Clinical Disorders and Clinical Manifestation of Food

8/11/2019 Clinical Disorders and Clinical Manifestation of Food

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Clinical Disorders and Clinical Manifestation ofFood AllergyFood hypersensitivities develop in genetically predisposed individuals, presumably when oral tolerance fails to develop normally or breaks

down. IgE-mediated reactions develop when food-specific IgE antibodies residing on mast cells and basophils come in contact with and bind

circulating food allergens and activate the cells to release potent mediators and cytokines. As depicted in number of IgE-, cellular-, and mixed

IgEand cell-mediated food hypersensitivity disorders have been described. There is little evidence to implicate antigen-antibody complex

mediated hypersensitivity in food-related disorders.In addressing possible food-induced allergic disease, the clinician must consider a variety of adverse reactions to foods that are not food allergies,especially because more than 20% of adults and children alter their diets for perceived adverse reactions/allergies. Adverse reactions that are not

classified as food allergies include host-specific metabolic disorders (eg, lactose intolerance, galactosemia, and alcohol intolerance), a response to apharmacologically active component (eg, caffeine, tyramine in aged cheeses triggering migraine, and histaminic chemicals in spoiled dark-meat fish

resulting in scombroid poisoning masquerading as an allergic response), or toxins (eg, food poisoning). Additionally, psychologic (food aversion and

anorexia nervosa) or neurologic (eg, auriculotemporal syndrome manifested by a facial flush from tart foods or gustatory rhinitis manifested by

rhinorrhea from hot or spicy foods) responses can mimic food allergies

It is conceptually and diagnostically helpful to categorize food-induced allergic disorders based on immunopathology among those that are and are not

mediated by IgE antibodies. Disorders with an acute onset of symptoms after ingestion are typically mediated by IgE antibody. Food-specific IgE

antibodies arm tissue mast cells and blood basophils, a state termedsensitization. On re-exposure, the causal food proteins bind to the IgE antibodies

specific for them and trigger the release of mediators, such as histamine, that cause the symptoms. Another group of food hypersensitivity disorders aresubacute or chronic and are mediated primarily by T cells. A third group of chronic disorders attributed to food allergy are variably associated with

detectable IgE antibody (IgE-associated/cell-mediated disorders). The features of a spectrum of the most common food-induced allergic disorders

categorized by pathophysiology. The table does not include disorders such as recalcitrant childhood gastroesophageal reflux, constipation, and irritablebowel syndrome, which are sometimes attributed to food allergy. Detection of IgG antibodies to foods is not considered diagnostic of food allergy.

However, Heiner syndrome, a rare infantile disorder characterized by pulmonary hemosiderosis triggered by milk protein, is associated with increased

milk-specific IgG antibodies. Celiac disease and the related skin disorder dermatitis herpetiformis can be considered food allergies because an immune

response to gluten in grains, such as wheat, rye, and barley, is responsible, but these disorders are not discussed further here. Dietary (food) proteininduced enteropathy is another malabsorption syndrome, but unlike celiac disease, it is usually caused by cows milk, is transient, is not associated withmalignancy or dermatitis, and, for unclear reasons, has been rarely described in the past decade. Although symptoms of mucous and bloody stools in

breast-fed infants have typically been attributed to dietary proctitis/proctocolitis caused by immune responses to maternal ingestants, such as cows milk,

studies have recently emphasized that alternative causes, such as infection or other inflammatory disorders, should be considered. Thus empiric maternal

dietary interventions should be undertaken with consideration that alternative explanations might exist, and retrials of the avoided allergen can be

considered shortly after resolution of symptoms if other signs of allergy are absent. Lastly, contact dermatitis has also been attributed to foods,particularly with occupational exposure.

Food hypersensitivity disorders


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IgE mediated

Gastrointestinal Oral allergy syndrome, gastrointestinal anaphylaxis

Cutaneous Urticaria, angioedema, morbilliform rashes and flushing

Respiratory Acute rhinoconjunctivitis, bronchospasm (wheezing)

Generalized Anaphylactic shock

Mixed IgE and cell mediated

Gastrointestinal Allergic eosinophilic esophagitis, allergic eosinophilic gastroenteritis

Cutaneous Atopic dermatitis

Respiratory Asthma

Cell mediated

Gastrointestinal

Food proteininduced enterocolitis, food proteininduced proctocolitis, food

proteininduced enteropathy syndromes, celiac disease

Cutaneous Contact dermatitis, dermatitis herpetiformis

Respiratory Food-induced pulmonary hemosiderosis (Heiner syndrome)

Gastrointestinal food hypersensitivity reactionsThe number of gastrointestinal food hypersensitivities have been described. As indicated above, the pollen-food allergy syndrome (oral allergy syndrome)is elicited by a variety of plant proteins that cross-react with airborne allergens, especially birch, ragweed, and mugwort pollens.32Patients with ragweed

allergy might react to fresh melons and bananas, patients with grass pollen allergy might have symptoms when ingesting raw tomatoes, and patients with

birch pollen allergy might have symptoms after the ingestion of raw potatoes, carrots, celery, apples, pears, hazelnuts, and kiwi. Because the allergensresponsible for these reactions are easily broken down by heat or gastric enzymes, most patients only experience allergic symptoms in the oral and

pharyngeal mucosa. Gastrointestinal anaphylaxis typically presents as acute nausea, colicky abdominal pain, and vomiting and generally occurs with

allergic manifestations in other target organs.1


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DISORDER MECHANISM SYMPTOMS DIAGNOSIS

and

angioedema

swelling RAST; challenge

Chronic

urticaria andangioedema IgE mediated

Pruritus, hives, and/or

swelling of >6 wkduration

Clinical history; SPTs or

RAST; elimination diet;challenge

Atopicdermatitis

IgE and cellmediated

Marked pruritus;

eczematous rash inclassic distribution

Clinical history; SPTs;

CAP-System FEIA (ie,

quantitative IgE);

elimination diet and foodchallenges

Contactdermatitis Cell mediated

Marked pruritus;eczematous rash Clinical history; patch test

Dermatitis

herpetiformis Cell mediated

Marked pruritus;

papulovesicular rash

over extensor surfaces

and buttocks

Skin biopsy (IgAdeposition); IgA anti-

gliadin and anti-

transglutaminase

antibodies; endoscopy

source: J Allergy Clin Immunol.2003;111(suppl):S540-7.

Respiratory food hypersensitivity reactionsFood allergy can induce a number of disorders in the respiratory tract, as depicted in Table V. Acute respiratory symptoms caused by food allergygenerally represent isolated IgE-mediated reactions, whereas chronic respiratory symptoms represent a mix of IgE- and cell-mediated reactions. Isolated

rhinoconjunctivitis is rarely the result of a food-induced allergic reaction, although it frequently occurs in association with other food allergy symptoms.

Asthma is an uncommon manifestation of food allergy, although acute bronchospasm is usually seen with other food-induced symptoms.70However,

airway hyperreactivity and worsening of asthma also can be induced in the absence of marked bronchospasm after the ingestion of small amounts of foodallergens in sensitized subjects.71Interestingly, food allergy recently was found to be a major risk factor for severe life-threatening asthma. Roberts

reported that about one half of asthmatic children requiring intubation for severe asthma had food allergy compared with about 10% of asthmatic patients

seen at the same hospital. Vapors or steam containing proteins emitted from cooking food (eg, fish) can induce asthmatic reactions and even anaphylaxis.

It has been estimated that about 1% of asthma in adults might involve reactions to inhalational exposures to food, especially in the workplace. Similarly,

particulate matter, such as peanut dust in airplanes, can induce allergic reactions, whereas the smell of peanut butter, primarily organic solvents, is not


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likely to induce allergic symptoms. Food-induced asthmatic symptoms should be suspected in patients with refractory asthma and a history of atopic

dermatitis, gastroesophageal reflux, food allergy, or feeding problems as an infant or a history of positive skin test responses or reactions to a food.Heiners syndrome is a rare form of food-induced pulmonary hemosiderosis typically caused by cows milk.

Respiratory food hypersensitivities

DISORDER MECHANISM SYMPTOMS DIAGNOSIS

Allergic

rhinoconjunctivitis IgE mediated

Periocular pruritus,

tearing, and

conjunctivalerythema, nasal

congestion,

rhinorrhea, sneezing

Clinical history, SPTs,

elimination diet, food

challenge

Asthma

IgE and cell

mediated

Cough, dyspnea,

wheezing

Clinical history, SPTs,

elimination diet, food

challenge

Heiners syndrome ?

Recurrent pneumonia,

pulmonary infiltrates,hemosiderosis, iron-

deficiency anemia,FTT

Clinical history,

peripheral

eosinophilia, milk

precipitins (if causedby milk), lung

biopsy, eliminationdiet

source J Allergy Clin Immunol.2003;111(suppl):S540-7.

Food-induced allergic disorders

IMMUNOPATHOLOGY DISORDER

KEY

FEATURES

ADDITIONAL

IMMUNOPATHOLOGY

TYPICAL

AGE

MOST

COMMON

CAUSAL

FOODS

NATURAL

COURSE

IgE ant body dependent


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KEY

FEATURES

ADDITIONAL

IMMUNOPATHOLOGY

TYPICAL

AGE

MOST

COMMON

CAUSAL

FOODS

NATURAL

COURSE

(acute onset)

Urticaria/angioedema

Triggered byingestion ordirect skincontact(contacturticaria);food

commonlycauses acute(20%) butrarely chronic(2%) urticaria

Children >adults

Primarilymajor allergens

Dependingon food

Oral allergysyndrome (pollenfood related)

Pruritus, mildedemaconfined tooral cavityUncommonlyprogresses

beyond mouth(

7%) oranaphylaxis(1% to 2%)Might increaseafter pollenseason

Sensitization to pollenproteins by the respiratoryroute results in IgE that bindscertain homologous, typicallylabile food proteins (incertain fruits/vegetables (eg,apple Mal d 1 and birch bet v1)

Onset afterpollen allergyestablished(adult > youngchild)

Rawfruit/vegetablesCooked formstoleratedExamples ofrelationships:

birch (apple,peach, pear,carrot),ragweed(melons)

Might belong-livedand vary

with seasons

Rhinitis, asthmaSymptomsmightaccompany afood-induced

Infant/child >adult, exceptforoccupational

General: majorallergensOccupational:

wheat, egg, and

Dependingon food


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KEY

FEATURES

ADDITIONAL

IMMUNOPATHOLOGY

TYPICAL

AGE

MOST

COMMON

CAUSAL

FOODS

NATURAL

COURSE

allergicreaction butrarely anisolated orchronicsymptomSymptomsmight also betriggered byinhalation ofaerosolizedfood protein

disease (eg,bakers asthma)

seafood, forexample

Anaphylaxis

Rapidlyprogressive,multiple organsystemreaction canincludecardiovascularcollapse

Massive release of mediators,such as histamine, althoughmast cell tryptase levels notalways increased Key role ofplatelet-activating factor Any

Any but morecommonlypeanut, treenuts, shellfish,fish, milk, andegg

Dependingon food

Food-associated,exercise-inducedanaphylaxis

Food triggers

anaphylaxisonly ifingestionfollowedtemporally byexercise

Exercise is presumed to altergut absorption, allergendigestion, or both

Onset morecommonly laterchildhood/adult

Wheat,shellfish, andcelery are mostdescribed

Presumedpersistent

IgE antibody associated/cell-mediated (delayed


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KEY

FEATURES

ADDITIONAL

IMMUNOPATHOLOGY

TYPICAL

AGE

MOST

COMMON

CAUSAL

FOODS

NATURAL

COURSE

onset/chronic)

Atopic dermatitis

Associatedwith food in

35% ofchildren withmoderate-to-severe rash

Might relate to homing offood-responsive T cells to theskin

Infant > child >adult

Majorallergens,particularly eggand milk

Typicallyresolves

Eosinophilicgastroenteropathies

Symptomsvary onsite(s)/degreeof eosinophilicinflammationEsophageal:dysphagia andpainGeneralized:ascites, weightloss, edema,andobstruction

Mediators that home andactivate eosinophils play arole, such as eotaxin and IL-5 Any Multiple

Likelypersistent

Cell-med ated (delayedonset/chronic)

Dietary proteinenterocolitis

Primarilyaffects infantsChronicexposure:emesis,

Increased TNF- response,decreased response to TGF- Infancy

Cows milk,soy, rice and

Usuallyresolves


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KEY

FEATURES

ADDITIONAL

IMMUNOPATHOLOGY

TYPICAL

AGE

MOST

COMMON

CAUSAL

FOODS

NATURAL

COURSE

diarrhea, poorgrowth, andlethargy Re-exposure afterrestriction:emesis,diarrhea, andhypotension(15%) 2 hoursafter ingestion

oat

Dietary proteinproctitis

Mucus-laden,bloody stoolsin infants Eosinophilic inflammation Infancy

Milk (throughbreast-feeding)

Usuallyresolves

Reference :

Sicherer SH, Sampson HA. Food allergy.J Allergy Clin Immunol. Feb 2010;125(2 Suppl 2):S116-25.

Scott H. Sichererand Hugh A. Sampson. Food Allergy: Recent Advances in Pathophysiology and Treatment. Annual Review of Medicine Vol.

60: 261-277 (Volume publication date February 2009)

Sampson H. Update on food allergy.J Allergy Clin Immunol2004 113 (5): 805819.

Julie Wang and Hugh A Sampson. Food allergy: recent advances in pathophysiology and treatment. Allergy Asthma Immunol Res. 2009

October; 1(1): 1929. Lemon-Mule H, Sampson HA, Sicherer SH, Shreffler WG, Noone S, Nowak-Wegrzyn A. Immunologic changes in children with egg allergy

ingesting extensively heated egg.J Allergy Clin Immunol. 2008;122:977983

Shreffler WG, Castro RR, Kucuk ZY, Charlop-Powers Z, Grishina G, Yoo S, et al. The major glycoprotein allergen fromArachis hypogaea, Ara

h 1, is a ligand of dendritic cell-specific ICAM-grabbing nonintegrin and acts as a Th2 adjuvant in vitro.J Immunol. 2006;177:36773685

Meyer S, van Liempt E, Imberty A, van Kooyk Y, Geyer H, Geyer R, et al. DC-SIGN mediates binding of dendritic cells to authentic pseudo-

LewisY glycolipids ofSchistosoma mansonicercariae, the first parasite-specific ligand of DC-SIGN.J Biol Chem. 2005;280:3734937359

Commins SP, Satinover SM, Hosen J, Mozena J, Borish L, Lewis BD, et al. Delayed anaphylaxis, angioedema, or urticaria after consumption ofred meat in patients with IgE antibodies specific for galactose-alpha-1,3-galactose.J Allergy Clin Immunol. 2009;123:426433


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Anna Nowak-Wgrzyn, Hugh A. Sampson. Future therapies for food allergies. Journal of Allergy and Clinical Immunology March 2011 Vol.

127, Issue 3, Pages 558-573

Scott H. Sicherer, Hugh A. Sampson. Journal of Allergy and Clinical Immunology February 2010 Vol. 125, Issue 2, Supplement 2, Pages S116-

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Stephan Steckelbroeck, Barbara K. Ballmer-Weber, Stefan Vieths. Potential, pitfalls, and prospects of food allergy diagnostics with recombinant

allergens or synthetic sequential epitopes. Journal of Allergy and Clinical Immunology June 2008 Vol. 121, Issue 6, Pages 1323-1330 A. Wesley Burks, Mimi Tang, Scott Sicherer, Antonella Muraro, et al. ICON: Food allergy. Journal of Allergy and Clinical Immunology 24

February 2012

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Clinical Disorders and Clinical Manifestation of Food

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