Diagnosis of Food Allergy

Accurately diagnosing patients complaining of adverse reactions to foods requires a certain amount of detective work that begins by obtaining a complete history. The initial step involves identifying the food or foods suspected of causing symptoms.

Obtaining a list of all foods ingested within a few hours before the onset of the reaction is suggested when patients present with an acute reaction after a meal but are uncertain of the causative food.

Foods eaten since the reaction in similar amounts without symptoms are removed from the list, whereas those foods not subsequently ingested remain suspect. Complaints of chronic symptoms not temporally associated with food ingestion, or symptoms reported to be significantly delayed in onset after ingestion of the suspected food, often pose a diagnostic challenge.

Determining the source, ingredients, and manner of preparation of the suspected food occasionally provides an explanation for a lack of reproducible symptoms with each exposure, or implicates a previously unsuspected food, food ingredient, or contaminant as the cause of reactions.

All ingredients in suspected foods should be identified, and ingredient labels for processed foods should be examined for the presence of substances capable of causing reactions. Cooking denatures heat labile food allergens while others are heat stable.

For example, patients who experience isolated oropharyngeal symptoms after ingesting raw fruits or vegetables, often report tolerating these foods when cooked. Patients allergic to raw egg who tolerate cooked egg have been reported, as have patients who react to rare beef, but tolerate thoroughly cooked beef.

Occasionally, contamination of the suspected food with other food allergens, either intentionally as exemplified by the addition of spices, or accidentally during meal preparation, is the cause of the reaction.

The ability of nonfood allergens contaminating foodstuffs to cause reactions is exemplified by reports of reactions in dust mite allergic individuals after the ingestion of dust mite contaminated pancakes, waffles or beignets, or latex as a contaminant in foods.

Obtaining a list of foods eliminated from the patient’s diet and documenting whether the elimination of these foods led to a reduction in symptoms provides useful information.

The patient’s current diet should be thoroughly reviewed, not only for nutritional adequacy, but to determine whether the suspected food is being inadvertently ingested in significant amounts (as a hidden ingredient in other foods), or whether a food with significant immunologic cross reactivity to the suspected food remains in the diet.

In some instances, patients thought to be on elimination diets continue to have symptoms because of the unrecognized continued ingestion of the culprit food as an ingredient in other foods. Alternatively, the ability to tolerate hidden sources of suspected foods in the diet raises suspicion as to whether these foods are truly causing symptoms.

For example, a patient suspected of being milk allergic who tolerates goat’s milk should raise suspicion, given the documented extensive cross reactivity between homologous proteins in goat’s and cow’s milk. Similarly, the patient considered to be wheat allergic, who tolerates spelt, may not be wheat allergic, given that spelt is an ancient variety of wheat.

After the foods suspected of causing symptoms are identified, a precise description of each previous reaction should be obtained, including the suspected route of exposure, the estimated dose, the symptoms experienced, the timing of symptom onset in relation to food exposure, and the severity of symptoms.

In addition, the duration of the reaction, the treatment, the response to treatment, the reproducibility of reactions, and the date of the most recent reaction should be ascertained. While the majority of reactions to foods are caused by ingestion or topical contact, symptoms resulting from the inhalation or injection of food allergens have been documented.

Fortunately, unless a large surface area is exposed or the patient is exquisitely sensitive, contact reactions are generally localized to areas of contact and self-limited, rarely progressing to systemic reactions. For reactions triggered by ingestion, determining the amount of food ingested before each reaction provides one means of gaining insight about the patient’s level of sensitivity.

In regards to reactions triggered by the ingestion of miniscule amounts of the offending food, these place the patient at higher risk for more frequent reactions, and suggest the potential for more severe reactions if a larger dose of the food is ingested.

Increasingly severe reactions following the ingestion of a similar amount, or symptoms caused by the ingestion of significantly smaller portions, suggests an increasing level of sensitization. Alternatively, tolerating exposure to amounts of the food that previously caused reactions could be an indication that sensitivity to the food is waning.

A dose response relationship in regard to the amount of food ingested and the severity of symptoms encountered is commonly observed in patients with allergic reactions to foods. For example, some children tolerate milligram amounts of egg as an ingredient in baked goods, but have significant reactions when foods containing larger amounts of egg are ingested.

Threshold doses and target organ involvement for specific foods vary considerably from patient to patient and among different foods in the patient with multiple food allergies.

Studies attempting to determine the lowest threshold doses for allergic reactions to common foods allergens have documented patients with reactions after the ingestion of milligram amounts of these foods during blinded, placebo-controlled food challenges.

Allergic reactions to foods affect different target organs, either individually or in combination. The most often-involved target organs are the gastrointestinal tract, the skin, and the upper and lower respiratory tract. Although urticaria is frequently encountered in allergic reactions to foods.

The lack of urticaria does not rule out an allergic reaction, as fatal allergic reactions to foods have been observed in the absence of urticaria. Fatalities from allergic reactions to foods are usually caused by extensive laryngeal edema, severe bronchospasm, or refractory hypotension.

Most allergic reactions to foods begin within minutes to hours of ingestion of the offending food, and last from approximately one to several hours, although cases of biphasic and protracted anaphylaxis to foods have been observed. Often patients describe reactions that are similar in onset and progression when a comparable dose of allergen is ingested.

Inconsistencies in the timing and severity of allergic reactions to the same food may result from a difference in the amount consumed, the manner of food preparation, the presence of other foods, or factors such as vomiting, which impact digestion or absorption, changes in the patient’s level of sensitivity, and the ingestion of medications such as antihistamines, that can mask symptoms.

The time elapsed since the last reaction is of interest, as some patients develop tolerance after prolonged successful elimination of the food from their diet, whereas recent reactions document continued sensitivity. In rare instances, the ingestion of a food must be accompanied by another stimulus in order for a reaction to occur.

For example, food-dependent exercise-induced anaphylaxis is an interesting form of anaphylaxis that occurs when the ingestion of a specific food is followed within several hours by exercise. Ingestion of the specific food in the absence of exercise does not cause symptoms, even though the patient usually has a positive skin test to the food.

Alternatively, exercise not preceded by ingestion of the specific offending food is well tolerated, except in rare cases where the ingestion of any meal before exercise triggers symptoms. A wide variety of foods have been implicated in causing these reactions, such as fish, shellfish, wheat, celery, mushrooms, and fruit.

The typical age of patients with food-dependent exercise-induced anaphylaxis extends from adolescence through the late thirties, with women outnumbering men. The mechanism responsible for these reactions remains to be defined. This entity should be considered when reactions occur only following exercise preceded by food ingestion.

Skin testing the patient to foods ingested shortly before the exercise preceding the reaction may aid in identification of the offending food. Other factors that could cause confounding symptoms or impact the course of an allergic reaction, such as an acute illness, drug ingestion, alcohol ingestion, vigorous exercise, or psychologic distress, should be considered.

A history of illness in others ingesting the same food raises concern about food poisoning rather than food allergy. Because most patients with food allergy have other family members with allergic disease and a personal history of other allergic disease, questioning to obtain this information is indicated.

Studies examining fatal allergic reactions to foods suggest that food allergic patients with asthma are at higher risk for fatal or near-fatal reactions. These same studies reveal that the majority of patients suffering from fatal allergic reactions to foods were aware of their food allergy and ingested the offending food unknowingly.