So far, I've talked about the LPCR (late-phase cutaneous reaction, a.k.a. "delayed skin test") and to briefly summarize what I started in part I, the "conventional wisdom" on the LPCR is:  1.  We know the LPCR is a real phenomenon, but we don't know what it really means clinically 2.  The LPCR is not an "allergic response (in the IgE mediated sense of the term).   And because most allergists suffer from a lack of curiosity (and subsequent inattention to the patient's clinical history), they largely ignore the LPCR in the clinical setting.  And that's a shame.  Before I go any further, I'm going to wax a bit philosophical on you at this time, and give a quotation from Hindu Prince Gautama Siddharta, the founder of Buddhism, 563-483 B.C:

 “Do not believe in anything simply because you have heard it. Do not believe in anything simply because it is spoken and rumored by many. Do not believe in anything simply because it is found written in your religious books. Do not believe in anything merely on the authority of your teachers and elders. Do not believe in traditions because they have been handed down for many generations. But after observation and analysis, when you find that anything agrees with reason and is conducive to the good and benefit of one and all, then accept it and live up to it.”

Nowhere is this quote more appropriate than when we look at the LPCR...especially the part of the quote stating "do not believe in traditions because they have been handed down for many generations", but we should always use "observation and analysis" to come to the Truth.  Facing the truth sometimes requires change...

And allergists like change the way dinosaurs liked meteors. 

And please understand that what I'm going to tell you in my entry below, do not believe at face value...just as I have asked you not to believe the "conventional wisdom" at face value.  In short, check it out yourself, by your own careful observations of your patients. Be observant.  And be curious! 

Pearl #1:  When a patient has LPCR; their symptoms will follow the course of the LPCR. 

You like Tuesdays?  For me  they are one of the most interesting  work-days of the week.  Here's  why:  because when I see a patient has LPCR's on their testing, and they flare 24-48 hours later, it stands to reason that their symptoms will flare 24-48 hours later.  And I have a whole bunch of people who basically "hang out" at their desk job Monday thru Friday, and then on the weekend--often Sunday--they finally get down to "real work"--you know, sweeping out the root cellar or the garage, working on the compost pile, mowing the lawn, cleaning out the old leaves from the gutters, etc. etc. etc.  And you know what?  Often they have no reaction--for a while.  Then they have a rough nite sleeping Sunday, feel terrible Monday morning, get typically worse throughout the day, and end up talking to me on Tuesday.  So when you see a strong LPCR to any allergen, always query the patient about symptoms 12-48 hours after such an exposure in the future.  When the patient with a LPCR to dust sweeps the garage out, his most important symptoms will be 24-48 hours later, and he/she will have symptoms that you and your patient will likely miss unless you're observant and curious!  The same idea applies to the mold sensitive patient who tends their garden or mows their lawn--how do they feel 12-24 hours later?  48 hours later?  This idea is the single most important "pearl" I have learned from my patients regarding the LPCR.  

Pearl #2:  Symptoms in the patient with LPCR typically tend to be more systemic in nature than immediate skin test patients.  Of course, since this is a non-IgE mediated reaction, if you just "ask for" IgE symptoms like ocular itching, sneezing, etc. you usually won't see them.  Instead, if you query patients, you'll find they will complain of nasal/sinus congestion, progressive fatigue and flu-like symptoms, and sometimes headaches and neurological symptoms hours after an inciting exposure.  

Pearl #3:  Molds are the most characteristic inhalant to trigger LPCR's although they can occur from virtually any inhalant antigen.Virtually any inhalant can cause LPCR's but in our midwest location, I have seen that time and again that mold antigens are the overwhelming culprits.  I see alot of people with seasonal sinus congestion and seasonal malaise and aching in the spring and fall, and their immediate skin test reactions are disappointing.  But their LPCRs typically are NOT disappointing at all--especially to molds.  However, exceptions do occur.  For example, I can recall recently a  patient of mine with seasonal sinus congestion triggering migraine headaches each spring,  who ended up having extremely strong delayed reactions to tree pollens.  In fact, after we did IDT on her and she had no immediate reaction the day of testing, 12 hours later severe sinus congestion and eventual migraine ensuded; in retrospect these were likely precipitated by our prior skin tests.

Pearl #4:  When you see a patient in your practice "for a second opinion" who has had failed attempts at prior immunotherapy because of delayed reactions at their injection sites and trouble building up their dose, pay particular attention to the LPCRs that occur, and strongly consider SLIT as an alternative (more about this in part III).  As a consulting allergist, I often see patients for a "secocnd opinion" who have seen another allergist and had one or more failed courses of immunotherapy.  They haven't been able to build up their immunotherapy adequately, and one of the biggest causes is LPCR's.  As you'll see in my next journal entry, SLIT works slick for this problem, with a few caveats which I'll give later. 

Pearl #5:  If a patient has LPCRs to inhalants--such as molds, dust, or other antigens, they are "delayed reactors" and this will be their modus operandi for other allergens, such as foods.  Another big reason why patients aren't well after a course of immunotherapy is often a hidden food sensitivity, which in these types of patients is often of delayed-onset type, just like their inhalant sensitivities. 

Pearl #6:  If a patient has LPCRs to inhalants, the former sites of skin testing may exhibit a curious phenomenon of "memory", whereby a subsequent exposure to the offending allergen can cause inflammation and itching at the prior skin test site.  I have seen patients who had delayed reactions to molds, and sometimes dust, who on subsequent heavy exposure to their allergen will have pruritis and even some redness occur at prior skin test sites, even months after testing has occured.  Ingestion of food yeast can trigger itching at sites of prior skin tests to molds, and excessive regrowth of Candida in the body after antibiotics can trigger itching and redness at the site of a former Candida skin test.

As I have already mentioned, probably the greatest "pearl" I can give you with this journal entry is to not always accept at "face value" the "conventional wisdom" handed down to us but in your work with allergy patients, be curious, be observant, and analyze.  The rewards are great!