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Eaton's Sign

 Clinical medicine--including the specialty of allergy-- is about sight, touch, smell, and hearing--not just about the latest medical article we've read in the Annals of Allergy or JACI.  One thing we've tended to underemphasize  in our profession is late-phase skin test reactions--something we can see and touch hours after the test has been applied--if we just look for them.  But there is another  item that I've never seen described or documented in the lilterature--and that is the curious phenomenon of intradermal skin test "recall" days or even months after intradermal skin testing was done.  Under certain occasions, it seems as if the site where a skin test was formerly applied  retains a "memory" for furher reaction  when a similar antigen is encountered in our environment many days later. 


What do I mean?  For example, I've seen patients receive intradermal skin tests for molds, and end up with strong delayed rections to them.  Upon getting a subsequent  airborne mold exposure many days later, (for example, mowing the lawn), the patient may note pruritis and swelling at the site of his former tests.  If you ask patients about this phenomenon, they will frequently volunteer that it does indeed occur.  Interestingly, I had a chance to examine this phenomenon first-hand in my office one day, in  a patient who I had previously tested for mold allergy.  She had had strong delayed reactions to mold when I initially tested her. .  When she saw me, she had just had a major symptomatic mold exposure the day before.  On her arm, there were faint areas of erythematous swelling and puriritis where I had previously tested her to mold on an earlier occasion.   

I'd like to call this phenomenon "Eaton's Sign", named in memory of the late Dr. Keith Eaton, M.D. 

I remember meeting Dr. Eaton in Manchester, England, when he excitedly came up to me and asked if I thought that heavy mold exposure could trigger depression in susceptible individuals.  He was one of the earliest members of the BSACI (British Society for Allergy and Clinical Immunology), and a student of Professor Jack Pepys. He was a prolific writer, publishing some 80 papers, and specifically wrote about the delayed reaction to molds on intradermal testing,  and described it thoroughly in his publications.  He felt the delayed mold reaction, although obscure in cause, was "not without biological significance".  In retrospect, his interest in mold was probably stimulated by his wife Susan's serious illness from mold, and a serious case of "dry rot" in his house!  He was a consumate clinician and researcher, who tragically passed away with pancreatic cancer.  Dr. David J Freed has this to say about him in his memorium:  

 

As a doctor he was loved by his patients—they too could not get a word in edgeways, but did not seem to want to either because Keith intrigued and entertained them as well as giving sound medical advice. When lecturing at formal medical gatherings he used an impish sense of humour to illustrate points that might otherwise have been difficult for doctors to comprehend, as, for example, his famous comment on the cause of atopic eczema. To judge by the prescribing behaviour of doctors, he dryly noted, it must be caused by betamethasone deficiency! He was also multitalented, and few of us saw all sides of the man. Whatever he turned his attention to he became absorbed in and became good at, whether it was painting, sculpting, or restoring vintage cars (during his general practice years he could often be seen, on dry days, driving his open-top Alvis or Gilbern around the practice to visit patients, fully kitted out in goggles, beret, and huge motorman’s gloves...
So what do we know about Eaton's sign?  A few intriguing points I've found:

1.  It only occurs after intradermal--and not prick--testing.  A heavy dose of antigen is needed.
2.  It mainly occurs in patients who have experienced delayed "late phase" intradermal reactions.
3.  It mainly occurs with either dust or mold.  It may occur with pollens but I'm not sure I've seen it
4.  The sign consists of pruritis, and sometimes observable swelling and erythema at sites of previous intradermal        tests to mold or dust mite, upon having a recent relatively heavy exposure anywhere in the preceeding 24-48 hours.  
5.  The onset of the reaction may be variable, and may occur within minutes of the subsequent allergen exposure.  
6.  This phenomenon may be a variant of the "fixed drug eruption site" phenomenon observed by dermatologists...

So Keith, I say "Thanks for the memories"...and this sign's for you....

Later, Dude











 


Posted on Sunday, October 5, 2008 at 02:30PM by Registered CommenterGeorge F Kroker MD FACAAI in | Comments4 Comments

The Tale of the Storyteller: A Case Report

Throughout our lives, allergists listen to tales...and in the end, we become a storytellers, full of fascinating clinical viginettes from our experiences in caring for allergy patients.  A recently article, entitled "The tale of the Allergists life:  A series of interesting case reports" by Ray Slavin, M.D.  in Allergy Asthma Proc. 2008 Jul-Aug;29(4):417-20, emphasizes this fact.  A few quotes from the article are worth noting:

"The practicing allergist has the unique opportunity to see an extraordinary variety of fascinating patients.  Identifying the precise cause of the patient's complaints makes for a satisfying intellectual endeavor...To get to the heart of the matter, rather than simply starting a new drug or increasing the dose of the present medications, makes for an intensely gratifying intellectual experience and one that also benefits the patient.  What a great way to make a living!"
It is ironic that one of my most interesting tales comes from an elderly man I met, who was actually a professional storyteller (and flute-player).  It was a pleasant day in March of this year, when I turned the doorknob and entered the exam room.  

 

"I want help with my neuropathy", he said.  "I've been to the University of XX and after a detailed workup, they diagnosed idiopatic neuropathy.  I began gabapentin in 2005.  I continued with my symptoms and saw another neurologist for a second opinion, and after a further series of tests, I was given Lyrica to counteract the pain in my feet and legs in 2006.  However, Dr. X is questioning the diagnosis of peripheral neuropathy, because I have tingling in my face, neck and back as well as my feet and legs, and he prefers to call it an immune or inflammatory neuropathy."  

 

"I began weekly infusions of one gram of methylprednisolone in April of last year (2007), and these were changed to every other week in June of this year (2008).  I immediately noticed benefits--dramatic lessening of need to take Gabapentin for pain, I had better balance, and a return of skin sensitivity where I was previously numb." 

 

"Tell me about your current symptoms", I said.

He looked at me sadly, then began:

"I have a real struggle with my balance for the last couple of years, but the big thing is that I have terrible numbness and  tingling in the legs and feet, below the knees.  There is tingling, and some pain however, in all areas above the knees, including the face, neck, back, hands, and arms. The feet and lower leg pain and numbness is present most of the time, but can be reduced by the steroid infusions, which reduce the need for pain meds consideratly.  I take the infusions on Monday and initially get good relief, but by Thursday, the pain and tingling in the lower legs recurs with a terrible vegance."

 

"Tell me about your alcohol ingestion", I said.  

He looked at me.  

"I'll be honest with you.  I had considerable alcohol consumption from about 1966 to 1975, then a period of no consumption lasting until about 1983.  Then I again had heavy consumption lasting until about 1995, then again a period of no consumption for 4 years.Then I began to drink heavily again, and haven't had a drink since Feb of 2004.  I attend AA meetings now."  

 

"Any respiratory problems?" I asked.

"I've got some nasal drainage and cough in the fall, but that's a minor issue" he said.

 

"How about your diet and your intestinal function?" I asked.

"Well, I am bothered by alot of intestinal bloating and gas" he admitted.  "I've also found that some foods aggravate my pain--yogurt, peanut butter, nuts, citrus all intensive the symptoms in my feet and legs so I avoid them. "

 

I looked at the personal questionnaire he had typed out before the visit.  He had a litany of problems in addition to his presenting one:  glaucoma, rosacea, gout, sleep apnea, venous stasis dermatitis, tinnitus, hypertension, and a prior history of nasal polyposis.  

When I examined him, he needed a cane for walking, and although his Romberg was intact, he had a very unsteady heel-to-toe walk, for which he needed assistance.  He had decreased knee reflexes bilaterally, but at the time of exam, sensory exam was intact to light touch on both legs.  Pedal edema was noted bilaterally.  Mild pharyngeal posterior nasal drainage was seen.  

                                  Tests:

IgG RAST:

Egg--Class II

Dairy--Class II

Wheat--Class I

Corn, peanut, soy, yeast, gluten--Negative


Celiac Antibodys:

Gliadin IgA    9.45 (nl <5)

Gliadin IgG   6.98  (nl <7)

Tissue Transglutaminase IgA    2.31 (nl <20)


Challenge Tests:

milk:  increased pain, tingling in feet, swelling sensation in feet, imbalance & unsteady; flu-like sensation throughout body; increased pain in forehead & cheeks; increased impairment on heel-to-toe walking (on exam)

corn:  increased impairment on heel-to-toe walking (on exam), slight numbness in feet

gluten: incresed impairment on heel-to-toe walking (on exam), weakness on walking

yeast:  heavy sensation in legs "felt like wooden blocks"., slightly unsteady heel-to-toe walk

Candida:  pain increasing from feet up to legs, heavy sensation in legs, 


IDT Tests:

Antigen                          Immediate rxn               Delayed rxn

dust                                  8mm dil 2                         +

alternaria                           9 mm dil 1                        ++

Cladosporium                    9 mm dil 1                        ++

Candida                            8 mm dil 2                        +++

Histamine control              10 mm dil 2

Pollens (tree/grass/weed)    6 mm dil 2    


Assessment:

1.  Neuropathic pain, multifactorial, related to former alcohol abuse,--variant nature of pain related to celiac disease, food sensitivities, and Candida related illness.

2.  Abnormal celiac antibodies, with evidence of gluten sensitivity clinically on challenge

3.  Abnormal IgG antibodies to dairy & egg, with evidence of dairy sensitivity clinically on challenge

4.  Abnormally strong ID delayed reaction to Candida, with evidence of Candida and food yeast sensitivity on challenge

5.  Impaired gut integrity, with increased intestinal permeability likely, as a result of chronic alcohol use, and celiac disease, and enhanced carriage of Candida in gut secondary to chronic antibiotic use for rosacea

6.  Chronic Tinnitus probably aggravated by allergy

7.  Mild mold sensitivity causing seasonal fall congestion.

8.  Sleep apnea

9.  Hypertension

10. Rosacea

11. Glaucoma

12. Chronic tinnitus

13. Venous stasis dermatitis

14. Penicillin allergy

15. s/p nasal polyposis

16. gout

Discussion

Here is my "discussion" that I shared with my patient in writing: 

 

"I mentioned to Mr. X that I felt it would be possible that low grade food sensitivities have been worsened following a probable increase in intestinal permeability that could have occured as a result of chronic alcohol ingestion historically.  His use of antibiotics chronically since 1999 for Rosacea could have caused Candida overgrowth and further impairment in intestinal integrity and heightened intestinal permeability or "leaky gut". The combination of alcohol ingestion and increasing Candida growth could have, in summary, caused a leaky gut with more food reactions developing.  Clinically, he is already aware that certain foods bother him and seem to increase neuropathic pain.  This would include yogurt, raspberries, peanut butter, nuts, and citrus.  The fact that he has a very atypical neuropathic pain problem, with no concurrent muscle wasting, and the fact that his symptoms include intestinal issues, and areas of involvement outside of his lower legs per se would suggest that food sensitivities and yeast issues are aggravating his condition..."  
Treatment Plan:

 

1.  SLIT for offending foods

2.  Rotary-diversified elimination diet, both gluten and dairy free, and also eliminating eggs, yeast, citrus, corn, tomatos, nuts.  

3.  Nystatin antifungal medication, probiotics

4.  Continuation of medications, except for doxycycline

5.  Continuation of vitamin supplements already on


Treatment course:

When I saw the patient back in the clinic, he was no longer using a cane.  His heel-to-toe walk was unimpaired, and could be done without assistance.  He handed me a written summary of his progress: 

"My strength and stamina have increased dramatically since going on the diet 3 months ago... I have rapidly lost 40 pounds to date, and have eliminated the taking of protonix and gabapentin.  I have reduced the steroid infusions to once every three weeks.  Neuropathic pain still remains if I don't take Lycra, but greatly reduced.  It appears that an element of neuropathy is reversing as I seem to have more control over the awareness of the need for urination and defecation and sexual responsiveness is improved.  
So, can celiac disease or/or  food sensitivities cause or contribute to peripheral neuropathy?  His neurologist currently thinks so, based on this patient's response and his improvements.  I would refer you to an excellent review of the Subject by Grossman, published a few months ago in April 2008, entitled "Neurological complications of celiac disease:  what is the evidence?"  In Pract Neurol.  

 

As Grossman points out in his article, , 

"This literature has become quite controversial, with disputes over the definition of coeliac disease and gluten sensitivity, whether neurological complications are caused by coeliac disease or are epiphenomena, and whether the proposed complications respond to a gluten-free diet."
However, although the literature may be controversial, my patient really doesn't see any controversy to be concerned about on a personal level.  He's getting better, and that's what matters to him.  And the purpose of this tale?--simply to arouse our curiosity as allergists, and to "think outside the box" with our patients.  And it all gets back to listening to tales...and becoming storytellers ourselves.  But with one important difference.  We try to end each story on a happy note... for the benefit of our patients.

 

Later, Dude




 


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Posted on Sunday, September 28, 2008 at 12:56PM by Registered CommenterGeorge F Kroker MD FACAAI in | Comments1 Comment

Allergy Aphorisms--An Idea whose time has come...

I love aphorisms...and those of you with keen clinical eyesight will now see that I have a list of personal allergy aphorisms listed in the rightside menu bar of my Blog....Aphorisms give us memorable insights into the minds of others, and ideas to mull over....and it was in that spirit that I provide them...Maybe my love for aphorisms is because I was academically raised on them...while I was at the University of Iowa one of my attending physicians was the late Dr. William Bean

 Dr. Bean interned on the Osler service at Johns Hopkins, and he was named Sir William Osler Professor of Medicine at the University of Iowa.  One of my most treasured medical posessions is a signed textbook I received from him, entitled "Sir William Osler:  Aphorisms from his bedside teachings and writings".  These aphorisms were collected by Dr. Bean's father (Robert Bennett Bean), who was a medical student under Osler, and my attending physician William Bean edited and published them. After 30 years, I still have the textbook.  Through Dr. Bean, I felt I had a direct connection to the life of Osler--Dr. Bean stated "my memory does not go back to the time when Osler was not a household word...almost even a household god..." Dr. Bean remembered how personally devastated his family was at Osler's son's death.  And the book of Osler's aphorisms I got from Dr. Bean?  You can only imagine how they influenced my own thinking as an embryonic physician entering the grand specialty of medicine....

  ...But what about allergy?  Do we have our "own" aphorisms, written and recorded by the giants of allergy?  In truth, hardly any.  Why?  Perhaps it's because allergy is seen nowindays as a technical/immunological field...after all, how many aphorisms can you write about dust mite exposure modifying the effect of functional Il10 polymorphisms on allergy and asthma exacerbations?  In this time and age, the patient may be seen more as a complex roadmap of cytokine interactions rather than a living, breathing organism. ...I am again reminded of one of Osler's aphorisms:  

               "The greatest art is the concealment of art, and I may say that we of the medical profession excel in this respect..."

There was, however, one article on the subject I found:  "Aphorisms and Facetiae of Bela Schick, written by I.J. Wolf M.D. and published in Clinical Pediatrics, pp 495-497, 1968, subsequently made into a book.  .   Some great aphorisms abound:

               "It is too bad we cannot cut the patient in Half to compare two regimens of therapy..."

              "You can always make a theory.  In making theories, always keep a window open so that you can   throw one out if   necessary.  Twenty theories can be made in five minutes"

              "There was no diagnosis--that's what makes the case interesting"  (in responding to someone who remarked that                   a case was interesting)

               "The human body is like a bakery with a thousand windows...We are looking into only one window of the bakery  when we are investigating only one particular aspect of a disease..."

Now think about this one:  Allergy as a profession is nearly 100 years old.  We have only one article and one textbook of aphorisms about only one allergist.   Aphorisms breathe "art" into the "science" of clinical medicine.  They help us to remember what's really important in our life as clinicians.  They are an endangered species.  We must preserve them.  

Later, Dude








Posted on Sunday, September 14, 2008 at 02:41PM by Registered CommenterGeorge F Kroker MD FACAAI in | CommentsPost a Comment

Chronic angioedema and urticaria: The Strange case of the water management employee...and the Tyranny of IgE

No one likes Dictators or Tyrants.  Especially in this country...the Land of the Free and the Home of the Brave, right?.  But do you know that one of the smallest tyrants in the world is also the most powerful?  Yep, it weighs in at barely 200,000 Daltons....

It's IgE.  

 


    Webster's dictionary defines a Tyrant as "an absolute ruler" who "uses power to oppress it's subjects".  And it's my contention that most allergists fall under IgE's overly oppressive power to define who--and who not--to treat as allergy patients.   Next month I'm going to launch into some allergy aphorisms of mine, and it is from these thoughts about IgE that one of my favorite aphorisms was born:   "IgE is a cruel taskmaster".   And the following case illustrates this perfectly...

...It was a hot August day in 2007, and I was sitting in my office, trying to mind my own business.  The pleasant quiet of the day was abruptly diminished when I heard a "plop".  I looked up.  My nurse dropped a "new patient" chart on my desk.  

Back to work. I put my journal down.  The fact that my investigation into reading about Toll-like receptor heterodimer variants that protect from childhood asthma...well, it just would have to wait.  So would Adenosine induction of airway hyperresponsiveness through activation of A3 receptors on mast cells.  It was difficult to do, but I tore myself away from the JACI.  Self-discipine, pure and simple.  I had to see the patient.  And the JACI would have to wait.  Again.  


I walked into the room.  A pleasant, middle-aged man sat in a chair, next to his wife.  

"You've got to help me." he said.  "It's been a living nightmare for 3 years.  I get swollen lips, eyes, and tongue, and sometimes I break out in hives all over my body.  And nobody can help me. Nobody.   I heard about you."  

He had been worked up at a large midwestern university.  I liked that, because the workups are usually thorough, and it leaves me to look into the mundane.  And he had been worked up well...Zebra-hunting didn't turn up a thing.  Hereditary or acquired C1 esterase inhibitor deficiency had been ruled out, based on normal C4, C1Q,, C1 esterase inhibitor (both functional and nonfunctional), and he had a normal tryptase, and no eosinophilia on CBC.  An IgE level was entirely normal.  Thyroid studies were normal and anti-thyroid antibodies were negative.  Allergy evaluation included negative skin prick testing to a wide panel of seasonal and perennial allergens as well as common foods.  

"I'm on a bunch of medications, but they don't really help", he said.   He had been on zyrtec, Zantac, prilosec, and Prednisone.  The latter was for short bursts, and only transiently helped.  

"Any other symptoms?" I asked.  "yes, I've got some GERD and some bad post nasal drainage" he replied.  "I think dust makes my drainage worse", he said.  "I sometimes have so much sinus drainage I can hardly sleep because of my coughing".  "Flonase, nasonex, Astelin--I've tried them all, and they don't touch it" he said.  

Another one of my axioms (aphorisms)  popped into my mind--that is, the patient with upper respiratory drainage from presumed  aeroallergens who also suffers from GERD has a food sensitivity until proven otherwise.  It's been my experience that in diagnostic conundrums, two distinct possibilities often emerge:  the patient either has a "Zebra" (i.e., a rare disease), or he has a horse painted with black-and-white stripes (i.e., a common disease with rare manifestations).  The latter possibility took shape with my patient...so in view of the above, we talked some more. ..Specifically, we talked about his diet...

"You know," he said, "I had something really strange happen in Colorado a couple months ago.  I went into a coffee shop, ate an organic bran muffin, and then seemed to immediately swell up and have hives.  Last night, while driving to La Crosse to see you, I ate at a local restaurant here.  I had the same experience".  

"What did you eat?" I asked.   

"Well, I had a sirloin, baked potato, salad, and bread from the bread basket", he said.  (Italics mine).  

"How do you do with beer?" I asked.  "Well, my sinuses get worse with it so I don't drink it any more" he said.  

 

Test results:

ID tests:  dust mite:       9 mm dil 1

 

                 alternaria:    10 mm dil 1

                 aspergillus:   9 mm dil 1

                penicillium     9 mm dil 1

all other test results negative

RAST tests:

IgE:  milk, wheat, oat, corn, beef, baker's yeast, gluten:  all negative.  0.00 IU/ml IgE

IgE:  milk, wheat, oat, corn, beef, baker's yeast, gluten:  all negative


 

Discussion:  

My working diagnosis was that this patient suffered from a combination of non-IgE mediated food sensitivities, coupled with minor prick test-negative but mild ID-positive inhalant sensitivity to dust and mold.  The combination of these contributed to his three major presenting symptoms:  urticaria/angioedema, chronic PND, and GERD.  

 

Treatment: 


We placed this patient on the following program: 

 

1.  Rotary Diversified Elimination diet, avoiding major food suspects (wheat, dairy, corn, sugars, yeast, beef)

2.  SLIT for dust and mold

3.  Temporary continuation of his medications as previously prescribed

4.  Trial of Gastrocrom for restaurant meals only


 

Clinical Course

Within 48 hours of beginning the diet, his daily urticarial lesions and facial swelling began to subside.  His stomach began to feel better, and he went off his prilosec.  He reduced his zantac by 50%.  He used Gastrocrom when eating out, since this seemed to block reactions when eating at Red Lobster.  I last saw him 2 weeks ago.  His congestion was alot better on SLIT, and dust wasn't bothering him like before.  He was afraid to stop his Zyrtec and Zantac, but...

 his urticaria and angioedema were in remission.  

"I can eat just about everything you took me off of, but I still have to be careful that I don't overdo wheat.  Mahybe once or twice a week is ok, but if I have more, my skin prickles". "I'm glad you suggested probiotics.  They seem to have helped me."   "My GERD is gone".  "I feel great".  
 

Comments: 

I've said it before, but I'll say it again.  The most valuable diagnostic ally in the allergists armamentarium isn't a skin test or a blood test...it's a good clinical history coupled with a healthy sense of curiosity.  When this patient told me about the curious incident involving eating a whole bran muffin, and noting an immediate reaction, I began to think along the lines of a non-IgE mediated food sensitivity.  If we eat a food, it is in our system (assuming a normal GI transit time) of about 3 and 1/2 to four days.  So if this patient is having wheat products daily, he always has a constant "load" of wheat in his system--which fluctuates from day to day.  Walter Vaughn wrote in his textbook that he had a patient who could eat wheat twice weekly, but not daily--otherwise she would have symptoms.  His prior allergists had shut out the possibility of extrinsic factors triggering a reaction--since his total IgE was normal.  No IgE?  No reaction, right?  Wrong. ...


Life is good.  

And  you know what?  Life would be even better....without dictators and tyrants.  

Later, Dude


 

 

 

 








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Posted on Sunday, September 7, 2008 at 01:37PM by Registered CommenterGeorge F Kroker MD FACAAI in | Comments1 Comment

The Strange Case of the Peruvian Missionary

  So there I was in my office last September, 2007, feet up on the desk and reading the latest JACI issue about some obscure immunological aberration of questionable practicality . when a "new patient" chart was dropped on my desk.. the nurse pointed me toward examination room 6  I reluctantly put the JACI issue down...I hadn't known that Yin-Yang 1 regulates effector cytokine gene expression and Th2 immune responses , but I somehow felt better for it, so dropped the issue, and in I walked...and there I found a pleasant 20 year old dark-haired young girl from Minnesota, who had an interesting story to tell...

"I want help with my stomach", she said; "it's upset 24 hours a day, and I have pain after eating." 

When I asked her about a past allergy history, I realized I had indeed opened up a Pandora's Box...

She had been diagnosed as having allergic rhinitis in childhood, and I reviewed the medical records she brought with her; indeed, they revealed she had been on prior injection immuntherapy for dust mite and grass , from 1996 through 2000.  Since that time, she had been doing well, without any significant respiratory problems, until a year and a half before she saw me, when...

...she went on an extended mission trip to Peru.  While there, she was working under extremely poor conditions with presumably heavy dust exposure.  Four months into her trip, upon consuming a meal containing cayenne pepper, her hands became red, burned, itched, and she developed urticarial lesions on her arms.  Two weeks later, while eating in a Peruvian restaurant, 20 minutes later she developed dizziness, throat closure, and generalized urticaria for which she took Benadry.  There were no peppers in this second meal, which admittedly contained nothing unusual for the patient, but nevertheless this reaction was worse than the first one.  One month later, in February of 2006, while still traveling in Peru, she ate a fairly regular meal containing potatoes, vegetables, chicken, and no spices at all.  Within 20 minutes,  her ears began to burn and itch, and her throat began to close. Her stomach cramped, and she began to have nausea and vomiting and collapsed.  She was taken to a local emergency room, where she received emergency treatment, and was advised to see a local Peruvian allergist.  Records from this visit were unavailable for review, but he apparently tested her and told her that she had "probably reached a threshold of tolerance on heavy dust mite exporsure in Peru".

She returned home from Peru in March of 2006, and ate mainly ad lib, with no severe reactions; she felt most of her problems were behind her...However, in June of 2006, she had a cappucino while on a family trip, and within 5-10 minutes, she felt severe stomach pain, and had nausea and vomiting, accompanied by urticaria.  In the spring of 2007, several months before seeing me in the fall, she had an episode of eating pecan pie from Perkins, and developed severe stomaches and diarrhea...

"...and since that point in time my stomach has been continually upset", she told me...Although she had minor spring and fall rhinitis issues, these were not a concern.   Understandably, her stomach issues were her major concern, and severely impacted her quality of life...

...Two months before seeing me, her local clinic had done a medical workup, including normal CBC, sed rate, stool for O&P, abdominal/pelvic CT,   peripheral smear for malaria--all of which were normal.  A GI consult was pending...Allergy prick testing was done and had showed strong sensitivity to cat, dust mite, and horse dander, and moderately strong reaction to trees, grasses and weeds.  Prick testing to a battery of foods was negative.  

What next??

Her physical exam was generally unremarkable, except for mild nasal turbinate congestion.  She had no dermagraphism, and abdominal exam showed no h/s megaly or point tenederness.  Remainder of exam was not noteworthy.

IDT testing

Dust mite:    10 mm        dil #7

Ragweed:    13mm         dil #3

Grasses       13mm        dil #3

Tree mix      13mm        dil #3

Cat                 8 mm        dil #5

Alternaria      6 mm       dil #2

Candida       8 mm         dil #2    blistered at 48 hours


RAST testing IgE

dermatophygoides farine   Class IV      8.22 IU/ml

Cow's milk                              Class I        .07  IU/ml

 All others negative:  wheat, corn, beef, potato, baker's yeast, apple, chicken, bell pepper

RAST testing IgG


Cow's milk                             Class III       22.48 ug/ml

Wheat                                     Class II         9.68 ug/ml


Discussion:
Certainly, the squalid, filthy living conditions she encountered on her missionary trip to Peru gave her large concentrations of dust mite exposure.  But "not all dust mites are dust mites"--and certainly not in Peru...Croce and colleagues in J Investig Allergol Clin Immunol 5:286-8, 2000 pointed out that the mite Blomia tropicalis was the organism most frequently detected in 59% of peruvian house dust samples, with dermatophagoides pteronyssinus second place at 15.9%.   Chortoglyphys arcuatus and Tyrophagus putrescentia were also found, and these four mites, taken together, accounted for more than 90% of the mites detected.  No specimen of Dermatophagoides farinae was detected.   What's the cross reactivity between D. farinae (which we did with RAST) and Blomia tropicalis? Again, this was studied this year by Croce and colleagues and published in P R Health Sci J 27: 163-70, 2008.   They found that although (as expected) cross-reactivity between homologous allergens from Dermatophagoides spp. is high, it is low to moderate to Blomia tropicalis.  It would certainly be possible that her severe reactions in Peru might be accounted for by the difference in mite populations between Peru and the U.S. 

Another factor to consider in her severe reactions in Peru would be whether she had a variation in "pancake syndrome" or oral mite anaphylaxis, as pointed out in the article by Hannaway and Miller in the Annals of Allergy in  Allergy Asthma Immunol 4: 397-8, 2008.    Storage mites in grains grow under humid conditions, and as pointed out by Croce, Lima Peru is a city of tropical climate located along the Pacific coast, and the relative air humidity is 80-90% in the districts they studied...
Certainly, who knows how many mites she was eating in some meals the locals prepared for her?...Was she gradually ingesting more and more mites?...

Finally, what about the patients current commplaints--her continual GI tract pain and nausea?  Could the presumed heavy dust-mite associated anaphylaxis inflammed the patients GI tract, and made it more reactive to foods (i.e., milk, wheat?) and Candida?  An intriguing paper by Magnusson J in J Allergy Clin Immunol 112:45-50, 2003 indirectly addresses this question, when they studied the GI tract in individuals with seasonal birch pollen allergy.  Although the pre-season intestinal biopsies were normal,  nearly half of the post-seasonal biopsies showed intestinal inflammation...the authors stated that "birch pollen exposure triggered a local inflammation with an increase in duodenal eosinophils and IgE carrying mast cells in patients...there is an interplay between immunologically active cells in the airways and gut..." could the same thing have happened to this patient, with oral mite anaphylaxis aggravated a food sensitivity? 

Why the IgG RAST in my workup?  Although IgG RAST is controversial, there is a study by Dixon published in Otolaryngol Head Neck Surg 123:48-54, 2000, on 114 consecutive patients suggesting help in diagnosing the "hardest of the hard"--the delayed food reaction...and I thought it might be of help here, given the patients history of chronic daily gastrointestinal distress.... 

Finally, this is where SLIT shines...the other allergist she had seen just before her arrival in our clinic was "not interested" in giving her SCIT again, especially with her predominantly GI complaints and her prior severe reactions to dust mite.  But with the safety profile of SLIT, we can begin right away, and treat her comprehensively for all factors contributing to her total "allergy load"...and for those who have read my prior entries, I am a BIG believer in the total allergy load!!

 
Diagnosis:
1.  Dust mite anaphylaxis, with possible pancake syndrome and preferential sensitivity to Blomia tropicalis over dermatopagoides spp.

2.  Coexisting low-grade food sensitivities contributing to GI upset
3.  Abnormal delayed reaction to Candida antigen
4.  Irritable bowel syndrome with  inflammation aggravated by dust mite and food sensitivities
5.  Seasonal pollen sensitivites aggravating seasonal congestion in spring and fall, and heightening susceptibility to GI flares at those times

Treatment:
1.  SLIT to offending inhalants:  dust mite, grass, ragweed, tree
2.  Reduction in dairy, wheat in diet
3.  Short course of oral cromolyn sodium
4.  Short course of low-dose diflucan, 100 mg twice weekly x 1 month to reduce intestinal carriage of Candida

Clinical Course
On this treatment program, the patients gastrointestinal symptoms gradually subsided and within 3 months her stomach was improved, she had had no urticaria or anaphylaxis requiring emergency room visits, and she felt better..  By her last visit May 22, 208, she had had an excellent interval report, with no gastrointestinal distress, urticaria, or seasonal problems.  Spring season was going well, with no congestion.  She remained on SLIT, and was eating her dairy and wheat products carefully.  Life is good. 

Later, Dude
 

Posted on Sunday, August 17, 2008 at 01:00PM by Registered CommenterGeorge F Kroker MD FACAAI in | CommentsPost a Comment