When I picked up the phone, I noted the desperation in her voice..."I'm going crazy trying to figure out what's causing my rash", she said.  "I've been everywhere, and no one has helped me..."

...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 

I've just finished reading "The Hound of the Baskervilles" for the umpteenth time...I love detective stories, and I especially love the archetypical detective, Sherlock Holmes.  And in the following case history, one of Holme's axioms is employed--here it is, repeated multiple times in various settings:

 "Eliminate all other factors, and the one which remains must be the truth" (from The Sign of Four)

"How often have I said to you that when you have eliminated the impossible, whatever remains, however improb able, must be he truth" (again, from The Sign of Four) 

"When you have eliminated all which is impossible, then whatever remains, however improbable, must be the truth" (from The Adventure of the Blanched Soldier)

"We must fall back upon the old axiom that when all other contingencies fail, whatever remains, however improbable, must be the truth" (from The Adventure of Bruce-Partington Plans) . 

Keep this Sherlockian rubric in mind with the next story...it'll pay off...

...Besides reading books, I also like to read newspapers--they're full of interesting stuff.  So I was especially intrigued by the newspaper headline "Mystery Illness Plagues Former Pentagon Worker".  I was even more intrigued when it was handed to me by my new patient, a young woman walking unsteadily with a cane, which appeared incongruous in such an attractive, young individual.

She had a litany of complaints--well described in the newspaper article about her case--a cornucopia of neurologic and "allergic" symptoms:  Burning and numbness in her extremities, balance difficulties, muscle spasms and twitching, , chronic mucous in her throat and sinuses...as well as more systemic complains of  chronic exhaustion and  cognitive dysfunction.  There were gastrointestinal symptoms too, including  mucous in her stool, and diarrhea.  If I picked an organ system, she seemed to have a symptom in it.  (The dreaded "positive review-of-systems" that most doctors recognize). 

The only thing bigger and longer than her list of complaints were her prior medical records--she had worked for the Pentagon, and there was page after page of diagnostic tests by impeccable Washington medical institutions, with test result after test result.  But no firm diagnosis had been made.  I  decided to do something totally radical--I put all her prior test reports aside, and decided I'd take her history myself.  And her history was interesting too:  She knew she had allergic disease earlier in life--and she came to see me to see if there was any "tie-in" between her current plethora of symptoms and allergies.  In the 1990's she had episodes of recurrent/chronic sinusitis and tonsillitis.  Prior allergy testing via RAST had shown positive results to dust mite, Kentucky blue grass, elm and cottonwood.  She had a history of classic seasonal allergic rhinitis causing quite a bit of throat, nose, and eye irritation for which she had periodically used fexofenadine.  However, all of these issues were perceived by her as being relatively "minor" issues until November of 2004, when troubles really began...

In November of 2004, while working at the Pentagon, she ate what she thought in retrospect was some contaminated fish and had a sudden, protracted episode of gastroenteritis.  As the months wore on, she had recurrent episodes of further diarrhea and abdominal cramping, followed by some constipative tendencies.  By October of 2005 she was having trouble getting up in the morning and progressive malaise and fatigue were setting in.  In November of that year she began to develop pain in her lower back and hips, and she experienced difficulty walking.  She again saw her physician, who at this time felt she might have pelvic inflammatory disease, despite negative cultures and a monogamous marriage.  She was given Flagyl and Levaguin, and began to feel markedtly worse within 24 hrs.  She began to have bilateral paresthesias in her legs and hands, and her feet ached and her grip got weak, she got progressively weaker,  and was hospitalized and had a thorough neurologic workup.  An LP, EMG, MRI of her brain and spine were all negative.  Celiac disease was ruled out.  She was given  IVIG and a preliminary diagnosis of "atypical laboratory negative Guillian Barre Syndrome".  Of note is the fact she had a rash on her hands while hospitalized which she described to me to be suspiciously like the distribution of an "Id reaction."  Her neurologists, however, were puzzled by the fact that she "should be getting better" and she had a very protracted convalescence, with a 3 week stay in the National Rehab Hospital. 

She never returned to her job at the Pentagon, and in April of 2006 moved to the midwest, where another neurologist there took over her case, and again extensive neurologic tests were run, without a firm diagnosis being made. She became  self-employed as a Defense Contractor Analyst, but because of her multiple symptoms, she was barely able to function on a day-to-day basis.  

Physican exam:  Positive Chvostek sign, positive Romberg, nasal drainage.

Medications:   omeprazole, skelaxin, dilaudid, meclizine, oral contraceptive

Diet history:   Craves chocolate, steak.  Has sweet tooth.  Favorite foods pasta and beef.  Very heavy wheat ingestion. 

Intradermal testing by IDT:

Grass Pollen:   11 mm dil #5

Ragweed:       16 mm dil #3 

Dust mite:      10 mm dil  #4

Tree mix:        9 mm dil# 3 

Oral Challenge testing:

Gluten:     dizzy, lightheaded

Milk:         cognition impaired, unsteady in walking; shakey legs

Beef:        cognition impaired, legs tingling & shaking

Candida:  very tired, aching in legs and shoulders, legs shakey

RAST test: 

IgE:  Negative to:  milk, wheat, soy, tomato, beef, yeast, potato, garlic, onion, gluten 

IgG:  Class II:  milk, Candida, beef, garlic  

        Class i:  wheat, soy, tomato, potato

        Negative:  onion, gluten

So what's going on?  

Again, the beauty of understanding diagnostic synthesis in complex allergic diseases is that you can make sense of a history, that superficially, is horrendously complex and puzzling. After I took this history, here's how I put it together chronologically:

longstanding history of inhalant allergies, leading to

recurrent sinusitis, leading to

recurrent antibiotic use, leading to

excessive Candida growth--

acute food poisoning reaction in 2004--chronic intestinal inflammation with enhanced intestinal permeability, leading to

Candida sensitization (and possibly food sensitization at that time)

Levaquin and  Flagyl given, with drug reaction occuring, and further Candida growth

Id reaction in hospital is further evidence of Candida sensitization

Underlying grass pollen sensitivity sets her up for cereal grain sensitization in presence of leaky gut syndrome; may have had a longstanding milk allergy all her life, made worse with leaky gut; 20 percent of people sensitive to milk react to beef, and she sure did!

Furthermore, her chronic diarrhea and Candida overgrowth set her up for a serious magnesium depletion state, with a positive Chvostek sign on exam and multiple muscle spasms throughout her body.  Peripheral vasospasm contributes to neurogenic ischemia, aggravating her paresthesias.   

All of this can be deduced by her history, before any allergy testing is done.  

Treatment Plan: 

She obviously wouldn't be a candidate for SCIT--she's too unstable, and has too many neurological symptoms.  She's a great Candidate for SLIT, however.

Plans--

1.  Rotation-elimination diet to reduce antigenic burden:  avoiding milk, beef, refined sugar, wheat gluten

2.  Fluconazole with probiotics to reduce Candida antigenic burden

3.  SLIT to inhalants , treating her dust, ragweed, grass, pollen, tree, and Candida sensitivities (note--she had scarring from her Candida and TCE injection sites, and dosing was given for Candida only after receiving information on her delayed reports, to avoid overdosing, and using the strongest negative delayed reaction wheal on her Candida IDT)

4.  SLIT to foods--gluten, milk, beef 

5.  Magnesium Chloride Elixir, 12.5%, 2 tsp orally per day for magnesium repletion

Clinical Course:

When she returned to see me 3 weeks after her first visit, she still had scars on her arm from the prior Candida & TCE IDT tests, but she was feeling much better.   Her balance was dramatically better, and she was no longer using her cane, and had stopped her meclizine, dilaudid, and had reduced her Skelaxin.  Her gastrointestinal function was markedly improved, and the generalized burning in her torso was gone, and her energy and cognition were dramatically better.  I last saw her informally in our hallway 2 weeks ago--this was about a year after I had first seen her; her symptoms were in complete remission, and she was now pregnant.  She was bringing in...guess what...another friend of hers, a young nursing student, for assessment for idiopathic chronic fatigue and aching issues...and the beat goes on...

Important points to ponder:

Were this patients neurological symptoms related to "allergies?"  And before you're too quick to pass judgement, remember the Sherlockian phrases I listed above.  Read them again.  Then reconsider. Neurological manifestations of allergic disease states are a great unexplored frontier.  And this is a tragedy--and one of our own making, I might add, because of our arbitrary demarcation of allergic disease to the respiratory tract. Should we, as allergists, be more interested in neurologic manifestations of allergic disease?

It's Elementary, my dear Watson.

Later, Dude 

Go ahead.  Try it out.  Make my day.  Try to find case histories on SLIT in medical journals.  Sorry, pal, but you won't find any.  None at all.  Zip.  Well, somebody has to start producing case reports on Sublingual Immunotherapy (SLIT) use, right?  Alright, it's a dirty job, but somebody has to do it, and so, since I've had 27 years of experience with SLIT, here goes....

You already know where I stand on the importance of case reports; in my prior entry on The Iatrogenic Atrophy of the Case Report, I gave a Case Report on...you guessed it...the Case Report--since The Annals of Allergy Announced they were no longer going to accept unsolicited case reports in their journal. So here's another unsolicited case report, which I'm publishing online, to outline the versatility of  SLIT in treating a complex case of allergic disease...

Case Report 

Patient X was referred to me by a local allergist on January 4, 2007.  This 20-something patient was referred by her allergist to me, principally to help deal with a loss of food tolerance and progressive food sensitivities.

Background history: 

Patient X had a history of eczema transiently as a young child, and had a lifelong history of asthma beginning in childhood.  Throughout childhood she had recurrent sinusitis.  She was treated symptomatically with antihistamines, and steroid inhaler medications, and overall was doing acceptably well in her teenage years.  As a college student, she was under much stress, working 15 hours part-time and taking 15-18 hours of college credit per semester.  Things were going well until...

The fall of 2005 she suffered from a serious aggravation of upper and lower respiratory tract allergies in Sept & October, followed by bronchitis in October and November.  In December 2005 she developed her first migraine headache, and migraines have been bothersome since then. Interestingly, they were helped partially with benadryl useage...

Not only were migraines bothersome, but in the fall of 2005 she began to notice nausea, satiety, and general stomach distress with eating.  She reduced her food intake and lost about 40 pounds.  Her stomach distress was significant enough to keep her from concentrating on her academic studies. In December of 2006  she had formal gastrointestinal  evaluation;  esophageal biopsies  demonstrated short segment  Barrett's,  and mid-esophageal biopsies demonstrated 25 eos per HPF, borderline for eosinophilic esophagitis.  Her gastric emptying study demonstrated a mild delay to solid phase gastric emptying. 

Past medical history:  Remarkable for multiple concussions playing basketball, with heavy NSAID use; infection while traveling overseas requiring doxycycline useage for 2 months, June-July 2006. 

Prior Allergy Testing & Treatment 

Her referring allergist had enclosed records from still ANOTHER allergist (!!), who had previously done prick testing for inhalants, revealing strongly positive ++++ pricks to ash, aspergillus, curvularia, fusarium, pullularia, rhizopus, stemphylium, mucor, and +++ prick tests to dust mite, alternaria, botrytis, ragweed. 

Prick testing to foods revealed ++++ pricks to corn, +++ to carrot, soybean.   

RAST testing had revealed IgE class I to corn, banana, almond, potato, and soy.  Additional RAST testing had revealed IgG class IV to casein, corn, soy, and IgG III to wheat. Gliadin antibody to wheat was negative. 

She had peripheral eosinophilia at 8%.   

She did not receive immunotherapy. She initially tried to eliminate wheat and corn from her diet, and noted a reduction in migraine headaches for about one month, only to return with a vengance after that.  

Status on Presentation 

Patient's X's major goal was "to help my health so I can complete college."  She had lost 40 pounds, and was afraid to eat.  She had dropped out of school because of her multiple illnesses.  She had chronic migraine headaches, and continual stomach distress.  She was afraid her asthma would again act up in the fall and cause even more problems, but on a day-to-day basis she struggled with frequent migraine headaches and stomach upsets.    

Medications on arrival:  Allegra 180 mg/d, Topamax 50 mg BID, Prevacid 30 mg/d, Advair 500/50 1-2 x per day, depending on season, albuteral prn, midrin prn, skelaxin 800 prn.   

Current diet:  avoiding wheat, corn, corn, milk, beef, soy, bananas, carrots, rye, pork, MSG.  Craving peanut butter.   

Physical Exam:  remarkable for nasal turbinate congestion, coated tongue, cold hands with poor capillary filling.  Lungs clear at time of presentation.  No hepatosplenomegaly or localized abdominal tenderness.

Our Initial Test Results:   

IDT Testing: immediate test results

dust:             9mm       dil #4

Ragweed:    15 mm      dil #5 

Grass:          11 mm      dil #5 

Alternaria:  11 mm      dil #5 

Fall pollen   10 mm      dil #5

Candida       11 mm      dil #1

Mold mix      10 mm      dil #3

Rast Tests: inhalants

Kentucky/June grasses:               IgE Class III

Alternaria mold:                         IgE Class III

Ragweed:                                   IgE Class III

Rast Tests: selected foods in diet currently eating

Egg:                                            IgE Class II

Pea                                             IgE Negative          IgG Class II

Peanut                                        IgE Class I

Almond                                       IgE Class II             IgG Class III

Tomato                                       IgE Class II             IgG Class III

Potato                                        IgE Class I              IgG Class II

Chicken                                      IgE Negative

Candida                                      IgE Negative         IgG Class III

Oral Challenge Testing:

Peanut challenge--immediate severe migraine (eating daily)

Egg challenge--immediate exhaustion (eating frequently)

Potato challenge--immediate sinus pain and pressure

Milk challenge--stomach distress

Candida challenge--exhaustion 

Assessment & Discussion:

On the "surface", this patient suffers from multiple problems:

1.  Bronchial Asthma
2. Seasonal Allergic Rhinitis
3. Recurrent sinusitis & Bronchitis
4. Chronic gastrointestinal distress, nausea, anorexia
5. Migraine Headaches
6. GERD with Barrett's esophagus
7. Eosinophilic Esophagitis (borderline)
8. Gastrointestinal hypomotility
9. Multiple food sensitivities
10. Multiple inhalant sensitivities
11. Oral allergy syndrome from fresh carrots, bananas
    

However, it's necessary to use a chronological, "flow-chart" approach to really appreciate what the hell is going on.  Believe it or not, getting an "integrated" view of this case isn't really that hard if you go back to some of the principles I outlined in my prior entry Diagnostic Synthesis in Multiple Food Sensitivities.  Basically, here's how I saw it on the first day I saw her: 

She has had a lifelong history of multiple allergic sensitivities, beginning in childhood with  manifestations of eczema and asthma.  These were not treated with disease-modifying immunotherapy, but "patched up" with inhalers, antihistamines, etc.  Her high-stress college-environment made her susceptible to a flareup in her allergic condition and a further "allergic march to other organ systems.  In fact, it turns out she  had an allergic march through her life--not just the usual respiratory "allergic march", but a VERTICAL allergic march involving her GI tract and Neurological systems (migraine) when she hit the fall allergy season and had an overload of ragweed and alternaria exposure. 

She had enhanced permeability brought about by high NSAID useage and Candida overgrowth.  (Prior concusions and high NSAID use followed by 2 months of doxycycline immediately before the onset of her symptoms).  Enhanced intestinal permeability subsequently caused aspread of food sensitivities during the fall mold season; Candida growth was further aggravated by the additional antibiotics she took in the later part of the fall for bronchitis.  Since enhanced intestinal permeability was her real problem, it didn't surprise me to hear she was only temporarily better on a wheat and corn free diet.  It didn't surprise me she had a migraine triggered by peanut on her first visit, since this cross-reacts with soy protein, already a formerly diagnosed food allergen.  (The beauty of food challenges is you can actually see what "target organ" is affected by a particular food.  For example, peanut triggered a migraine, but milk triggered intense stomach upset.)

Treatment Plan 

This involved 3 major areas:

1.  Improve intestinal integrity:

     ---Probiotics, oral cromolyn sodium, and short-course  fluconazole

2.  Reduce inhalant and food sensitivities with immunotherapy:

      ---SLIT immunotherapy to inhalants & foods (including all molds), titrated off RAST & IDT tests

3.   Offer patient food choices in a structured manner, since she was afraid to eat anything when first seen:

      ---Rotary Diversified Elimination Diet avoiding initially wheat, peanut, soy, carrot, banana, melon, egg, almond, pork, milk, corn, tomatos, MSG but allowing other foods on rotation

4.  Prevent a recurrence of a "crash" in the fall of 2007, like she had in the fall of 2006, by using highpotency preseasonal Ragweed treatment. 

Clinical Course:

We had first seen this patient on Jan 4; by Feb 5 (one month later) she her migraines were in complete remission and she was feeling well enough to return to school and complete her course requirements.  On her March 5 visit she related she had 1 migraine (stress from midterms).  She found improved food tolerance on SLIT, and at that point was able to reintroduce milk and beef back into her diet on rotation.  By May 2007 she was able to taper off of gastrocrom, and able to handle most foods, but still had problems with wheat and soy.  Her eosinophilia of 8% had improved by July to 2%.  She took high-potency preseasonal Ragweed treatment for 6 weeks before the ragweed season.  When she was last seen by me in November, she related she had an excellent fall allergy season, especially in light of camping out 3 weekends in August!  She was delighted she did not have her bronchitis episodes in the late fall like she had last year.  Food tolerance continued to improve, migraines were in remission, she was gaining weight, and only used gastrocrom when eating out at restaurants but still took SLIT for inhalants and foods faithfully.  She was off of Advair ("I don't need it") and her FEV1 was 4.546, 116% of predicted. 

Important Points:

There are actually several points to be made with this Case Report:

1.  Bad things can happen to a patient with multiple allergies who receives no disease-modifying immunotherapy approach, especially if their allergic "load" continues to build in a hidden fashion.    

2.  The "allergic march" can include not only the classic upper/lower respiratory tracts and skin, but also the development of neurological symptoms, including migraine headaches, and (arguably) eosinophilic esophagitis.

3.  The concept of a "critical allergic mass" is important in this case--the patient began to decompensate during the fall ragweed/alternaria mold season, when the additional load of inhalant allergens on previously existing occult food/Candida sensitivities put her in an "overload."

4.  Enhanced intestinal permeability needs to be addressed to stop the spreading of food sensitivities.

5.  SLIT can be safely used, even in patients who are polysensitized.

6.  Eosinophilic esophagitis is one more manifestation of a broadening allergic picture in this patient, rather than a totally distinct issue to be dealt with separately.  Interestingly, I have had one more patient (a doctor's son) treated with SLIT for eosinophilic esophagitis, who had a repeat biopsy confirming complete remission (the current patient has not had a repeat biopsy). 

7.  High-potency preseasonal ragweed SLIT helped the patient enjoy a healthy fall allergy season, with no recurrence of previous chronic bronchitis or other serious respiratory illness.

Her referring allergist was initially skeptical of SLIT useage, indicating in his first letter to me that "I would be somewhat hesitant to use SLIT, taking into account her current gastrointestinal complaints."  His most recent letter to me is as follows:

"I am very impressed with your management of patient X.  You and your staff have done a very nice job in managing a patient who is difficult to manage with the standard allergy management.  Keep up the good work.  

 It is gratifying to have tools to help complex patients such as this.  SLIT is one of them.  

Later, Dude   

I love Case Reports.  And I love the Annals of Allergy.  Conclusion?  I love to read Case Reports in the Annals.  What don't I love?  Any change in the status of Case Reports that might threaten to diminish their importance.  The Editorial in this month's issue of the Annals, entitled "Annals Evolution--The Next Phase" states that "The Annals will no longer accept unsolicited case reports" Instead there will be a new "Letters" feature to replace this. OOOHHHH BOY.  So what's the Angry Allergist to  do?

Well, like the song says, "I gotta be me", so I'm offering a Case Report...on...you guessed it...The Case Report.   Why am I publishing this case report here and not in the Annals?  If you don't know the answer, you haven't been paying attention:  like I mentioned earlier, the Annals is no longer accepting unsolicited case reports...so here goes: 

Iatrogenic Atrophy of the Case Report:  A Case Report and Review of the Literature

Introduction 

Case reports are undoubtedly helpful in the progression and advance of medical knowledge.  They have been a time-honored medical communication for many years.  We describe a case of iatrogenic atrophy of the Case Report, relegated to "Letters to the Editor" status, from its former status with more formal article format in this prestigious major allergy journal.

Case Report:

C.R. presented to the Annals of Allergy with a longstanding history of good health.  A vigorous contributor to medical knowledge and academic medical advancement, C.R. was unexpectedly downgraded to "Letters to the Editor" status in The Annals of Allergy, from its former status amongst its peer articles in the Annals.  C.R.'s past history had been excellent--it had regularly visited the Annals for years, and frequently praised for its work.  However, In an article entitled "Annals Evolution--The Next Phase", it was unexpectedly stated that "The Annals Editorial Office will no longer accept unsolicited case reports".   Iatrogenic atrophy of The Case Report is expected to soon follow. 

Literature Review:

Vandenbroucke, in an article entitled "The Importance of Case Reports as Compared to Evidence-Based Medicine and Molecular Explanation" asks the rhetorical question, "Does the case report still have a place in modern medical science?"  He then states "The answer is an emphatic yes."  Clinical case reports form the basis for detecting new ideas--new disease entities, new etiological clues, new side effects, and new treatments.  In an article entitled "In Defense of Case Reports and Case Series" he writes that "Case reports and series have a high sensitivity for detecting novelty and therefore remain one of the cornerstones of medical progress..For example, Morris, in an article entitled "The Importance of Case Reports", relates the Case Report appearing in the summer of 1981 in The American Journal of Dermatopathology.  Gottlieb, et. al. wrote a very small, unassuming case report entitled "A preliminary communication on extensively disseminated Kaposi's sarcoma in young homosexual men".  In the article, the authors raised an interesting question--something characteristic of any good case report: 

"This sudden, very high incidence of the condition in male homosexuals suggests an epidemic and raises the possibility of an infectious cause." 

Arguably, this was one of the first (if not THE first) article describing what we would now call AIDS.  

In addition to giving us a forum for new ideas which would suggest new medical hypotheses and stimulate further medical research, the Case Report forms a time-honored tradition in medical education--the Clinical Pathological conferences where difficult or rare cases are discussed/described for the benefit of all.  They are necessary for medical education.  They are an excellent means of describing important adverse drug effects, and even offer a way for neophyte, young authors to find their way into the medical literature.   

 But enough with the generalizations.  Why are case reports particularly crucial in the allergy literature?  Easy.  Because in our own specialty, we are often dealing with highly sensitive individuals with multiple unique sensitivities.  No two people are exactly alike.  Yet we are deluged with randomized, controlled studies investigating ONE variable in otherwise homogeneous patient populations--let's say grass pollen allergy--and see how a particular SINGLE modality (antihistamine, SLIT, etc.) helps.  The typical allergy patient (if there is such a thing) is usually "messy"--they have multiple sensitivities involving multiple target organs.  An ideal situation for case reports--and not so ideal for randomized trials.  And an ideal situation for keeping the Case Report in a prominent position--and not in the backwaters of "Letters To The Editor" at the tail end of the Annals.