It's Wednesday morning at 10:15 AM.  And you're sitting in your allergy office with Mrs. X, a doctor's wife.  Frankly, you'd rather be somewhere else.  Anywhere-else.  In fact, very frankly, you'd like to be as far away from Mrs. X as humanly possible.  Because Mrs. X. isn't an atopic patient loaded with IgE.  And that means only one thing:  Trouble--trouble with a capital T. 

When Mrs. X. presented to your office yesterday, she complained of seasonal chronic sinus congestion in the spring and in the fall.  So you  tested her and found negative prick tests to all allergens, but just to "make sure" you had done some ID's to molds as well.  Fortunately, she had only a slight reaction which you told her was "insignificant"--you were secretly glad because you knew that injection immunotherapy doesn't do squat for mold allergy anyway.   You confidently told her that she "had no allergy", gave her the latest, greatest flavor-of-the-day nasal spray with the most colorful box you could find, and sent her on her way, reassuring her that all was well.  After all, you'd get reimbursed for the skin tests by her insurance company, and she got a free nasal spray sample out of it as well.  Life is good... Schazam!--Another case solved...

Then, unfortunately, she called you back early this morning, and that's when the problems began... after leaving your office she said later that evening she began to notice some  "strong reactions" at the sites of some of her former intradermal mold tests; they continued to grow overnight and now she feels miserable today after her prior testing the day before. In fact, she feels exactly like she feels during a bad day in the spring or fall mold seasons.  So she's now back in your office demanding an explanation as to what these events mean, and expects you to treat them.   

So now what?

Near as I can figure, you've got  3 choices on what you could do at this point: 

a:  you could let your p.a. see her and duck out the back door

b.  you could tell her that "we don't know what the "late phase cutaneous reaction" (LPCR) means" and ask her what she's got against using the latest & greatest nasal spray you gave her yesterday--and lay a heavy bill on her for good measure

c.  you could explain that her LPCR's mean she is a delayed reactor, explain the nature of her symptoms--that they correlate with the time course of the LPCR-- and treat her effectively with SLIT

If you scored "c" you're the sharpest tool in the shed.  Because SLIT works for LPCR's.  And I mean it really works... But to do SLIT on LPCR's you first have to get an idea of "how strong is strong?" for the LPCR.  You need to calibrate it, through doing three very basic things:

1.  Do repeat testing with serial IDT on the items she had LPCR to.   

2.  Observe at 12, 24, 48 hours.

3.  Start SLIT at the strongest IDT titration that is negative for LPCR.  That is, if she had positive LPCR's which swell at 24-48 hours on dilutions 2 & 3, and none at 4, then start SLIT at 4. 

Never "buildup" or give "high dose" SLIT treatment (like the European preseasonal rush protocols) to a patient with LPCR's and no immediate skin test positivity.  European preseasonal rush protocols work great for the atopic patient--I've done plenty of them--but they spell disaster for non-atopic patients with LPCR's.  When treating the LPCR, only go stronger on SLIT  if you repeat the testing first, and firmly establish that a higher dilution now causes no LPCR like it had previously done on earlier testing.  Only then can you could step up to the next higher dilution.  Remember:  this isn't IgE mediated sensitivity.  You don't need high dose treatment.  Low dose treatment at the threshold of the LPCR is enough. 

As mentioned earlier in this series, SCIT (not SLIT) for patients with immediate AND delayed reactions has been shown in 4 controlled trials to result in a reduction in delayed reactions.  SLIT does the same.  However, for patients with no immediate reactions, but a strong LPCR, SLIT is the way to go. You can successfully treat these patients. Over the years I've effectively treated LPCR's to dust, mold, and the occasional pollen that gives strong LPCR's but no immediate reactions--all with virtually no side effects and great clinical response.  Generally, over time, when repeat testing is done in a patient on SLIT, a reduction in LPCR's occurs, as evidenced by observing stronger IDT dilutions required to have any LPCR at all. 

And it works.  Believe me, dude, it works. 

I've been using variations of this approach for "problem" patients like Mrs. X for 25+ years, and I've found SLIT is the only thing that effectively addresses LPCR's to molds, dust, or pollens when there is a minimal immediate reaction or none at all, and the majority of the reaction is delayed.  And patients love it.  I love it because I no longer dread seeing Mrs. X.  And Mrs. X in turn thinks I  walk on water and sends all those atopics to me that I so lust after.  And life is good afterall...