The ‘Golden Rules of Pediatric Allergy’: a lesson in history.

I was recently purging my files and came across this handout. Unfortunately there is no date, no author, and there are no references for these statements. This was given to me during my pediatric clerkship at Rainbow Babies and Children’s Hospital (Case Western Reserve University School of Medicine, Cleveland, Ohio). Pediatrics was my first clerkship. So, I have had this since the fall of 1978. This document was a handout for a lecture on allergy given to the medical students.

My recollection is that an allergist by the last name of Rome was the speaker. Since this was well before the days of the internet, I was unable to verify Dr. Rome. I would like to reference the author of the ‘Golden Rules of Pediatric Allergy’ and try to get a fix as to when these were written. My guess is that this is from the  1960’s. These golden rules are almost 50 years old. How have these withstood the test of time?

I love history. If you know your history you know where you come from and that helps when you set your sites on where you need to go. Where did these come from? Was there evidence to support the contentions that not just became rules but became ‘Golden Rules’?

Some of these statements have gone by the wayside- many have been disproven over time (that is what evidence-based medicine will do), some have never been proven to be true, some may be dangerous given our current knowledge, and some still remain true to this day- especially rule #33.

Some of these rules are still being practiced, prescribed and proscribed. You could almost tell when a physician was trained when some of these re-surface. I had rule #45 present recently. It made me wonder where I had heard/seen that before, it may have been one of the ‘Golden Rules’.

This will be a dynamic document. My plan is to look into each rule, try to determine why it became a rule. Then see what we have in the 21st century to support or refute it.

So, I will need your support on this project. Please feel free to help with comments and hopefully references. Do you think something is true, do you think it is not, do you see it another way, share your perspectives.

Also note that I retyped the ‘rules’ and was exact in my work. What follows is verbatim, including any and all grammatical and  spelling errors.

The Golden Rules of Pediatric Allergy

Comments appear after the rule in blue.

1. Although you may have used it and ’got by’, never use morphine for asthma. This is akin to not using morphine derivatives such as codeine as cough suppressants in someone with known asthma. Asthma is a sputum producing condition. Children with asthma need to cough. Cough is a protective mechanism for children with asthma. Do not suppress that cough. This rule stands.

2. Antihistamines are worthless topically either in the nose or on the skin. Antihistamines gained popularity in the 1940s, during World War II, for their use in motion sickness.  By the end of the 1940s, though, drug companies had realized the potential therapeutic effects of oral and topical antihistamines for pruritis.  However, reports were also made during this time regarding several adverse reactions, including contact dermatitis, due to many of the topical antihistamines.  An article published in Pediatrics in 1973 discussed these concerning reactions and the AMA’s recommendation that topical antihistamines not be used because of their sensitizing potential and adverse reactions.

Since then, several studies have been conducted, looking at the efficacy of topical antihistamines versus placebo.  The results varied from statistically significant to inconclusive.  Multiple review articles have been written to better assess the evidence, the most recent being in 2010 in the Journal of Drugs in Dermatology.  Unfortunately, the authors revealed that the studies varied considerably and further studies needed to be conducted.  They did point out, however, that only one study had looked specifically at the efficacy of topical diphenhydramine (or Benadryl) and showed no statistical significance in its therapeutic effects for pruritis.

Similarly, studies have looked at the effect of nasal antihistamines for reduction of allergic rhinitis symptoms.  A study reported in 1998 in the Annals of Allergy, Asthma, and Immunology concluded that nasal corticosteroids had a greater reduction of symptoms when compared to nasal antihistamines.  However, a study reported in 2006 in the same journal showed a statistically significant difference between an intranasal antihistamine (azelastine) and an oral antihistamine (cetirizine) in reduction of allergic rhinitis symptoms.  Most recently, a review published in 2011, again in the Annals, concluded that intranasal antihistamines were superior to oral antihistamines in the treatment of allergic rhinitis, but likely equally beneficial as intranasal corticosteroids.

Ultimately, it appears that although topical antihistamines are widely available and commonly used, there has not been definitive studies showing greater efficacy in treating pruritis or allergic rhinitis as compared to other therapies.

References:

1.     Berger W, Hampel F Jr, Bernstein J, Shah S, Sacks H, Meltzer EO. Impact of azelastine nasal spray on symptoms and quality of life compared with cetirizine oral tablets in patients with seasonal allergic rhinitis. Ann Allergy Asthma Immunol. 2006 Sep;97(3):375-81.

2.     Eschler DC, Klein PA. An evidence-based review of the efficacy of topical antihistamines in the relief of pruritis. J Drugs Dermatol. 2010 Aug;9(8):992-7.

3.     M.A. Kaliner, W.E. Berger, P.H. Ratner, C.J. Siegel. The efficacy of intranasal antihistamines in the treatment of allergic rhinitis. Ann Allergy Asthma Immunol, 106 (suppl) (2011), pp. S6–S11

4.     Stern MA, Wade AG, Ridout SM, Cambell LM. Nasal budesonide offers superior symptom relief in perennial allergic rhinitis in comparison to nasal azelastine. Ann Allergy Asthma Immunol. 1998;81(4):354–358.

5.     Yaffe S, Bierman CW, Cann HM, et al. Antihistamines in topical preparations: statement of the Committee on Drugs, American Academy of Pediatrics. Pediatrics. 1973;51:299-301.

 Thanks to Dr. Seethal Jacob- a third year pediatric resident at Riley Hospital for Children for her work on Golden Rule #2.

3. Bacitracin remains the only antibiotic which is really safe for local application.

4. Ask the child with cyclic vomiting if he hurts anywhere. He may have migraine.

5. Canker sores inside the lower lip may be due to tooth paste. Also consider orange, tomato, food dyes (pop, Kool Aid, bubble gum etc.)

One of our recent medical students, Dr. Tassey took this ‘Golden Rule’ and wrote the following;

The association between canker sores, or aphthous ulcers, and toothpaste most likely originates from a chemical substance commonly used in toothpastes and some food products that require an emulsifier, known as sodium lauryl sulfate (SLS). SLS is also frequently referred to as Lauryl Sulfate sodium salt or sodium dodecyl sulfate (SDS) (1). Sodium dodecyl sulfate (SDS) may sound familiar to some because it is the detergent component used in SDS-PAGE, an electrophoresis protocol.  When used in SDS-PAGE, SDS is responsible for breaking down membranes of molecules so that proteins can be separated out by their size during the electrophoresis process (2). This well-known effect of SDS on cellular membranes may help explain the damaging properties the chemical can have on squamous cells in the mouth, leading to aphthous ulcers in some susceptible individuals.

According to Colgate, around 1945, soaps that were used in toothpastes began being replaced with SDS in order to create a smoother paste or emulsion (3). The anionic surfactant has since become widely used in nearly all toothpastes, additive to foods and cosmetics to decrease surface and allow products  to spread over a larger surface area(1).

Over the last 20 years, many studies have attempted to assess the proposed association between aphthous ulcers and SDS-containing products, especially toothpastes. One single-blinded, crossover study conducted in 1997 found a significant difference in the occurrence of aphthous ulcers in study participants over a 2 month period (4).  A variety of other, smaller studies have concluded similar results: that use of SDS (or SLS) free toothpastes significantly reduces the number of aphthous ulcers (5, 6).

As SDS is widely used in numerous oral care, cosmetic and food products the association between the emulsifier and its ability to cause aphthous ulcers in some individuals is generally accepted, but continues to undergo investigation. Despite some debate as to the chemical’s ability to cause aphthous ulcers, today many “SLS-free” and “all natural” toothpastes exist for individuals who believe they are extremely sensitive to the chemical and experience recurrent aphthous ulcers when SDS-containing products are used.

References
1. Australian Government Department of Health and Ageing. NICNAS Existing Chemicals Information Sheet.
Sodium Lauryl Sulfate, CAS No: 151-21-3. 9 Oct 2003. Accessed on 07/25/2011

URL: http://www.nicnas.gov.au/publications/information_sheets/existing_chemical_information_sheets/ecis_sls_pdf.pdf
2. Department of Biology, Davidson College.  SDS-PAGE (PolyAcrylamide Gel Electrophoresis).  Davidson, NC 28036 Copyright 2001. Accessed on 7/31/2011

 URL: http://www.bio.davidson.edu/courses/genomics/method/SDSPAGE/SDSPAGE.html

3. Colgate. The History of Toothbrushes and Toothpastes. Last updated: 6/12/2006. Accessed on 7/31/2011

URL:http://www.colgate.com/app/CP/US/EN/OC/Information/Articles/Oral-and-Dental-Health-Basics/Oral-Hygiene/Brushing-and-Flossing/article/History-of-Toothbrushes-and-Toothpastes.cvsp

4. Chahine L, Sempson N, Wagoner C. The effect of sodium lauryl sulfate on recurrent aphthous ulcers: a clinical study. Compend Contin Educ Dent. 1997 Dec;18(12):1238-40.
PubMed PMID: 9656847. (Unable to access full paper)

5. Herlofson BB, Barkvoll P. Sodium lauryl sulfate and recurrent aphthous ulcers. A preliminary study. Acta Odontol Scand. 1994 Oct;52(5):257-9. PubMed PMID:7825393

6. Herlofson BB, Barkvoll P. Oral mucosal desquamation of pre- and post-menopausal women. A comparison of response to sodium lauryl sulphate in toothpastes. J Clin Periodontol. 1996 Jun;23(6):567-71. PubMed PMID: 8811477.

 

6. In urticaria, ask about recent penicillin or overindulgence in citrus fruits, fresh tomato, chocolate, or egg. Also consider aspirin, sulfonamides, shrimp, walnut and pecan, fish, or pork.

7. The most common source of recurrent or persistent diarrhea in children is food allergy.

The origins of this golden rule are truly unknown. I went through the Ruth Lilly Library website with the terms food allergy and diarrhea and tried to find the earliest published reports and opinions on that topic. I came across articles written by the ‘founders’ of allergy; Greer, Rowe, and Ratner. The earliest publication was from 1920 by Oscar M Schloss (American Journal of Diseases of Children 19:433,1920). Clearly the origins of the consideration of food allergy causing diarrhea are almost 100 years old. This article was a study of 122 children that the author had seen over 7 years. “That certain infants develop acute gastro-enteric disturbances when fed small amounts of raw cow’s milk, is a matter of common observation”. Some of these infants had hives, edema, and marked generalized ‘disturbances’ . This later group all had a positive skin test to cow’s milk protein (Anaphylaxis). A second group had less acute symptoms which did not appear until the milk was ingested for a few days. These symptoms were loss of appetite, followed by vomiting and diarrhea, irritability, and at times, fever. This group rarely showed a positive allergy test to milk. Some could tolerate formula made of dried cow’s milk but did poorly with raw or pasteurized milk.

The article ‘Diarrhea Caused by Food Allergy’ by Rowe (Journal of Allergy 27;424, 1956) listed 9 references to support the statement that food allergy as a cause of colic and diarrhea…. In infants and young children has long been recorded. So the origins of this golden rule date back many years.

How does this golden rule of pediatric allergy stand up to current findings? My thanks to Dr. D. Slifko, one of our Riley residents who offered the following;

According to Nelson’s Textbook of Pediatrics and a Peds in Review article from 2005, this statement is NOT true.  The most common reason for persistent diarrhea, or diarrhea lasting greater than 14 days is often infection, usually due to bacteria.  While viral infections can cause diarrhea in the acute setting, these episodes usually resolve after 1 week.  Persistent bacterial infections, however, can be due to Campylobacter, Salmonella, and Yersina, and can last from 2 weeks up to several months in infants.  These are by far the most common cause of recurrent or persistent diarrhea in children.  After infectious causes, post-infectious sequelae or Post-Enteritis Syndrome is the next most common causes of chronic diarrhea.  Following a bought of diarrhea, the brush border of the intestinal lining is often damaged and inflamed.  This leads to an inability to resorb nutritents, especially sugars, which results in a transient osmotic diarrhea.  The brush border of the intestinal villi is rich in diasaccharidases, including lactase which is the enzyme required to break down the milk sugar lactose.  After a child sustains damage to the intestinal lining, lactase may be transientenly less effective, thereby resulting in a temporary lactose intolerance and leading to diarrhea with drinking milk.  Still, this does not qualify as an allergy and is more of a result of infection.  Furthermore, there is a very long list of possible diagnoses that may cause chronic diarrhea in children and infants which includes Abnormal Digestive Processes, such as CF, Anatomical Abnormalities, Malapsorptive Syndromes, Structual Defects, Motility Disorders, and Allergic and Inflammatory disorders.  Food allergies and inflammatory disorders are a common cause of diarrhea in children, especially Cow’s Milk allergy as children are often exposed to milk in infancy.  However, this usually presents with bloody stools and is not the most common cause of persistent diarrhea.  Therefore, while Milk Protein Allergy or food allergy is an important differential to consider in the pt with persistent diarrhea, it is by no means the most common or the only diagnosis that may be present.

Sources:

  • 1.  Kleigman:  Nelson’s Textbook of Pediatrics, 19th Ed.  Ch. 33: Chronic Diarrhea
  • 2.  Keating, James P.  Chronic Diarrhea.  Pediatrics in Review. 2005;26:5-14

8. When the complaint is foul breath, think of food allergy, especially milk, or less commonly, egg.

9. If a mother says her young child has fever following the eating of a certain food she is probably right. Fever from allergy is not rare.

10. Hand sweating is common in infants with milk allergy.

11. In infants with profuse nasal discharge and blocking, don’t overlook choanal atresia. See if a nasal catheter appears in the pharynx.

12. “All that wheezes is not asthma”. Think of a bronchial foreign body.

 

All that wheezes is not asthma”. Think of a bronchial foreign body

Wheezing is a common presenting symptom in children reported by their parents/caregivers.   Typically the examiner has to do some investigation to identify the source of the wheeze and determine if the noisy breathing by the child is indeed wheezing.  Many parents refer to any noise and change in their child’s breathing as a wheeze.  A good history and physical can usually clue in the physician as to whether the child is indeed wheezing versus having other respiratory issues of the airway like stridor.    

While wheezing can definitely be associated with asthma, we need not forget the many other causes of wheeze in children.  The Golden Rule of Pediatric Allergy “All that wheezes is not asthma” certainly remains true to date and will continue to remain true for many years to come.  This adage was coined by Chevalier Jackson, an American laryngologist, about a century ago from the patients he was seeing in his practice.  Jackson noted that foreign bodies in the airway can produce a noisy breathing that mimics the wheeze of a patient with asthma, and thus when one hears a wheeze we must not assume it is due to asthma.  In fact, some patients with asthma never wheeze.  During his career, Jackson developed methods to safely remove foreign bodies from the airway and esophagus and some classify Jackson as the inventor of modern endoscopy.   Given the nature of Jackson’s practice, he would definitely advocate to never overlook the possibility of a foreign body in the patient who wheezes.  Often time, a good physician can rule in or out foreign body aspiration given the history like the toddler who plays with small toys who started wheezing acutely.   Radiological imaging may be necessary to identify a foreign body, however some materials like food (ie peanuts, popcorn) are radiolucent and will not show up on an X-ray and other modalities will be necessary like performing a bronchoscopy to visualize the airways.   While a bronchial foreign body can produce a wheeze, there are many other conditions to consider. 

The differential diagnosis for a child that wheezes can be vast and can be separated into acute and chronic (or recurring) wheeze.  In the child with acute onset of wheeze, asthma and foreign body aspiration are definitely possibilities however, you also have to think of and rule out other conditions like bronchitis, bronchiolitis, and tracheitis.   Children with chronic wheeze may have structural and/or functional abnormalities.  Structural abnormalities affecting the respiratory tree include tracheal web/stenosis,  vascular web/compression, tumors and lymphadenapthy causing compression, tracheo-bronchomalasia, and cardiomegaly.  Functional abnormalities include asthma, gastroesophageal reflux, recurrent aspiration, retained foreign body, cystic fibrosis, vocal cord dysfunction, bronchopulmonary dysplasis, primary cilia dyskinesia, interstitial lung disease, bronchiolitis obliterans and pulmonary edema.   Therefore the next time you see a child who wheezes, always remember “All that wheezes is not asthma”.   Remembering this adage can help improve patient care and make diagnosis of any of the above conditions more timely and allow for appropriate and efficient management and treatment of the wheezing child. 

References:

Broom, T and Okereke, C.  “All that wheezes in not asthma.”  Emergency Medicine Journal,      2008;25:311.                  <http://emj.bmj.com/content/25/5/311.full>.

“Chevalier Jackson.”  The University Archives and Special Collections at Thomas Jefferson      University. <http://jeffline.jefferson.edu/sml/archives/exhibits/notable_alumni/              chevalier_jackson.html>.

Fakhoury, K.  “Approach to wheezing in children.”  UpToDate. 2013. <http://www.uptodate.com.                 proxy.medlib.iupui.edu/contents/approach-to-wheezing-in-children?source=search_result                 &search=wheezing+in+children&selectedTitle=1%7E150>.

 

Submitted by Shaylar Padgett, MD, PGY1  on 4/1/13

Thanks Dr. Padgett! Nice work

13. Allergic children generally do poorly in moldy houses or in houses shared with cats and dogs.

14. Before giving penicillin or horse serum, take a few seconds to ask about previous reactions. Skin test, of course, for horse serum.

15. Do not overlook the possibility of allergy in the “nervous” child.

16. Ragweed patients should avoid the insecticide, pyrethrum.

Dr. Amanda Walter took on this very interesting ‘Golden Rule’.

In the botanical classification system, ragweed is of the family Asteraceae , genus Ambrosia and is a long-known cause of allergy or “hay-fever” in the late summer/early fall. Pyrethrum (referring to a group of plants including chrysanthemum, feverfew, golden feathers, and pellitory) belongs likewise to the family Asteraceae, genus Chrysanthemum.5 It is not as widely known as ragweed for environmental/seasonal allergy; but due to its shared umbrella within the family Asteraceae, pyrethrum is believed to cross-react with allergen receptors in ragweed sensitive patients to elicit similar “hay fever” symptoms upon exposure.1

Concern of pyrethrum as an allergen was noted as early as the turn-of-the-century in a 1930 article questioning whether pyrethrum-containing insecticides could be responsible for allergic rhinitis, asthma, or anaphylactic dermatitis is susceptible individuals. Pyrethrum powder (obtained by crushing dried chrysanthemum flowers) had been used for its natural insecticide properties since the mid 1800’s with noted case reports of dermatitis, sneezing/itching eyes/difficulty breathing after termination of ragweed season, and one case of anaphylactic dermatitis all in pyrethrum handlers. These patients displayed positive skin testing to pyrethrum and were found to be positive to ragweed, as well, heightening suspicion for cross-reactivity of ragweed and pyrethrum allergens. The conclusion of the 1930’s article was that pyrethrum was a “questionable” allergic component of insecticides affecting some individuals.3

More recent manufacture of pyrethrum-based insecticidal materials (powders, sprays, creams, shampoos) employs advanced extraction methods compared to those used at the turn of the century. Instead of using whole, crushed pyrethrum leaves, only the active insecticidal component of the plant is extracted and refined, removing many allergenic imprities found in crude pyrethum. This refined pyrethrum extract is known as pyrethrin and is one of the major ingredients in insecticides along with pyrethroids (synthetic insecticides similar in structure and action to pyrethrin but modified to increase potency and stability in the environment). Therefore, all pyrethrum-based insecticidal materials on the market today contain purified pyrethrin extract or synthetic pyrethroid and are “not expected to contain the allergic component found in [crude] pyrethrum”.4 There are, however, incident reports that bring to question a potential association between pyrethrin/pyrethroid exposure and allergy/asthma. Based on an extensive review conducted by the EPA (with data collected from the FDA), “adverse event data [does] not support an association between use of pyrethrins or permethrin pharmaceutical pediculicide and scabicide products and allergic or asthmatic responses, despite . . . [instances of direct] application and  . . . high [environmental] exposure levels”.4

Of note, all OTC insecticide drug products (including those using pyrethrin extract and synthetic pyrethroids) for the treatment of head lice and scabies have an FDA warning that reads: “Ask a doctor before use if you are allergic to ragweed. May cause breathing difficulty or an asthmatic attack”.4 This warning is reflective of limited case reports of severe reactions in patients using a pyrethrum-containing product. In general, pyrethin-containing products (i.e. pyrethrin shampoo) should not be used by individuals allergic to chrysanthemums, and patients with ragweed allergies should be warned that they may experience wheezing and dyspnea.1 This is likely due to the fact that pyrethrin is a natural extract of the pyrethrum plant and may inadvertently contain some allergic-inducing impurities, though more recent studies have shown current extraction techniques to remove all allergic components.2 Pyrethroid-containing products (i.e. permethrin) should not cause allergic reactions due to the synthetic nature of this component and are considered safe for use regardless of ragweed or pyrethrum allergy.1

References:

  1. Burkhart CG, MPH, MD. Relationship of Treatment-Resistant Head Lice to the Safety and Efficacy of Pediculicides. Mayo Clinic Proceedings. 2004; 79:661-666.
  2. Franzosa JA, Osimitz TG, Maibach HI. Cutaneous contact urticarial to pyrethrum-real?, common?, or not documented?: an evidence-based approach. Cutaneous and Ocular Toxicology. 2007; 26(1): 57-72.
  3. Ramirez MA, MD. Pyrethrum: An Etiologic Factor in Vasomotor Rhinitis and Asthma. Journal of Allergy. Jan. 1930; Vol. 1, Issue 2: 149-155.
  4. US Environmental Protection Agency Office of Pesticide Programs. A Review of the Relationship between Pyrethrins, Pyrethroid Exposure and Asthma and Allergies. Sept. 2009. Available online: http://www.epa.gov/oppsrrd1/reevaluation/pyrethrins-pyrethroids-asthma-allergy-9-18-09.pdf.
  5.  An Online Botanical Encylopedia: Scientific and Botanical Systems of Classification. ePlantScience.com, available online: http://www.eplantscience.com/index_files/medicinal_plants/classification_and_identification/scientific_and_botanical_systems_of_classification.php.

Submitted by Amanda Walter, MD (Pediatrics, Riley) September, 2011. 

17. Patients allergic to chocolate should avoid related kola nut of cola drinks, and patients allergic to peanuts are probably allergic to beans and peas.

My thanks to Dr. Srivastava for the following;

Fortunately for most people, true allergy to chocolate is extremely rare. More than likely, a person with a “chocolate” allergy is sensitive to one of the components, such as milk or nuts. The kola nut is a plant native to Western Africa, and became famous as one of the main ingredients in the original formulation for Coca-Cola. Although it is not as commonly used, it is making a comeback as part of the trend of “all-natural” cola drinks. No data exists to support that having a true chocolate allergy predisposes an allergy to kola nut containing compounds, including cola drinks.

Peanuts are legumes, and come from the same general family as soybeans, beans, and peas. Likewise, there is no published data that supports a consistent reaction between peanuts and other members of the legume family. If you are part of the 1% of the population who do have a peanut allergy, the best way to know if you need to avoid other legumes is to consult an allergist.

Source for the rule:

Speer, F. Food allergy: the 10 common offenders. Am Fam Physician. 1976 Feb 13 (2): 106-12.

 Contemporary Source:

Chapter 40: Food Allergy. Clinical Allergy. Current Clinical Practice. 2009. 1-40.

18. “Dust shots” are ineffective if the patient does not avoid heavy exposure to house dust. This is also true of ragweed and molds.

19. A patient (or his mother) rarely “imagines” he is allergic to a food or drug.

20. Death has followed the injection of ivy extract in the treatment (not prophylaxis) of ivy dermatitis. A safe shot is ACTH.

21. Do not minimize the danger of insect stings, especially those of wasps and bees.

 The following was submitted by Dr. J. Rybka, Pediatrics Riley Hospital, October 2011

 Finding an original article on this topic is difficult. The earliest record of an allergic reaction to an insect appears in hieroglyphics in the tomb of King Menes of Egypt. This first report was in 2641 B.C. and referred to the king’s death due to the sting of a wasp or hornet.

Hymenoptera are a large group of insects that include honeybees, bumblebees, wasps, hornets, yellow jackets, and ants.  These insects can be very dangerous for people who are sensitive to their venom. In fact, hymenoptera stings account for more deaths in the US than any other envenomation.  Ants sting 9.3 million people each ear.  Other hymenoptera species account for more than one million stings annually. A review of animal related deaths in 2005 determined that Hymenoptera stings accounted for 533 deaths in the US from 1991-2001, which represents 70.2% of all venomous animal related fatalities in the US.  Wasps and bees themselves cause 30-120 deaths yearly in the US.  The true incidence of fatal reactions may even be higher as sudden deaths occurring outside may be mistakenly attributed to heart attacks and strokes. 

 The hymenoptera venom consists of mixture of biologically active substances, which include various enzymes, peptides and low-molecular-weight compounds.  Toxic components include phospholipase, histamine, bradykinin, acetylcholine, dopamine and serotonin.  Many of these peptides cause degranulation of mast cells, which results in the reactions seen.  Not only can activation of this cascade cause severe and life threatening reactions but a large venom load can also be sufficient in and of itself to cause fatal injury.  Several types of reactions can develop after being stung by hymenopteran insects.

 Reactions can be non-allergic and local in nature, which would involve pain, minimal edema, and redness at the site of the sting.  Large local reactions occur in 17-56% of those who are stung.  The reaction can be allergic in nature and can either be local with more extensive swelling exceeding 10 cm and persisting longer than 24 hours or can be anaphylactic which involves generalized urticaria, bronchospasm, hypotension, cardiovascular collapse, and loss of consciousness. Anaphylaxis secondary to Hymenoptera envenomation affects roughly three percent of the general population.  One may also experience a systemic toxic reaction with edema, vomiting, diarrhea, headache, hypotension, seizures, and altered mental status.  Systemic reactions leading to life threatening manifestations occurs in approximately 0.4-0.8% of children and 3% of adult patients.  There have been some unusual reactions reported which include cardiac ischemia, renal failure, and encephalomyelitis.

It is important to know that fatal allergic reactions can occur as the first generalized reaction.  In fact, about one half of patients who die as a result of hymenoptera induced anaphylaxis did not know that they had an allergy.  It is more common, however, for a fatal reaction to follow a previous milder generalized reaction. Venom allergy is very likely to be under-recognized and underdiagnosed which is why insect stings should be taken very seriously.  

 Sources:

Ciszowski, Krzysztof and Mietka-Ciszowska, Aneta.  Hymenoptera Stings.  Przegl Lek. 64(4-5):282-9, 2007.

 Emedicine.medscape.com, key word Hymenoptera stings.

 UpToDate.com, key word Hymenoptera stings.

 

22. Never prescribe a drug if the patient says he is allergic to it. You have nothing to gain and everything to lose.

23. T and A is probably never of benefit in asthma. It may precipitate asthma in allergic children.

Dr. Keena, one of our medical students, evaluated this Golden Rule. He offers the following:

This rule probably originated with a 1931 study in the Journal of Allergy.  The study involved 600 patients with nasal or pulmonary allergy symptoms, 300 of which received adenotonsillectomy, and 300 that did not.  The study concluded that the positive results and failures within the two groups were “almost identical.”1

The same study also did a ten year follow-up on 2000 children, half of which underwent adenotonsillectomy at age 5 or 6.  The other half had been advised to undergo adenotonsillectomy, but had opted not to.  The study found that a slightly greater number of children who received the procedure developed allergic symptoms than those that did not.

Currently, there validity of this rule is somewhat controversial.  While the rule is correct that asthma alone is not an indication for adenotonsillectomy, newer studies in Laryngoscope (2010)2 and Acta Oto-Laryngologica (1996)3 that suggests that adenotonsillectomy may improve asthmatic symptoms and decrease asthma medication requirements.  It may be the case that improving the upper airway in children may lead to improvement of the lower airway in asthmatic children.

 References-

  • Bullen, S.S., The effect of tonsillectomy in allergic conditions. Journal of Allergy 2:310,1931
  • Busino, R. S., Quraishi, H. A., Aguilla, H.A.. Montalvo, E., Connelly, P. The impact of adenotonsillectomy on asthma in children. Laryngooscope 120 Supplement 4: S221, 2010.
  •  Saito, H., Asakura, K., Hata, M., Kataura, A., Morimoto, K., Does adenotonsillectomy affect the course of bronchial asthma and nasal allergy? Acta-Oto-Laryngologica Supplement 523:212-5.

24. If the allergic child’s mother insists that he must be protected from outdoor exposure she is probably right.

25. From 0.05 cc to 0.10 cc is the correct dose of epinephrine. Over dosage can scare you and the family badly.

26. Although skin testing for inhalants is accurate, skin testing for foods is not.

27. Suspect milk allergy in the child with an unusual craving for it.

28. Antipruritic ointments are of little use in allergic dermatoses and may make matters worse.

29. In infantile colic a change to a milk substitute such as Mullsoy or meat base should be considered. First give the infant time to get accustomed to the milk formula.

30. In the absence of an organic cause of projectile vomiting in the newborn, think of milk allergy.

31. Antihistamines are useful in nasal pollenosis, but not in asthma or much of anything else.

32. Not only is vaccination for smallpox contraindicated in children with eczema, but also in their siblings and playmates.

33. No matter what you owe other allergic children, you owe the asthmatic child the benefit of the most skilled allergist you can find.

34. In this day of synthetic vitamins do not prescribe orange juice for infants. They seldom like it anyway. The same could be said of egg yolk.

35. Infection and dehydration are hidden problems in status asthmaticus.

36. It has been shown that nursing babies may be allergic to foods in the mother’s diet. Common offenders: egg, milk, chocolate, citrus fruits. Common symptoms: colic and eczema.

Pediatric resident, Dr. Steele helped to sort out this Golden Rule;

It has been shown that nursing babies may be allergic to foods in the mother’s diet. Common offenders: egg, milk, chocolate, citrus fruits. Common symptoms: colic and eczema.It is difficult to find where this rule originated though I did see an article dating back to 1930 that researched the possible link between breast feeding
and eczema. Despite unclear origins, this allergy rule has persisted in public belief and continues to play a role in maternal choices.

Dietary changes during pregnancy and lactation have been proposed as methods to prevent or allieviate allergies in children, especially those with a family history. This does not apply to infants who manifest signs of allergic disease shortly after birth, as dietary interventions would be treatment rather than prevention.  The largest study of pregnant women with dietary avoidance was done in Sweden in the 1980s. 212 women received a diet free of cow’s milk and eggs compared to women who kept a normal diet. At 18 months and 5 years, there was no difference in rate of allergic rhinitis, atopic dermatitis (eczema), or asthma. At 5 years of age, the children actually had a higher rate of egg allergy if their mother had avoided eggs in pregnancy. The AAP does not recommend dietary avoidance during pregnancy as a means of primary prevention of allergic disease or eczema.

Avoidance diets of mothers who are breast feeding have been studied as a means of prevention as well. There have been studies with women avoiding egg, cow’s milk, fish, and nuts during lactation. The results have been mixed, with some trials showing decreased rates of eczema and allergies, others showing increased rates.  There was a Cochrane analysis done to pool the data together and their conclusion was that avoidance diets during breast feeding may reduce the risk of developing eczema and the severity during the first two years of life, but after that age, there is not enough data to have further recommendations.  The avoidance diets also need to be weighed agaist the benefit of nutrition.

Peanuts, as a non-essential food and one associate with allergic reactions, have also been studied in avoidance diets, as a means to prevent peanut allergies in children. Again, the data is mixed with some studies showing a benefit and some no benefit.  There is no current recommendation to support the general population from avoiding peanuts during pregnancy or lactation. There is a recommendation that families where one child has a peanut allergy could consider avoiding it during pregnancy and lactation.

I was unable to find any studies that looked at chocolate or citrus fruits in a controlled setting in regards to eczema rates. The evidence regarding chocolate and citrus with colic is limited and not sufficient to comment on though there continues to be frequent family reporting that this is a relationship.

Breast feeding itself has been proposed to have a protective effect from developing eczema. There have been studies to support and refute this claim but a 2001 meta analysis of 18 studies showed an overall protective effect for children who were exclusively breast fed three months.

References:

Gruleeetal. “The influence of breast and artificial feeding on infantile eczema.” J Pediatr 1930; 9:223.

Falth-Magnusson et al.”Development of atopic disease in babies whose mothers were receiving exclusion diet during pregnancy–a randomized study.” J Allergy Clin Immunol. 1987;80(6):868.

Kramer er al.”Maternal dietary antigen avoidance during pregnancy or lactation, or both, for preventing or treating atopic disease in thechild.”  Cochrane Database Syst Rev. 2006;3:CD000133.

Gdalevich et al. “Breast-feeding and the onset of atopic dermatitis in childhood: asystematic review and meta-analysis of prospective studies.” J Am Acad Dermatol. 2001;45(4):520.

37. If you use corticosteroids, use them only in extreme situation and not over 4-5 days. They are vastly over-rated.

38. Aminophylline suppositories are useful in asthma but must not be used in overdosage. Death is a possibility. I use 100mgm, for each 30 lb. of body weight, not oftener than q8h.

39. Topical use of respiratory vasoconstrictors (nose drops and asthma sprays) may lead to a sort of addiction, unusual dryness, and neglect of better treatment.

 The following is from Dr. Elizabeth Gates

This rule likely has its first published origins in the otolaryngology literature in 1931, where Dr. Fox was the first to describe the histological effects of chronic nasal ephedrine and epinephrine in rabbits. (1)   The term “rhinitis medicamentosa” was first used by Dr. Lake in 1946 and has since been used to describe the condition of “nasal rhinorrhea, postnasal drip, or sneezing that begins after using a nasal decongestant for more than three days” (2)

Over the counter topical decongestants nasal sprays fall into two classes.  There are the imidizolamines such as oxymetolazone (Afrin) and the sympathomimetic amines like phenylephrine (NeoSynephrine).  While they provide rapid vasoconstriction and relief of decongestion prolonged use can be harmful. 

While the various histologic changes associated with chronic use of nasal decongestants, the pathophysiology is not clear.  There is some thought that local norepinephrine production is reduced through negative feedback effects in the case of the imidazolamine derivatives.   Another theory is that the alpha adrenergic effect predominates during the first few days of use and then vasodilatation due to beta adrenergic action emerges when sympathomimetic amines are used..  Another hypothesis is that the preservative benzalkonium chloride aggravates the condition by impairing mucocilliary clearance. (3)

The physical findings in the condition can resemble those in infectious or allergic rhinitis, and the diagnosis is typically confirmed with a careful history, which may reveal that the patient has increased the dose and frequency of the decongestant in order to address the worsening symptoms.   

Treatment of rhinitis medicamentaosa begins with cessation of the medication.   Unfortunately, rebound congestion and worsening nasal stuffiness may occur.  In recent years, a number of trials have used corticosteroid nasal sprays and shown beneficial effects.  (4)

References:

1.)  Fox, N.  The Chronic Effect of Epinephrine and Ephedrine on the Nasal Mucosa.  Archives of Otolaryngology.  1931; 13(1):73-76

2.)  Ramey JT, Bailen E, Lockey RF.  Rhinitis Medicamentosa.  J Investig Allergol Clin Immunol 2006; Vol. 16(3): 148-155

3.)  Rizzo JA, Medeiros D, Silva AR, Sarinho E. Benzalkonium chloride and nasal mucociliary clearance: a randomized, placebo-controlled, crossover, double-blind trial.  Am J Rhinol. 2006 May-Jun;20(3):243-7.

4.)  Graf, P.  Rhinitis Medicamentosa.  Treatments in Respiratory Medicine.  2005(4) : 21-29

Clearly the overuse of topical decongestants can cause a significantly worse problem. Treating the ‘addiction’ of the nasal mucosa to topical decongestants is diffficult. The obvious treatment is to just stop the medication. However, I recall an article from the last century that suggested that the use of a topical nasal steroid may be of help. The plan was to stop using the decongestant on one side, but continue it on the other side for two weeks while a topical nasal steroid is used to both sides twice a day. Thanks Dr. Gates!

FEL 1-24-2012

40. No child should be ordered to another climate for relief of allergy without consultation with and allergist. It is of doubtful value and may ruin the family financially.

M. Pfederer, one of our medical students submitted the following (11-14-2100)

Today, runny nose, itchy eyes and sinusitis cause symptoms for up to 1 in 5 Americans.  For as long as we have attributed the symptoms of hay fever to plant pollen, escaping the geographic distribution of these invisible demons is a reasonable and popular proposal.  Couldn’t a severe birch tree allergy be tempered by staying 100 miles from the nearest birch tree?  Not reasonable, shouldn’t I at least cut the one down from my front yard?  Today countless anecdotes can be found on the blogosphere citing improvement and decline in allergic symptoms as people move around the country, but how can we reliably predict relief of hay fever by escaping the causative environmental exposure.  First lets look at the history and evolution of the escape from allergy. 

While I originally had trouble finding literature documenting this idea, I found a gold mine in journal article “Hay Fever Holiday” by Greg Mitman which reviews the cultural phenomenon of allergy escaping vacations in the 1800’s. 

            ” In mid-August each year, thousands of sufferers fled to the White Mountains of New Hampshire, to the Adirondacks in upper New York State, to the shores of the Great Lakes, or to the Colorado plateau, hoping to escape the dreaded seasonal symptoms of watery eyes, flowing nose, sneezing fits, and attacks of asthma, which many regarded as the price of urban wealth and education.”[1]

In his book Mitman goes on to outline how the culture of hay fever provided stimulus for growth of rail lines, cities and regions thriving off “hay fever holidays.”  While a cultural phenomenon, it was only vaguely understood that this “autumn catarrh” was associated with change of seasons and environmental irritants.

Have our scientific efforts in the field of allergy improved our ability to escape the suffering of hay fever?  To know how to properly run away, we first need to address what we are running away from.  Pollen, the reproductive mechanism of plants can come in two forms; anemophilous, literally wind loving, and entomophilous, insect loving.

Into the 20th century, as knowledge of environmental allergens grew, more drastic measures to prevent “hay fever” were taken by cities such as New Orleans to eradicate weeds.  This attempt was later proved futile by Morrill Wyman sampling of pollens via airplane at 15000 feet, which showed for the first time the traveling capacity of the causative agent.[2]  This was later corroborated when research found pollen up to 2000 miles from its source. [3]  We also know that a considerable amount of these allergens remain behind for weeks after the pollen is shed. In other words, the pollen is not only immunologically active the day it comes off the plant, but for weeks later. [4] This understanding of pollen helps us put together the framework for explaining seasonal allergies based on pollination seasons.   “Tree pollens are shed in the spring, grass pollens in early summer, and weed pollens (especially ragweed) in late summer and fall.”2  Given these facts, we could theoretically explain a “Yankee’s” bout of hay fever in snowy March from the early spring pollen season in the southern United States.

So if someone really did have an isolated birch allergy, staying a long flight away from birch in the spring months would theoretically provide good relief.  However another factor preventing successful escape from allergic rhinitis is the increasing breakdown of geographically specific species.  As people move, they took their plants with them, changing the environmental landscape. One allergy haven in Bethlehem, Maine noticed, “diminishing its immunity from Hay Fever” because reported by Professor Samuel Lockwood at the time “unless nature has been left to her virgin forms, complete relief could no longer be found.”  This problem continues to persist for parts of the country considered as “allergy havens.”  In some areas of the Southwest, laws were made outlawing Bermuda grass for disrupting their historically low pollen count.[5]   In 1984 National Geographic covered an anecdote of a man moving to Tucson, Arizona for relief only to find a bustling metropolis of pollen.[6]

In spite of all this trouble, there are still some geographical differences in plant, weed, and grass species.  Less ragweed, which affects 75% of sufferers is found in a band along the West Coast, the southern-most tip of Florida and northern Maine, so escaping to these areas could provide temporarily provide relief.  However, perhaps the most important issue preventing successful escape of environmental allergens is the idea of sensitization.  This is the idea that your immune system will learn to build an allergic response to a new allergen over time.  While literature was hard to pin down, clinical knowledge seems to suggest 2-3 years as a common time frame for sensitization.  Famous allergist, Dr, Max Samter puts it this way, The body’s immune system can rekey itself and develop an allergy to plants those places do have…God takes care of allergists.”6  Recently, Pfizer did a nation wide poll searching for geographic hot spots for allergy sufferers.  Percentages ranged from 49 percent in the Western region to 61 percent in the Mid-Atlantic.  If I were an allergist, I would suggest that you take this with a grain of pollen.  For me the evidence stacks up against escaping your allergies.  As long as pollen is in the air, sufferers will not be able to avoid their nemesis.

 [1]  Mitman, Gregg. “Hay Fever Holiday: Health, Leisure,and Place in Gilded-Age America.” Bull. Hist. Med., 2003, 77: 600–635

[2] A history of pollen mapping and surveillance: The relations between natural history and clinical allergy, journal of clinical immunology, November 2004

[3] HYDE, H. A.  Atmospheric pollen grains and spores in relationto allergy. II  Clinical Allergy, 1973, Volume 3, pages 109-126

[4] David Peden, Charles E. Reed, Environmental and occupational allergies, Journal of Allergy and Clinical Immunology, Volume 125, Issue 2, Supplement 2, February 2010, Pages S150-S160, ISSN 0091-6749, 10.1016/j.jaci.2009.10.073.

[5] Solomon and H. Hayes, Impacts of urban development upon allergenic pollen in a desert city. J Arid Environ, 3 (1980), pp. 169–178.

[6] Newman, Cathy. “Pollen: Breath of life and sneezes”. National Geographic, 1984, Volume 166 No. 4.

 41. The presence of fever in respiratory disease or rashes does not rule out allergy.

42. Before considering allergy in infantile eczema, examine the head for seborrhea. Treatment: Pragmatar of other sulfursalicyclic acid ointment.

43. The best local treatment of weeping eczema is Burrow’s solution, one Domeburo tablet to 24 oz. of water.

44. Although not often a primary factor, soap is the great secondary factor in everything from heat rash to poison ivy.

45. Erythema of the anus and/or vulva in infants is often due to allergy to fruits.

46. Although the results of prolonged treatment in asthma are excellent, the patient with nasal allergy must often settle for more or less reduction of the airway.

47. Common contact allergens are: vinyl plastic (bibs), diaper covers, chair upholstering, grass and weeds, perfumes in baby oils, etc., soaps, mercury (skin antiseptics, yellow oxide, ammoniated mercury), wool, nylon, dark dyes, starch, animal fur, feathers, latex (diaper covers), detergents, finger nail polish, metals. Be suspicious of all drugs applied to the skin.

48. Before considering allergy in rashes, think of the exanthmata chapping, seborrhea, herpes, impetigo, heat rash, ringworm, psoriasis, pityriasis rosea, or ichthyosis.

49. Avoid sedatives in allergic children. They tolerate barbiturates and tranquilizers poorly, but usually can take Benadryl and choral hydrate.

50. In the presence of itching papules, and hive, consider popular urticaria. Common causes in the Midwest: mosquitos (even in Winter), chiggers, fleas, and (rarely) lice and bedbugs.

51. A severe dermatitis tending to occur in streaks is characteristic of poison ivy.

52. The best local treatment for allergic conjunctivitis is still epinephrine (4 cc of 1:1000 to 3 cc of saline).

53. I.V. aminophylline is very effective in severe asthma. It is perfectly safe if given slowly, preferably in I.V. infusion, a practical office procedure.

54. Allergic asthma doses not harm the heart.

55. In dermatitis of the top of the foot, contact dermatitis from shoe dye is far more likely than athelete’s foot.

56. Myths about Penicillin-Cephalosporin cross- reactivity. This was not one of the original ‘Golden Rules’ but it comes up quite frequently.

Dr. Tyler Pearce, an Pediatric Emergency Medicine Resident picked this topic for a journal club discussion. We chatted about it quite often during the allergy elective. I encouraged him to share his findings.

Myths about penicillin-cephalosporin cross reactivity

 Myth:  Penicillin allergic patients will have an allergic reaction to cephalosporins 10% of the time.

This myth comes from older studies performed in the 1960s and 1970s when cephalosprins were first introduced into the market. The most prominent the early articles were a review of the literature by Dash in 1975 and two reviews by Petz in 1971 and 1978.  Dash concluded that 7% of penicillin allergic patients had allergic reactions to cephalosprins, whereas those who were not allergic to penicillin had only a 1% incidence of allergic reaction.  Petz reviewed clinical trials involving 15,708 patients treated with cephalosporins and found the rate of allergic reactions to be 8.1% in penicillin allergic patients and 1.9% in those without a history of penicillin allergy.  The 8.1% is likely where the widely cited, though rounded up, number of 10% comes from.  It was later discovered that early first generation cephalosprins were contaminated with trace amounts of penicillin, therefore overestimating cross-reactivity.  Another factor confounding studies reagarding penicillin-cephalosprin cross-reactivity is that patients who are allergic to penicillin are much more likely to develop reactions to any antibiotic.  Therefore, new reactions are impossible to fully separate from true immunologic cross reactions.

It was once thought that the beta-lactam ring was responsible for cross-reactivity between compounds, but in recent years, the R1 side chain off of the beta-lactam ring has been found to be the primary contributor to cross-reactivity, which is not shared with all cephalosprins.  Reviews of the literature have been performed in recent years, namely a review by Campagna et al in 2011, and by Pichichero in 2005.  Both conclude that the rate of overall cephalosporin allergy in penicillin-allergic patients is significantly less than 10%.  Cross-reactivity depends almost entirely on the similarities of the 3-postiion and 7-position side-chains between pcn, amoxicillin, and the cephalosporin in question. The Pichichero review estimates the attributable cross-reactivity to be less than 1% to first-generation cephalosprins and almost non-existant for 3rd and 4th generation cephalosprins (meaning IgE-mediated hypersensitivity reactions).  This figure, however, was taking into account the fact that the baseline risk of any individual to develop a primary cephalosporin allergy is 1-3%, and that pencillin-allergic patients have an estimated three-fold increased risk of developing a new reaction to any antibiotic.  The reactivity is higher for those first generation cephalospins with similar side chains as the antibiotic to which the patient has a primary allergy, such as cephalexin and amoxicillin, but decreased in those with dissimilar side chains, such as pcn and cefazolin.  Campagna et al estimate an overall cross reactivity between cephalosprins and penicillin in confirmed pcn-allergic patients to be 2.55% (IgE-mediated hypersensitivity reactions). 

Conclusion: The cross reactivity between cephalosporins and penicillins in pcn-allergic patients is significantly less than the widely quoted 10%, and greatly depends on the similarities between the side chains.  The risk of having an IgE mediated hypersensitivity cross reaction to a  3rd and 4th generation cephalosporin in patients allergic to penicillin is nearly zero, and for first generation cephalosporins with a similar side-chain is likely less than 5%. 

 

References:

1)      Anne S, Reisman RE. Risk of administering cephalosporin antibiotics to patients with histories of penicillin allergy. Ann Allergy Asthma Immunol 1995;74:167–70.

2)      Campagna, JD, Bond, MC, Schabelman, E, Hayes, BD.  The use of cephalosprins in penicillin allergic patients: A literature review. J of Emerg Med, pp. 1–9, 2011.

3)      Dash CH. Penicillin allergy and the cephalosporins. J Antimicrob Chemother 1975;1(3 Suppl):107–18.

4)      PichicheroME.Areviewof evidence supporting theAmericanAcademy of Pediatrics recommendation for prescribing cephalosporin antibiotics for penicillin-allergic patients. Pediatrics 2005;115:1048–57.

5)      Pichichero ME, Casey JR. Safe use of selected cephalosporins in penicillin-allergic patients: a meta-analysis. Otolaryngol Head Neck Surg 2007;136:340–7.

6)      Petz LD. Immunologic reactions of humans to cephalosporins. Postgrad Med J 1971;47(Suppl):64–9.

Submitted by Tyler Pearce, MD (Pediatric Emergency Medicince) September, 2011.

 Golden Rules of Pediatric Allergy- anonymous

 

10 Responses

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  4. Natalie Steve - November 15, 2011

    Wow that was unusual. I just wrote an really long comment but after I clicked submit my comment didn’t show up. Grrrr… well I’m not writing all that over again. Regardless, just wanted to say great blog!

  5. fleickly - November 16, 2011

    Natalie, thanks for your note. If you try it again, perhaps on a different page and I can place it where you want it. Thanks for the comments.

  6. fleickly - November 16, 2011

    Thanks for looking- is there any particular way the site helped?
    FEL

  7. fleickly - November 16, 2011

    I will think about that. The day is long enough with clinic and patient care. I would imagine that such a thing may be very time consuming. Thanks for the suggestion.
    FEL

  8. Alyson Elder - January 10, 2012

    I enjoyed reading these Golden Rules, Dr. Leickly. I would love to know more about number 15 (Do not overlook the possibility of allergy in the “nervous” child).

    I found #8 (When the complaint is foul breath, think of food allergy, especially milk, or less commonly, egg) particularly interesting since we have noticed foul breath in my 9 month old who was recently admitted to the hospital for major lip swelling. We are still unsure if it was the mac & cheese she ate, peanut dust from daddy’s shirt, or amoxicillin that she was on. Evalyn will be seeing you very soon! Her big brother, William, already saw you last July and has a peanut and egg allergy.

  9. fleickly - January 24, 2012

    Thanks for the comment. I just got back from a cruise- sorry for the delay. As you see, I have had the residents and students on rotation tackle these rules. I let them select which ones they want to work on. We are finding that some are myths and have no discoverable rationale in the literature. I will try to direct one to these questins – perhaps for extra credits.
    FEL 1-24-2012

  10. TC - May 6, 2012

    I think Allergies: A Leickly Story » The ‘Golden Rules of Pediatric Allergy’: a lesson in history. is a nice post and you do a complete job of posting unique info. Tommie – http://www.ep2p4u.com