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:  

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

"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..."  

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.  

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."

Later, Dude

                   -

 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

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:

                 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:  

Treatment: 

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

"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

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
 

We all like to "look under the lights" when we are searching for something valuable.  But sometimes remembering that valuable things aren't just what can be seen easily under the lights is worthwhile too. 

As I had said last time, there were two great men highlighted in the article by Cohen.  One was Walter Vaughan, and the other was Oscar  M . Schloss, M.D.   As I've said before, to get your picture published in the JACI you generally (1) have to be dead and (2) have made a VERY valuable contribution to the allergy field.  I talked about Vaughan in my last entry, so let's talk about Schloss...

Cohen points out in his article that Schloss held the positions of professor and chairman in the Departments of Pediatrics at Cornell Medical College and at Harvard.  As noted by Cohen: 

"In 1912, the controlled, in depth study of Oscar Schloss established the practicability of scratch tests for clinical hypersensitivity". 

                                           Indeed, he was....

Here's what Warren Vaughan says about Dr. Schloss (missing from the JACI article):

A child was brought to Dr. Oscar Schloss, a New York pediatrist.  There was a most unusual story of idiosyncrasy.  The lad had had diarrhea when ten days old and was treated with barley water and raw egg white.  This relieved the complaint and caused no unpleasant symptoms.  He received no more egg until he was fourteen months old.  Almost immediately after eating part of a soft-boiled egg he cried out, clawed at his mouth, and his tongue and mouth swelled until they were many times normal size.  Hives soon appeared around the mouth...When the boy was two years old his mother noticed that if he were to play with empty eggshells he would break out with hives on his hands and arms.  Schloss suggested that the boy's experience might be due to this new condition, recently receiving so much attention, called allergy....He injected the boys blood into a guinea pig.  Later he injected egg white.  The animal had typical shock...

 ...He mixed the white of a raw egg with water and diluted it so many times that you would scarcely have thought there was any egg left.  He fed this to the boy with a medicine dropper.  Nothing happened.  He kept on giving this curious medicine every day, increasing the number of drops each time and gradually increasing the strength of the solution...He finally increased the tolerance to such an extent that the lad could eat eggs in moderation with no consequent discomfort....Here again was something well worth telling to the world  Schloss published his report in 1912.

...Two methods of desensitization were now available--hypodermic and oral.  We use both today..." 
    

A physician in England, Dr. Alfred Schofield, wrote in 1908 about successfully treating a boy who suffered from angioedema and asthma because of an allergy to eggs.  (Schofield, Alfred:  A Case of Egg Poisoning, Lancet, p. 716, 1908).  This egg desensitization was confirmed by Drs. Keston, Walters, and Hopkins (Keston, B, Walters, I, Gardner, J:  Oral Desensitization to common foods.  J Allergy 6:431, 1935). 

.So SLIT for foods was documented by multiple doctors  at the turn of the 20th century, nearly 100 years ago. But Schloss deserves a major credit nonetheless.   Can we learn something from the classical literature?  You bet.  Schloss used a serial dilution technique for successful desensitization in a patient highly allergic to eggs...Seems to me that's important....We can also learn that we all have a bit of arrogance in "modern allergy" in "copping an attitude" that everything worth knowing in the field has been published within the last 10 years (or mentioned in the latest CME exercise we did...)   

...Open-mindedness and an obsessive sense of curiosity is  a hallmark of the Renaissance Allergist.  As Renaissance Allergists, we're interested in looking not just "under the lights" of our accepted (and preconceived) notions that SLIT for foods is a "new" idea and "new" treatment, never tried before. We look everywhere...whether it's under a light or not.  An interest in classical allergy literature pays many dividends for the Renaissance Allergist.  Here's one more.    

Later, Dude. 

"In 1930, Vaughan, in collaboration with Frances Wilson, an academic botanist, initiated studies of shared characters of plant-derived foods as the first stage in the development of a classification intended to serve as a rational and workable basis for selecting test allergens representative of members of a group.  ...Of special interest is a 75-year-retrospective review of Vaughan's contribution, noting that with few exceptions his compilation was valid and met the test of time"  

 As a Renaissance Allergist, I have an interest in classical (medical) literature, and an overwhelming sense of curiosity--basically, what else did Vaughan write--and what might it tell us in addition to Cohen's article? 

Here's some things not pointed out in the article by Cohen:  

First, Vaughan wrote on a wide range of topics he felt were related to the allergy field:  check these out:

1.  Vaughan, WT.  Allergic Migraine.  JAMA 88:1383, 1927.

2.  Vaughan WT.  Role of specific and nonspecific factors in allergy and allergic equilibrium.  J Lab & Clin Med 13:633, 1928.  

3.  Vaughan WT.  Allergic factor in mucous colitis.  South M J 21:894, 1928.

4.  Vaughan WT.  Atypical and borderline allergic manifestations as important factors in general medicine.  South Med & Surg 95:15, 1933.  

5.  Vaughan WT.  Food allergy as a common problem.  J Lab & Clin Med 19:53, 1933.

6.  Vaughan WT.  Food idiosyncrasy as a factor of importance in gastroenterology and in allergy.  Rev Gastroenterol 5:1, 1938.  

7.  Vaughan WT.  Palindromic rheumatism among allergic persons.  J Allergy 14:256, 1943.

Secondly, we know Vaughan was a brilliant physician.  ( For anybody to get their picture in the JACI, you've got to be brilliant).  Even his son was a brilliant doctor--John Heath Vaughan, was an internationally recognized authority on allergy and autoimmune diseases and a former member of the University of Rochester School of Medicine and Dentistry, who recently passed away at the age of 85 on Nov 11, 2007.  So why was  a brilliant physician like Vaughan writing about palindromic rheumatism and it's relation to allergy?  What does his "classical" writing tell us?  Are you curious? I was. 

In his article, Vaughan described 27 cases with recurrent or chronic joint symptoms among a large group of allergic patients, in whom the arthritic symptoms were attributed to food sensitivity.  He called this syndrome "palindromic rheumatism", a term used by Hench and Rosenberg 2 years earlier to imply recurring joint disease without articular residue.  Vaughan would note that about half of his patients seemed to have abnormal joint changes at the time of exam.  His original discription of this group of patients is repeated here for its remarkable accuracy:

"The second consideration was a small group of allergic persons with intermittent attacks resembling subacute rheumatoid arthritis in whom we have demonstrated specific food incitants.   The evolution of the attacks resembled those of intermittent hydroarthrosis, but multiple small joints were involved; often just one hand or foot was affected.  Sometimes the reaction occurred in more than one extremity, and at times one or two large joints became inflammed either simultaneously or independelty.  The local picture was of swelling, redness, paind, and tenderness.  The attacks would last from several days to a week, rarely longer.  In some, the joints were objectively normal between attacks.  In others, there were low grade arthritic changes..."

Now--be honest--how many allergists take rheumatic histories on our patients?  I do.  For example, I can remember the patient with a strong dust sensitivity who suffered an acute attack of palindromic rheumatism after sweeping out her basement.  In truth, being curious and delving into the older "classical" allergic literature---which was devoid of the built-in constraints of IgE-mediation, may offer us new insights.  Remember what I wrote last month about the mast cells and the synovium?  

Warren T. Vaughan was a Renaissance Allergist.  A brilliant clinician.  And he believed that palindromic rheumatism could be triggered by food incitants.  Renaissance Allergists in today's world need to follow-up on his meticulous & compelling observations. ...

Later, Dude.  

                          Renaissance

The word "renaissance" is of French derivation--for rebirth.  What characterized the Renaissance?--a "rediscovery" of classical literature/art, curiosity and objectivity, and an emphasis on individualism (among other things.)  The true "Renaissance Man" embodies these ideals in a multi-talented fashion.   In my (humble?) opinion, the allergy field needs more "Renaissance Allergists", and alot less "asthma docs".  We made a fundamental mistake as allergists when we anatomically delimited our field--because the field is basically not one to anatomically demarcate.  In that respect, it's alot like our "brother specialty"--infectious disease.  Imagine if the IDSA  (Infectious Diseases Society of America) changed their name, for example, to emphasize "bronchitis", and became the Infectious Diseases Society of America and Bronchitis?  What if you went to infectious disease meetings, and all they talked about was the respiratory infections they cared about?  How interesting would that be?  We've done that with our own societies--tagged "asthma" along with the official titles, as if to say that's "who we are". Asthma docs. 

And that's what the Renaissance Allergist is not.   What is he?  Easy.  He's a multi-talented physician first, an allergist second, and an asthmalogist (a distant) third.  He/she is interested in all immunological aberrations (both non IgE and IgE mediated) over all mucosal surfaces, as well as the skin and joints.  And come to speak of it, he's even interested in the human synovium, and how his allergic patients might respond there.  Remember--mast cells have long been known to be present in the human synovium, and mast cell numbers also increase 1-10 fold with diverse disorders, including juvenile and adult rheumatoid arthritis.  (See "Mast Cells and arthritis"  by Malone & Metcalfe, Ann Allergy 61:  27-30, 1988 if you're interested).  Yes, a spirit of curiosity, individualism, and love of classical literature are characteristics of the Renaissance--and of the Renaissance Allergist. 

Which brings me to the latest Allergy Archives, and Warren T. Vaughn.  But that's for another time, and another post.

Later, Dude

half-full glass of water...                                                                                     Is the glass half full?  Or half empty?  Which is the MORE accurate perspective?  Which viewpoint  tells us more?  In the field of allergy, the Angry Allergist has been concentrating on our shortcomings...and rightfully so.  We have a bucketful of them. I've outlined them in my "Allergy--a field in trouble" monograph in the right menu column.  In short, I've portrayed the Allergy Glass as pathetically half-full, or maybe even empty.  On the other hand, as I read our official allergy society newsletters, I've been greeted with moronic platitudes like "Nobody does it better than the Allergist"--and a marketing campaign dedicated to telling patients to see their local allergist for the best in allergy care.  This perspective treats the glass as completely full. Nothing more needed.  As allergists, we have all the knowledge and tools to effectively help our patients, even if we utilize our best tool--immunotherapy--in less than 20% of them.  Well, who's right? Is the glass half full, or half empty? 

 I've been looking for a word--a single word--that typifies what we need in the field of allergy--something typifying the act of "filling the glass".  Something to describe in a positive fashion what we--as a field--need to do.  And be.  And not what we lack. What word? 

 Renaissance.  

And I'll talk about why I chose this word.  And what it means for us as a specialty.  Because we need, desperately, to fill the glass.  Yes, it's probably half full.  I'll give you that.  But it wasn't designed to be half full.  And that's the point.    Let's fill 'er up.  And, like real life (at $4+ bucks a gallon)--it may be painful, but it's got to be done...

Late. Dude

Please Note:  When you come back to this site, you'll need to point your browser to a new web address:  www.renaissanceallergist.com. 

...usually I don't have time to talk to potential "new patients" on the phone, but I had an unexpected lull in the office the day she called...just hanging out and reading some journal article about some obscure immunological aberration that I would probably never see in my practice...so when I was paged I took the call.  The more I talked to her, the more interested I became.  "Ive been to xxxBLEEPxxx clinic, and they biopsied the rash and couldn't figure out what it was so they gave me a burst and taper of Prednisone and it still hasn't helped.  And my dentist keeps finding I am getting infections in my mouth for no reason.  I'm a TOTAL mess."  

... Well, at this point I figured I had about 5 minutes of time left on the phone, so I'd take a wild stab at this problem and decided to ask her what most physician't DON'T ask about and DON'T take a history on and DON'T factor into the differential diagnosis--her diet.  "So what do you typically eat?" I asked.  "I'm suspecting I have a food allergy" she said.  When the rash first began, I cut out most foods and now I'm eating green peas, hamburger, and brown rice and the rash is worse than ever..." 

...A thought crossed my mind.  "I want you to NOT change  your diet until I see you in the office," I said.  "And I think I know what's wrong with you.  We need to do a blood test to confirm it..."

...When she came into my office she appeared to be a frail, pleasant blonde who had a rash principally scattered over her lower extremities, but also seen on her back and the nape of the neck.  The lesions were punctate red excoriated areas with shallow scratch marks.  She proceeded to tell me her story, and brought in records for review: 

The rash had been insidious in onset, for about 2 years duration.  Her prior Immunofluorescence biopsy was negative for IgG, IgM, IgA, C3 and fibrinogen.  Skin biopsy reveated no evidence for dermatitis herpetiformis, lichen planus, vasculitis, or immunobullous disease.  There was no lupus band.   She had had fungal serologies and viral serologies, including herpes titers, and these were negative.  She had taken a systemic steroid course, followed by Cortaid application with occlusive dressings which did not help her symptoms significantly.  A boatload of blood work turned up nothing...her ANA, endomysial antibody and tissue transglutaminase antibody were negative (among others) , and she was told she had "neurodermatitis with excoriations". 

Wait...but there's more!  I found out that she would get diarrhea from eating most fresh fruits; she had known this for years:  as a child, she recalled that there was never any fresh fruit in the house  because her mother and sister couldn't tolerate it. Her gums looked somewhat sore.  She had dental problems, and so I ordered a

                         serum ascorbate level

I ran the test thru Mayo Medical labs, and the result was 0.3 mg/dl, with a normal range of 0.6--2.0.. 

Diagnosis? 

                                                Scurvy.  

I placed her on Vit C 500 mg tid, and a general multiple vitamin.   Her lesions healed in a month.  Also, her dentist was happy with me.  And her repeat Vit C level was 2.0. 

What made me suspect Scurvy?  Well, for one thing, her diet of green peas, meat, and rice had no significant Vit C and of course her lack of response to steroids suggested a cause other than immunological inflammation.  Once again, this shows the power of history-taking:  her case was figured out over the phone, and the blood test was merely confirmatory...(so much for her prior "million-dollar workup")

Comments:

There are several "morals to this story", and lessons to be learned:

1.  Not everything that a patient suspects is food allergy is actually food allergy.

2.  A prestigious medical institution missed the diagnosis because no one had bothered to take the patients dietary history.  And the cost (emotionally and financially) to the patient was enormous...

3.  She (and other family members) probably had a hereditary fructose intolerance, and she was probably marginally Vit C deficient her whole life, and then when the rash began, she restricted her diet further, taking out the vegetables out of her diet that were buttressing her Vit C level, and her skin rash and dental absesses began...

4.  Just because she had Scurvy didn't mean she was ONLY deficient in Vit C.  She desperately needed general vitamin repletion.  (I quickly checked a Zinc level with her dental problem as well, and she was also deficient in this).

5.  As allergists, we need to be aware of nutritional deficiencies for our patients.  It's not enough that we are "asthma doctors."  This patient wouldn't have been helped with inhalers or antihistamines.  Period.  

5.  If we're good doctors, we'll get more of our "bread and butter" allergy patients.  Ironically, this "non allergy patient" has referred me patient after patient for allergy care!

Later, Dude