All allergic diseases including asthma have shown significant increases in recent decades, the world over. Asthma in 12yr olds increased from 5.5% in 1988 to 27.3% in 2003 (UK, Burr Thorax 2006). UK, Australia and New Zealand have had some of the highest rates of asthma in the world (Global Burden of Asthma report, 2004) - predominantly a western English-speaking area disease!? But all world regions now affected (some S American countries now taking over eg Brazil, Costa Rica). Could this be a reflection of language viz wheezing translates with difficulty? Allergy. 65(2):152-167 2010 . Some suggestion that rates might now be declining – but no clear trends for any global region.
Admission rates for anaphylaxis rose from 6 to 41 per million between 1990/1 and 2000/1, and for food allergy rates 5 to 28 per million over this period (BMJ 327(7424) 2003).
An Isle of Wight population study found a doubling in the rate of peanut allergy and a tripling of sensitisation between the 1989 and 1994–1996 cohorts (J Paediatr. Child Health 2003; 39: 372–5).
Antigen response is initiated by Antigen Presenting Cells (APCs, specialized macrophages), expressing antigen on surface and presenting to T cells. Costimulating factors determine whether T cells then generate Th1 or 2 responses. Th1 (IL2, 12, IFNgamma) response suppresses allergy, whereas Th2 (IL4, 5, 13) promotes. If no costimulating factors, tolerance develops!
Costimulation initiated by tissue damage or microbe components. Inhibitory receptors on APC respond to IgG (mechanism of immunotherapy). Allergy develops when B cells switch Ig class to E.
IgE binds to tissue mast cells and circulating basophils to sensitize them. Type 1 hypersensitivity involves mast cell degranulation, with release of histamine (especially upper airway), tryptase, leukotrienes (esp lower airway), prostaglandins and kinins including:
Clinical response usually occurs within 2 hours but in theory can be delayed for up to 24hrs (later reactions are likely to be type IV delayed hypersensitivity rather than type 1).
Feeds back via IL4. Eosinophils respond more slowly to IL5 (6-72hr). Release peroxidases, Major Basic Protein etc with nonspecific cytotoxic (and so long lasting) effects. Consider size of parasite cf microbes, need to expel from tissue (so tissue disruption). This is the mechanism underlying eczema, GI allergy, late bronchoconstriction not responding to beta agonist.
So why do people become allergic? And why are rates increasing?
JACI 2006:117, 1063 - review
In asthma, initial response is IgE mediated, the late reaction is eosinophil mediated (both are Th2 responses). Hyperresponsiveness develops with an exaggerated diurnal variation and involves increasing sensitivity to non-specific stimuli eg cold air. Pollutants (esp diesel particles) and viruses may interact with IgE. Early onset asthma is usually associated with atopy; in later childhood, the relationship is less clear although severe asthma is associated with food allergies. In Westernized countries, asthma more likely to be associated with atopy eg 58% in Sweden, only 20% in Estonia. Sensitization to pollen predicts young wheezers who will have persistent and severe asthma.
In eczema, 50 to 81% of patients have food allergies! Seven foods (milk, egg, peanut, soy, wheat, cod, and cashew) responsible for most positive test results. Although food allergy and allergic eczema often resolve in early childhood, such individuals are at risk of developing other allergic sensitivities and atopic diseases, particularly asthma. This is the so called allergic march, whereby different diseases present sequentially, with hay fever being the last. Sensitization may be related to maternal food cravings in pregnancy (!), use of nipple creams, weaning foods.
House dust mite - arch-shaped-curve relationship between the levels of housedust mite allergen and the later prevalence of skin test positivity to the same allergen or of atopic wheeze. More obvious with house dust mite than with cat dander. These results suggest that reducing allergen exposure in infancy to moderately low levels may not result in a fall in the incidence of asthma and could increase it! Birth Cohort from Ashford, Thorax 2004;59:855–61
In food allergy, probably only a limited number of structural epitopes, shared across different species. 3D structure more important than sequence, hence cooking may render nonallergenic.
DoH advice to pregnant women with FH atopy to avoid peanuts and not to give them to their children until age 3yrs is out of date. Early peanut consumption in Israel associated with a low incidence! Current study at Evangelina hospital in London.
Early weaning (ie before 4 months) increases risk of allergy. Old recommendations to avoid common allergens eg egg in first year of life probably not helpful. See Nutrition.
In eczema, several studies suggest that the role of dietary avoidance in alleviating atopic eczema is greater than previously thought. A study by Agata and colleagues suggests that symptoms of atopic eczema improve if specific food allergens are eliminated from the patient's diet. In a double blind, controlled study, Atherton et al reported significant clinical improvement in many children with atopic eczema who received a diet free of egg and cow's milk. Because of maternal intake, cow's milk allergens are of clinical importance even in children with eczema who are exclusively breastfed.
Is it possible to prevent the "allergic march" - the evolution of atopy with age? Nishioka found that reducing dust mite exposure in infants with atopic dermatitis and egg, milk, or soybean allergy showed a significantly lower sensitivity to house dust mite even though they were not initially sensitive. In Warner's study, treatment with cetirizine has been shown to delay, and in some cases prevent, the development of asthma in children with atopic dermatitis. In the Preventative Allergy Treatment study, pollen immunotherapy in patients with seasonal rhinoconjunctivitis reduced the development of co-morbid asthma.
About 20% of adults in High Wycombe believed they had food allergy, only 1.4% shown to actualy have one!
History is extremely important. Allergy symptoms include:
In children, severe reactions virtually always include cutanous symptoms. Differential diagnosis of severe reactions should include vasovagal syncope, panic attacks, systemic mastocytosis. Identify triggers the child may have been exposed to in the previous 2 hours, particularly food, stings, latex, exercise.
Greenbook on immunisations has useful section comparing anaphylaxis and vasovagal syncope.
Cutaneous symptoms/signs resembling allergy may be caused by chronic idiopathic urticaria, hereditary angioedema (never urticaria, though!), viruses etc.
If trigger uncertain and/or reaction ambiguous, plasma Tryptase can confirm type 1 allergic reactions (mast cell derived proteinase). Do at 1,6 and 24 hours after reaction. If negative (persistently under 13) then reaction was not IgE mediated and so no risk of anaphylaxis. Still risk of reacting same way again though if non-IgE mediated.
If any testing is done, always consider testing for common food allergens, esp in asthmatics (increased risk of anaphylaxis).
Gold standard is double blind randomized controlled challenge. Some places do challenge with IV access if child has been prescribed Epipen in past. Isolated nausea is common, probably stress rather than allergy! About 2.5% of children will have symptoms only the next day! Mechanism?
NICE food allergy guideline highlights the poor quality and widely varying results of studies looking at allergy diagnosis. They suggest that atopy patch testing is probably the least reliable, and otherwise do not attempt to establish diagnostic criteria.
Traditionally, a skin prick weal of 3mm of greater has been considered diagnostic. But this level is aimed at achieving good sensitivity and negative predictive value rather than specificity/PPV, so is more useful for disproving rather than proving allergy. RCH Melbourne has established the following "100% specificity" cut offs:
| Milk | 8mm (6mm if under 2yr) |
| Egg | 7mm (5mm if under 2yr) |
| Peanut | 8mm (4mm if under 2yr) |
Ped All Imm 2004;15:435
Values betweent these cutoffs and the traditional 3mm standard produce variable clinical responses on challenge. In infants at risk (family history) who have never had the food in question, SPT is often falsely negative at 6 months, but the 100% specificity cutoffs are reliable in the 2nd year of life.
Note there are no established cut offs for wheat or soya. But such predictive values are probably less valuable than applying likelihood ratios to individual patients, according to history of reactions, associated atopy, etc (Pediatric Allergy & Immunology. 20(4):309-19, 2009 PMID 19538353).
European Academy of Allergology and Clinical Immunology (EAACI) has different rules, SPT is interpreted relative to size of 1% histamine weal, in HE units (=histamine equivalent). The idea is to control in variation in skin reactivity. Positivity is rated 4+ if weal double the size of the weal induced by histamine 10 mg/mL (1%); 3+ if weal size the same; and 2+ if the weal size is half. Only weals 2+ or more are considered positive.
Patients with dermatographism (ie positive response to negative control) or very high total IgE have a high chance of false positive results. Standardised food allergen extracts should be used where possible else unpredictable.
Warn patients to stop chlorphenamine for 48 hours, other antihistmines 7 days before doing skin prick. Need neg (saline) & pos (1% histamine) controls, lancet or orange needle, wipe off excess, then read @ 15 mins. Good for egg, milk, some nuts, fish and shellfish, bees/wasps, drugs eg penicillin, animals. Does have false negatives, so should go on to challenge if suspect. Safe (no fatal reactions have been reported), but systemic reactions may occur esp if active wheezing or intradermal.
IgE (previously called RAST but not actually radio-assays anymore, done as a ELISA dye test) appears to be as good as SPT, useful if no skin test reagent available (although you could always use a nonstandard preparation), if skin disease too severe to use skin prick, or if on antihistamines. Results vary with machine: different epitopes? Esp Pharmacia vs DPC. Cutoffs:
| 95% PPV | 50% PPV | |
| Egg | 7 (2 if under 2yr) | 2 |
| Cow's milk | 15 (5 if under 2yr) | 2 |
| Peanut | 15 | 2 [5 if no history of reaction] |
| Fish | 20 |
As with SPT, note that levels (ie sensitivity) seem to fall at younger ages. And similarly with SPT, no good cut offs have been obtained for wheat or soy.
The rate of decline of levels is predictive of tolerance too, esp in under 4 yrs. (Journal of Allergy and Clinical Immunology Volume 116, Issue 1 , July 2005, Pages 153-163)
Pediatric Allergy & Immunology. 20(4):309-19, 2009 PMID 19538353. Archives of Disease in Childhood 2005;90:826-831 PMID 16040882.
Patch testing can be done for type 1 allergy but prob best saved for cell mediated (ie type IV) contact dermatitis.
Symptoms occurring more than 4 hours after exposure are unlikely to have resulted from food allergy (and most will be within 60 mins). Typically, minor allergic symptoms last less than 1 hour, but severe reactions may be protracted.
For mild to moderate reactions (ie not severe), give chlorphenamine. Syrup is preferred as it may be difficult to swallow a tablet during a reaction. Some authorities use higher than standard doses. Repeat after 10mins if not improving & phone 999. Can also be used if accidental ingestion suspected. Not all throat symptoms are severe, can sometimes just be itch. Prolonged GI symptoms should possibly be considered as severe (see below).
Anaphylaxis is defined as an acute life-threatening allergic reaction that is usually - but not exclusively - mediated by IgE-antibodies. Criteria from EAACI given above. Anaphylactoid reactions are immediate systemic reactions that mimic anaphylaxis but for which an IgE-mediated immune mechanism can not be established - most people don't bother trying to make a distinction now. Differential diagnosis includes Exercise induced anaphylaxis, Mastocytosis and Familial Hereditary Angioedema.
EAACI anaphylaxis criteria (2007, from Sampson): any one of -
On logistic regression, confusion, collapse, unconsciousness, and incontinence were strongly associated with hypotension and hypoxia. Used to define severe reactions. Dizziness, vomiting, presyncope, dyspnea, stridor, wheeze, chest/throat tightness, nausea, vomiting, and abdominal pain had weaker, albeit significant, associations and were used to define moderate reactions. Reactions limited to the skin (urticaria, erythema, and angioedema) were defined as mild. These grades correlated well with epinephrine usage. Older age, insect venom, and iatrogenic causes were independent predictors of severity. Preexisting lung disease was associated with an increased risk of hypoxia. Journal of Allergy and Clinical Immunology Volume 114, 2004, 371-376
In a survey of kids with anaphylaxis, the mean latent period was 15.4 (SD27.5) minutes, ie 95% will react within 90 minutes of exposure. The type of allergy does not predict the latency well; however, age is inversely related, with younger children having more gradual onset. GI and cardiovascular symptoms tended to come later than skin/respiratory. 60% of anaphylactic reactions occurred in the home, and 10% happened in health care environments. Males predominate, particularly with regards exercise induced and insect venom anaphylaxis (PEDIATRICS Vol. 101 No. 4 April 1998).
About 20% to 30% of food-induced anaphylactic events have a biphasic or recurrent response, although only half of those severe. 90% of recurrent reactions within 12 hours. Delay in giving adrenaline increases risk of recurrence! Some anaphylactic reactions are persistent, going on for hours.
Exercise is an important factor esp in teenagers, can even (rarely) be the sole identifiable trigger! viz Food-Dependent Exercise- Induced Anaphylaxis and Exercise-Induced Anaphylaxis - see below.
Deaths - mostly in children over 5, despite the fact that food allergies are more common under 5 and usually lessen with time. Nearly all are in children with asthma. Of the 8 deaths between 1990 and 2000, 4 were due to milk, 2 peanut, 1 egg and 1 mixed (but see below for bigger study). Both the peanut deaths were in children over 13yrs. Children are over 250x more likely to die in road traffic accident.
See APLS guidelines on management of acute anaphylaxis from the United Kingdom Resuscitation Council. No distinction between anaphylactic and anaphylactoid reactions - confusing and may lead to inadequate treatment. Patients taking beta blockers may have a more severe reaction and respond less well to adrenaline. Adrenaline by the intramuscular route is safe. Repeat within five minutes if there is no improvement or if the patient's condition deteriorates - not based on any evidence! The role of the intravenous route is probably one of the more hotly debated topics in the literature and the courts. The consensus from the UK Resuscitation Council is that with an appropriate strength of solution (1/10 000 or 1/100 000, and never 1/1000) it is an acceptable route for patients with profound shock that is immediately life threatening, and should be given as slowly as seems reasonable. Use ECG monitoring. Should be given by someone appropriately experienced.
There is no mention of the use of nebulised adrenaline for treating stridor cf APLS. Reflects the lack of good evidence for either using or withholding nebulised adrenaline - concentrate on giving parenteral adrenaline!
Give sufficient intravenous fluid. Suggested preference for crystalloids.
BMJ 1999;319:1-2 ( 3 July )
Is an Epipen required? Risk factors would include nut allergy, asthma, previous anaphylaxis but potentially also teenagers, distance from medical facilities, cutaneous/airborne triggers. Prescribing a pen is only part of the overall management: nothing worse than prescribing a pen that does not get used with a subsequent anaphylactic reaction. In various studies, prescribed EpiPens were only used in a third of recurrent episodes, despite being available and in date in two-thirds of episodes. The reason(s) for the non-use of an EpiPen requires further study: parental questionnaires indicate that parents have a poor recall of anaphylactic symptoms and how to use the EpiPen despite training.
Video available at Epipen support website.
Training checklist (from GOS):
They come in two different doses--the EpiPen (containing 0.3 mg) and the EpiPen Jr. (containing 0.15 mg), with the EpiPen Jr prescribed for younger children (15-30kg) and the regular EpiPen prescribed for older children and adults (30kg+). If patient is under 15kg, need to balance risk of anaphylaxis with risk of drug error from drawing up adrenaline from vial with syringe and needle.
Anapen has a smaller needle and is cheaper, but has a different technique which is likely to cause confusion to all concerned.
2 pens? There has been good evidence published indicating that one-third of children with anaphylaxis require a second dose of epinephrine (Kornblat P, et al Allergy Asthma Proc. 1999; 20: 383–6), and deaths have occurred despite a single injection. Some expert recommendations have been published indicating that patients should have a second pen available to give if the first dose is insufficient. This is more likely to be an issue with big teenagers (eg over 45kg).
Do reactions get progressively worse with time? Probably not - the severity of the initial reaction generally gives a good clue to what kind of reactions are likely in the future: in a survey of peanut allergic adults and children, those whose first reaction was severe would mostly report that their last reaction was also severe (78%) whereas in those cases with a mild first reaction would only report a severe (most) recent reaction in 32% of cases.[Hourihane] The presence of asthma increases the risk of death or a severe reaction; seems reasonable to recommend an Epipen for those with both asthma (requiring preventer treatment) and a food allergy (esp peanut, given that combined mortality figures from USA, UK and Sweden found three quarters were associated with peanut or tree-nut reactions. Deaths from egg and cows milk sensitivity are much less common despite being among the most common food allergies detected.
Does reacting to only a trace of something indicate a more severe allergy? In adults, repeat challenges of peanut protein are pretty consistent in the threshold doses required to elicit clinical reactions.
Does the size of the skin prick test predict severity? In a large group of both adults and children, overall skin prick test size did correlate with severity (P = 0.04), but not in a very useful way, as there was substantial overlap between groups. But some people will include it as a factor.
Kemp AS, J Paed Child Health2003:39:372-5
EAACI task force guidance - schools should avoid providing food containing nuts. Sharing of food/utensils/containers should be discouraged. Menus should be provided in advance to families, with ingredients stated. School staff should be indemnified for administration of emergency medicines.[Allergy 2010]
Or CMPI (Cow's milk protein intolerance). Can even affect exclusively breast fed infants if sufficient milk proteins transmitted in breast milk. Associated problems eg lactose intolerance may complicate! Early reactions seen including anaphylaxis, else more chronic delayed GI symptoms seen. Delayed reactions are not usually IgE mediated, and include:
In patients with eczema, a mixture of reactions can be seen (and immediate reactions may be seen on re-introduction even when only delayed reactions seen initially). There may be a threshold level below which a patient is asymptomatic. With delayed reactions, diagnosis may be on history, or endoscopy. 3mm SPT wheal considered positive; when doing IgE/SPT tests, also check egg (high cross-reactivity) and soy (for formula substitution). If IgE/SPT neg do double blind challenge. Because of theoretical risk from phyto-oestrogens in soy, use Neocate/Nutramigen instead of soy formula if under 6 months. Soya cross reactivity seen in 25% of young infants, only 5% of over 6 months; plus, theoretical risk from phyto-oestrogens. Soya milk usage is also associated with increased risk of subsequent peanut allergy (RR=2.6)! About 10% of infants will not tolerate even extensively hydrolysed formula and may require an amino acid based formula; anaphylaxis has been described with hydrolysed formula. See Nutrition.
Lactose sometimes seen as an ingredient - can be contaminated with milk protein.
Exposure does encourage tolerance. In studies, after 6 months of oral desensitization, 11% had had positive food challenges cf 40% for abstainers. And in the abstainers, the threshold of sensitivity tended to be lower, and symptoms more severe (Eur Ann Allergy Clin Immunol. 2007 39:12-9. PMID 17375736).
Most non IgE reactions will have resolved by the age of 5yrs. About half of IgE reactions resolve by the age of 8.
Journal of Paediatrics & Child Health. 45(9):481-486, 2009.
Associated with use of creams containing peanut oil in infancy, esp with eczema. Also associated with soy milk, probably not just because of other allergic manifestations, ?cross sensitization.
Patients with peanut allergy with a peanut IgE of less than 5 kUA/L have a good chance of outgrowing their allergy. It is recommended that patients continue to keep epinephrine available until they can prove tolerance to peanuts over a 1- to 2-year period of consistent intake before the allergy is confirmed to be outgrown. Recurrence to peanut allergy, once outgrown, may occur - risk is about 10% but usually only happens in patients who continue to avoid nuts after a successful challenge.
Nuts found in Chinese & Indian takeaways. Arachis oil is peanut oil - most allergic patients are OK with peanut oil unless it is cold pressed (ie unrefined, gourmet).
Usually diagnosed in first 2 yrs. Half will grow out of it by the time they are 5, two thirds by the time they are 7. Likelihood of future tolerance is related to:
Journal of Allergy and Clinical Immunology Vol 110, 2002, P304-309 PMID 12170273
Negative food challenges had a median egg white SPT weal of 3mm (cf 5mm), and an egg/histamine index of 0.7 (cf 1). A history of allergic rhinitis reduced your chances of having a negative challenge J Allergy Clin Immunol. 2006;117:842–847 PMID 16630943.
Rate of decline in IgE levels also predictive.
Egg (or albumin) found in mayonnaise (eg coleslaw), royal icing (not normal icing), Tunnock's teacakes and Milky Way bars. Batter eg nuggets, croquettes and glazes eg sausage rolls may contain egg. Lecithin (E322) can be egg but is usually soya in origin. Loprofin is an egg substitute.
See Greenbook for more information.
Apart from food, egg allergy also has implications for vaccinations:
Exposure does encourage tolerance. In studies, after 6 months of oral desensitization, 30% had had positive food challenges cf 49% for abstainers. And in the abstainers, the threshold of sensitivity tended to be lower, and symptoms more severe (Eur Ann Allergy Clin Immunol. 2007 39:12-9. PMID 17375736).
Can be allergic to various wheat proteins, including gluten (but IgE, whereas coeliac is non-IgE). Potential cross-reactivity with barley, rye, oats, maize and rice. Most patients will develop tolerance before adulthood, but note that wheat-dependent exercise induced anaphylaxis is seen in older children and adults (see below). Wheat also found in beer, modified starch. Einkorn wheats lack some of the major allergens.
Latex is made from natural rubber. Found in some balloons, condoms, erasers, gym equipment (eg basket balls), vial bungs. Sensitization mainly occurs by wound or mucosal contact with latex esp surgery or by inhalation of powder from latex gloves. Usually only gives problems if mucosal contact eg chewing rubber on end of pencil, going to the dentist, safe sex.
Prevalence varies widely across populations and according to diagnostic method. Risk higher among:
Skin test involves 3 different strengths, then application of glove, then prick through glove, then application of glove to inside of mouth! Can be done double blind with sterile non-latex gloves which look similar.
Immunotherapy or specific premedication does not appear to be effective in preventing anaphylaxis perioperatively. Chiron make vaccines with non-latex bungs.
The extra cost of latex free gloves is far outweighted by the savings in occupational allergen testing, hospital admission/treatment for reactions, and worker's compensation.
Pediatric Anesthesia. 19(4):313-319, 2009.
Differentiate toxic, adverse, immune and non-immune allergic drug reactions.
Some people react to the IV form of something they tolerate orally - suspect carrier eg castor oil. Skin prick testing may not be reliable for IV reactions.
Some people react to Recombinant proteins eg insulin! Presumably structure differs from natural form, even if chemical identity is the same.
Desensitization to medications can be effective but the effect is often short lasting.
Aspirin and NSAIDs are associated with chronic idiopathic urticaria, through their action on COX receptors.
Stevens-Johnson Syndrome is a severe, diffuse mucocutaneous eruption causing erythematous or purpuric macules, blisters, target lesions, and no more than 10% skin detachment. Other manifestations are fever and mucosal lesions (stomatitis, conjunctivitis, or urethral inflammation) accompanied by at least 1 other visceral organ, such as hepatic, renal, or gastrointestinal involvement. Toxic epidermal necrolysis (TEN) involves 30% or more skin detachment; there is clearly an overlap in the middle. Treatment with IVIG has been disappointing; prednisolone might be better. Seems to be CD8 related CD56 reaction.
DRESS is drug reaction with eosinophilia and systemic symptoms. Can be due to HHV-6.
Contrast reactions can be managed by pretreatment with prednisolone for 13 hours then diphenhydramine for 1 hour, then using lower osmolality contrast.
J ALLERGY CLIN IMMUNOL FEBRUARY 2006 S464
It's often said that 15% of penicillin allergic are also allergic to cephalosporins, but this figure comes from studies of people with history of allergy, rather than evidence. In practice, most of those who think they are penicillin allergic probably never were, so the true risk of penicillin/cephalosporin cross sensitivity probably a few percent at best. If suspected penicillin allergy, but not anaphylactic, probably reasonable to try cefotaxime and ceftriaxone (appear to be safer than cephalexin and cephradine - see BNFc). But warn about possibility of sensitization in the future. IgE test vs penicillin is available, but best is probably skin prick, followed by intradermal test, then oral challenge.
Penicillin - reaction can be to any of the major or minor metabolic products; how many does test agent include? Penicilloyl-polyLysine is the most commonly responsible product - no longer available!? Of course, most suspected reactions turn out not to be allergic, but without it a large percentage of positives will be missed. So try test dose 5mg (unless blistering or mucocutaneous reaction; or hepatic/nephritic/aplastic reaction).
Risk with cephalosporins is higher with 1st and 2nd generation, down to 1-3% for 3rd and 4th generation. Seems to be that if skin testing for penicillin is negative then no risk! Otherwise, skin prick with 2ml/ml solution, then challenge.
Reactions to local anaesthetics are often reported, but given how often they are used, most turn out not to be allergic but rather toxic (eg to parabens or sulphite preservative) or autonomic. Where allergy is confirmed, it is often of a delayed hypersensitivity type eg 24-72 hours after exposure. Beware latex allergy and C1 esterase inhibitor deficiency too. Local anaesthetics come in 2 main groups, the esters (procaine, benzocaine) and the amides (lidocaine, bupivocaine). Cross-reactivity is common among the esters but not among the amides or between the 2 groups. Neomycin sensitivity may contribute to a reaction.
Testing can be done with preservative containing products, although a higher rate of false positives may be found. Skin prick testing should be done to non-adrenaline containing products, else reaction is impaired. There can be discordance between patch testing and intradermal testing. The final step should be subcut testing, perhaps blinded (Contact Dermatitis. 59(2):69-78, 2008 PMID 18759873 ).
If a vaccination results in a severe allergic reaction (any breathing problems or collapse) then Green book says further doses contraindicated. But important to consider differential diagnosis eg vasovagal (see Greenbook section on adverse reactions. Consider also allergy to bung (latex) or a specific vaccine component such as neomycin or gelatine. True allergic reactions are rare. Consider withholding further doses if patient already immune or at low risk of complications. Otherwise, skin prick with increasing concentrations of the same manufacturer's product, then do intradermal dose. Late reactions to vaccines rarely cause problems with subsequent doses, so administering in hospital is an option. Reactions with second doses are rare of course, since people with immediate reactions are unlikely to have further doses (Peds 2008;122:e771).
ie bee/wasp. A common cause of anaphylaxis, and interestingly, not related to atopy.
Hay fever is often considered a trivial complaint, but affects sleep, leisure activities, and evidence of decreased cognitive functioning, and impaired quality of life.
SPT is pretty good at finding causes - depends how many you screen for, of course! In a US study, 65% of patients (mixed adults/children) had a positive: HDM most commonly, else trees, weeds, moulds. Aspergillus and Penicillium are indoor moulds, Alternaria is outdoors. Cat allergens are commonl found in homes without cars,
To avoid pollens:
To prevent dust mite allergy:
To kill mites:
Allergy UK, PDF available
Cold compresses, artifical tears. Systemic antihistamines may be excessively drying. SAC and PAC (seasonal and perennial allergic conjunctivitis) are ideally treated with combination antihistamine/mast cell stabilizers - give rapid symptomatic relief coupled with long-term benefit of mast cell stabilization. The severe conditions of atopic keratoconjunctivitis (AKC) and vernal keratoconjunctivitis (VKC) are rarer: tarsal cobblestone-like papillae may also be present, else gelatinous yellow-gray infiltrates on the limbus, the circumference of which might appear thickened and opaque. There may be severe photophobia. Managed in the same way; consider pulse therapy with steroids. Ono SJ. Abelson MB. Journal of Allergy & Clinical Immunology. 115(1):118-22, 2005 Jan
IgE to moulds found in about 10% of normal population - so interpret in context, as for other allergy tests. Important as factor in asthma in terms of outdoor exposure, more controversial in indoor exposure (confounded with NO2, cockroach etc). Probably not very important in rhinitis/eczema. Besides skin tests you can also measure precipitins which are IgG antibodies, although no good cut offs.
These are the kids who get recurrent urticaria but not consistently to any particular agent and often without any explanation at all. Can significantly impair quality of life! More a disease of middle aged women, where it can last for years. Usually pruritis, often dermatographism (and similarly, pressure induced urticaria eg belt). Angioedema often co-exists, in which case lesions can be burny or painful (but improves with anithistamines, unlike isolated angioedema). Try long acting antihistamines eg hydroxyzine (Ucerax suspension, Atarax tab), Telfast (levocetirizine, 5mg od >6yr). About 30% of children with chronic idiopathic urticaria have autoantibodies against alpha chain of IgE receptor, in which case probably an autoimmune rather than an idiopathic condition, but evidence that this is the underlying mechanism is still lacking. If antihistamines don't work, try:
Allergy & Asthma Proceedings. 30(1):1-10, 2009. PMID 19331714
Complex form of allergy, where exercise alone can trigger symptoms, or only immediately after ingestion of a particular food esp wheat. No symptoms occur to the food alone. Wheat is the most common single identifiable trigger, but many are polysensitized, and presumably anaphylaxis only occurs after exposure to multiple antigens - but often difficult to reproduce. These children tend to be older cf those with food anaphylaxis, and often have a history of urticaria or angioedema (all are related to mast cell activity) (PEDIATRICS Vol. 101 No. 4 April 1998). Avoiding consumption of solids for 4 hours prior to exercise is the best prevention, at least in atopic individuals with a good history. IgE to Omega-5 gliadin is highly specific.
Common to find positive RAST (IgE) tests for multiple things,but not the same as clinical reactivity. Same true to a certain extent for skin prick tests. Approximate rate of clinical reactivity if allergic to:
There are some food allergy associations where there is no clear biochemical basis eg melon with avocado (and banana, kiwi, peach as above); celery-spice-carrot-mugwort syndrome (incl parsley, anise, fennel, caraway, pepper, paprika).
Immunotherapy is primary treatment for bee/wasp allergy, is well established for seasonal allergic rhinitis, but less well proved for asthma or house dust rhinitis. Venom immunotherapy is not necessary for children with large local reactions or mild systemic reactions but is warranted for children with moderate-to-severe systemic reactions. Golden DBK et al. N Engl J Med 2004;351:668–74. Gruchalla RS. N Engl J Med 2004;351:707–9.
In patients with asthma and house dust mite allergy who are receiving appropriate pharmacotherapy and have instituted environmental controls, house dust mite immunotherapy provides marginal additional benefits in asthma control. Sublingual immunotherapy for seasonal grass allergy can be safely administered by general practitioners (Grazax, £68 per month, only licensed for over 18yrs) but needs to start at least 4 months before start of season and symptom relief begins only in the second season of therapy. Metanalysis Chest 2008; 133:589, Journal of Allergy & Clinical Immunology. 115(4):676-84, 2005 Apr.
Anti-IgE therapy appeared promising in its first clinical trial, and further trials are ongoing. Recombinant protein vaccines with or without bound oligodeoxynucleotide sequences have shown promise in reversing peanut allergy (in mice). Li et al treated mice with peanut allergy with a herbal preparation, FAHF-1. A newer formula, FAHF-2, contains 9 herbs and provides extended protection from allergic symptoms. Like anti-IgE, FAHF-2 should provide protection to any food inducing an IgE-mediated reaction. Sampson HA. Journal of Allergy & Clinical Immunology. 115(1):139-41, 2005 Jan.
Monosodium glutamate is blamed for all kinds of reactions, from headache to wheezing but the evidence for it causing type 1 reactions (or any other reaction) is very limited. Clin Exp Allergy. 2009 PMID 19389112
Differential diagnosis to allergy. Basically Histamine poisoning rather than release of endogenous stores! Mild examples are not uncommon but severe cases rare. Clue is that several people who eat the same seafood meal fall ill with similar allergic symptoms! Histamine and other amines are produced by bacteria from certain amino acids (can occur during production eg Swiss cheese or by spoilage). Particularly affects fish of the Scombridae family (viz tuna, mahi mahi, bluefish, sardines, mackerel, amberjack, and abalone) but can be any food containing the right amino acids and subject to the right bacterial enzymes.
Initial symptoms not surprisingly include tingling or burning sensations in the mouth, rash, itching. Headaches are frequently seen. May progress to nausea, vomiting and diarrhoea.
Depending on the distribution of the histamine in the food, not everyone at a meal may be affected. Cooking or freezing do not reduce the toxic effect. Contamination is not apparently detectable by the eye or nose.
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