar and blood pressure and this goes cap in hand with pre eclamsia unfortunately which is why you would have been pre disposed to such--that and premature labour.

The very reason that LOCAH goes undiagnosed for so long in the past is that they seem to rely  on taking the ACTH and cortisol levels alone, which really would have appeared to be quite normal in most cases because of the above reason.  However, if Doctor’s just checked the 17 OHP and other anabolic hormones, they would find the "real" answer.  You have to imagine that since you can make a good deal of cortisol, the percentage that you cannot convert from cholesterol to cortisol is somewhat larger than the percentage left when a person with normal functioning adrenal glands makes cortisol.  So therefore the protion of cholesterol that is pushed fown that metabolic pathway to be converted to 17 OHP for LOCAH people, is slightly more than that shuttled down by the person with healthy adrenal glands.

Meanwhile the elevated 17 OHP is busy being converted to other androgenic steroids which are ALSO not exactly condusive to pregnancy either.  For example if we know that cortisol levels are higher at the end of pregnancy normally, we also know for certain that estrogen is at it’s highest, as estrogen favors those type of conditions.  Mother natures way of making us slow down and add a layer of fat for breastfeeding and whatever.  So higher than normal ababolidc steroids are out of place in that environment and could probably affect the placenta to my mind.  I mean post natally the estrogen levels go down and then we start to lactate which is caused by the plummet in not just estrogen but also the hormone changes in labour even. 

Also you may be interested to know that hormones linked with premature labour and causing contractions is prostaglandins which are released in response to a rise in other hormones such as anabolic I believe.  They are immune system stimulants, they cause muscles to contract, trigger inflammatory responses, assist with calcium absorption, prevent cholesterol from building up in the vessel walls, lubricate connective tissue and mucous membranes and moisturise dry skin. It is all sort of a culmination of things that generally occurs at 40 weeks gestation, but I guess it makes sense that if you start to have a rise in the other steroid sooner than 40 weeks, all the labour thing is brought forwards to an ealier time.