This is interesting. I read an article somewhere (wish I could find it again) that oral dhea works better for raising free test and sublingual was best for elevating DHEA-S levels. Maybe that's why you got an E2 spike.
Oral is notoriously unstable as it passes the liver and it is impossible to predict any conversion. What you are referencing is likely the following, which does outline the differences in administration. This general information is available readily through various publications.
Topical DHEA
If personal biochemistry does not allow for DHEA-S to be readily converted to DHEA, the topical route may be preferred.
When administered topically, DHEA restores skin elasticity, relieves symptoms of vaginal dryness and atrophy (with vaginal application), and generally improves many low-androgen symptoms [16]. The caveat with topical DHEA administration is that it does not undergo first-pass metabolism through the liver (no liver passage - no sulfation), so although a subsequent increase in salivary and blood spot DHEA is observed, DHEA-S levels remain unchanged. The levels of the hormone in saliva represent the "free" hormone fraction, available for tissue uptake. Animal studies show that with topical DHEA treatment, the unsulfated DHEA crosses into the brain and gives rise to DHEA-S right on site. With topical DHEA supplementation, the practitioner has to rely on monitoring the patient’s progress with improving symptomatology, which may be a challenge in and of itself. If low androgen symptoms persist with topical DHEA treatment, switching to oral dosing may prove to be a more effective strategy. It is important to know that topical DHEA therapy will raise serum and salivary DHEA levels, but have little effect on DHEA-S levels in these body fluids.
Oral DHEA
With oral DHEA administration we see a substantial spike in DHEA-S levels in all commonly tested body fluids (saliva, blood spot, serum, or urine) (undergoes first-pass metabolism and gets sulfated), and a marked improvement in symptoms as well. However, once DHEA becomes sulfated to DHEA-S, it is unable to cross the blood-brain barrier (DHEA is non-polar and crosses the blood-brain barrier easily, whereas DHEA-S is polar and does not cross into the brain from periphery). It is plausible to assume that DHEA-S that arises from first-pass metabolism after oral DHEA administration behaves in a similar manner to endogenous DHEA-S and contributes to the body’s biological reservoir of DHEA, readily converting to DHEA when the need arises.
Troche DHEA
How you take DHEA definitely impacts how much gets into the brain and how fast. For example, troche (sublingual) DHEA goes directly into the bloodstream (measured in serum) and because it’s not sulfated, it crosses directly into the brain and other tissues. Some patients are particularly sensitive even to small amounts (5 mg) of DHEA administered this way - with agitation being a common side effect. In this case, taking DHEA orally could have a more gentle uplifting sensation of wellbeing.