Effective management of allergic diseases relies on the ability to make an accurate diagnosis. Allergy testing can help confirm or rule out allergies. Correct diagnosis, counseling, and avoidance advice based on valid allergy test results reduces the incidence of symptoms and need for medications, and improves quality of life. To assess the presence of allergen-specific IgE antibodies, two different methods can be used: a skin prick test, or an allergy blood test. Both methods are recommended, and they have similar diagnostic value.

Skin prick tests and blood tests are equally cost-effective, and health economic evidence shows that both tests were cost-effective compared with no test. Also, early and more accurate diagnoses save cost due to reduced consultations, referrals to secondary care, misdiagnosis, and emergency admissions.

Allergy undergoes dynamic changes over time. Regular allergy testing of relevant allergens provides information on if and how patient management can be changed, in order to improve health and quality of life. Annual testing is often the practice for determining whether allergy to milk, egg, soy, and wheat have been outgrown, and the testing interval is extended to 2–3 years for allergy to peanut, tree nuts, fish, and crustacean shellfish. Results of follow-up testing can guide decision-making regarding whether and when it is safe to introduce or re-introduce allergenic food into the diet.

An allergy blood test is quick and simple, and can be ordered by a licensed health care provider ("e.g.", an allergy specialist), GP, or PED. Unlike skin-prick testing, a blood test can be performed irrespective of age, skin condition, medication, symptom, disease activity, and pregnancy. Adults and children of any age can take an allergy blood test. For babies and very young children, a single needle stick for allergy blood testing is often more gentle than several skin tests.

An allergy blood test is available through most laboratories. A sample of the patient's blood is sent to a laboratory for analysis, and the results are sent back a few days later. Multiple allergens can be detected with a single blood sample. Allergy blood tests are very safe, since the person is not exposed to any allergens during the testing procedure.

The test measures the concentration of specific IgE antibodies in the blood. Quantitative IgE test results increase the possibility of ranking how different substances may affect symptoms. A rule of thumb is that the higher the IgE antibody value, the greater the likelihood of symptoms. Allergens found at low levels that today do not result in symptoms can nevertheless help predict future symptom development. The quantitative allergy blood result can help determine what a patient is allergic to, help predict and follow the disease development, estimate the risk of a severe reaction, and explain cross-reactivity.

A low total IgE level is not adequate to rule out sensitization to commonly inhaled allergens. Statistical methods, such as ROC curves, predictive value calculations, and likelihood ratios have been used to examine the relationship of various testing methods to each other. These methods have shown that patients with a high total IgE have a high probability of allergic sensitization, but further investigation with allergy tests for specific IgE antibodies for a carefully chosen of allergens is often warranted.

Laboratory methods to measure specific IgE antibodies for allergy testing include enzyme-linked immunosorbent assay (ELISA, or EIA), radioallergosorbent test (RAST) and fluorescent enzyme immunoassay (FEIA).

There are three main classifications of anaphylaxis. Anaphylactic shock is associated with systemic vasodilation that causes low blood pressure which is by definition 30% lower than the person's baseline or below standard values. Biphasic anaphylaxis is the recurrence of symptoms within 1–72 hours with no further exposure to the allergen. Reports of incidence vary, with some studies claiming as many as 20% of cases. The recurrence typically occurs within 8 hours. It is managed in the same manner as anaphylaxis. Pseudoanaphylaxis or anaphylactoid reactions are a type of anaphylaxis that does not involve an allergic reaction but is due to direct mast cell degranulation. Non-immune anaphylaxis is the current term used by the World Allergy Organization with some recommending that the old terminology no longer be used.

Allergy testing may help in determining the trigger. Skin allergy testing is available for certain foods and venoms. Blood testing for specific IgE can be useful to confirm milk, egg, peanut, tree nut and fish allergies.

Skin testing is available to confirm penicillin allergies, but is not available for other medications. Non-immune forms of anaphylaxis can only be determined by history or exposure to the allergen in question, and not by skin or blood testing.

Skin prick tests can be used to confirm specific food allergies. Skin prick tests are designed to identify specific IgE bound to cutaneous mast cells. During the test, a glycerinated allergen extract drop is placed on the patient's skin. The patient's skin is then pricked through the drop. This procedure is repeated with two controls: a histamine drop designed to elicit an allergic response, and a saline drop designed to elicit no allergic response. The wheal that develops from the glycerinated extract drop is compared against the saline control. A positive allergic test is one in which the extract wheal is 3mm larger than the saline wheal. A positive skin prick test is about 50% accurate, so a positive skin prick test alone is not diagnostic of food allergies.

Diagnosis is usually based on a medical history, elimination diet, skin prick test, blood tests for food-specific IgE antibodies, or oral food challenge.

- For skin-prick tests, a tiny board with protruding needles is used. The allergens are placed either on the board or directly on the skin. The board is then placed on the skin, to puncture the skin and for the allergens to enter the body. If a hive appears, the person is considered positive for the allergy. This test only works for IgE antibodies. Allergic reactions caused by other antibodies cannot be detected through skin-prick tests.

Skin-prick testing is easy to do and results are available in minutes. Different allergists may use different devices for testing. Some use a "bifurcated needle", which looks like a fork with two prongs. Others use a "multitest", which may look like a small board with several pins sticking out of it. In these tests, a tiny amount of the suspected allergen is put onto the skin or into a testing device, and the device is placed on the skin to prick, or break through, the top layer of skin. This puts a small amount of the allergen under the skin. A hive will form at any spot where the person is allergic. This test generally yields a positive or negative result. It is good for quickly learning if a person is allergic to a particular food or not, because it detects IgE. Skin tests cannot predict if a reaction would occur or what kind of reaction might occur if a person ingests that particular allergen. They can, however, confirm an allergy in light of a patient's history of reactions to a particular food. Non-IgE-mediated allergies cannot be detected by this method.

- Patch testing is used to determine if a specific substance causes allergic inflammation of the skin. It tests for delayed food reactions.

- Blood testing is another way to test for allergies; however, it poses the same disadvantage and only detects IgE allergens and does not work for every possible allergen. Radioallergosorbent testing (RAST) is used to detect IgE antibodies present to a certain allergen. The score taken from the RAST is compared to predictive values, taken from a specific type of RAST. If the score is higher than the predictive values, a great chance the allergy is present in the person exists. One advantage of this test is that it can test many allergens at one time.

A CAP-RAST has greater specificity than RAST; it can show the amount of IgE present to each allergen. Researchers have been able to determine "predictive values" for certain foods, which can be compared to the RAST results. If a person's RAST score is higher than the predictive value for that food, over a 95% chance exists that patients will have an allergic reaction (limited to rash and anaphylaxis reactions) if they ingest that food. Currently, predictive values are available for milk, egg, peanut, fish, soy, and wheat. Blood tests allow for hundreds of allergens to be screened from a single sample, and cover food allergies as well as inhalants. However, non-IgE-mediated allergies cannot be detected by this method. Other widely promoted tests such as the antigen leukocyte cellular antibody test and the food allergy profile are considered unproven methods, the use of which is not advised.

- Food challenges test for allergens other than those caused by IgE allergens. The allergen is given to the person in the form of a pill, so the person can ingest the allergen directly. The person is watched for signs and symptoms. The problem with food challenges is that they must be performed in the hospital under careful watch, due to the possibility of anaphylaxis.

Food challenges, especially double-blind, placebo-controlled food challenges, are the gold standard for diagnosis of food allergies, including most non-IgE-mediated reactions. Blind food challenges involve packaging the suspected allergen into a capsule, giving it to the patient, and observing the patient for signs or symptoms of an allergic reaction.

The best method for diagnosing food allergy is to be assessed by an allergist. The allergist will review the patient's history and the symptoms or reactions that have been noted after food ingestion. If the allergist feels the symptoms or reactions are consistent with food allergy, he/she will perform allergy tests. Additional diagnostic tools for evaluation of eosinophilic or non-IgE mediated reactions include endoscopy, colonoscopy, and biopsy.

Skin prick testing is a common way of testing for an allergy. Other ways to test for allergies can be challenge testing, which consists in feeding a very small and measured amount of the allergen to the patient and monitor the reaction (O'Neil, Zanovec and Nickla). This should only be done by a doctor under surveillance.

Important differential diagnoses are:

- Lactose intolerance generally develops later in life, but can present in young patients in severe cases. It is due to an enzyme deficiency (lactase) and not allergy, and occurs in many non-Western people.

- Celiac disease is an autoimmune disorder triggered by gluten proteins such as gliadin (present in wheat, rye, and barley). It is a non-IgE-mediated food allergy by definition.

- Irritable bowel syndrome

- C1 Esterase inhibitor deficiency (hereditary angioedema), a rare disease, generally causes attacks of angioedema, but can present solely with abdominal pain and occasional diarrhea.

The majority of children outgrow egg allergy. One review reported that 70% of children will outgrow this allergy by 16 years. In subsequently published longitudinal studies, one reported that for 140 infants who had challenge-confirmed egg allergy, 44% had resolved by two years. A second reported that for 203 infants with confirmed IgE-mediated egg allergy, 45% resolved by two years of age, 66% by four years, and 71% by six years. Children will be able to tolerate eggs as an ingredient in baked goods and well-cooked eggs sooner than under-cooked eggs. Resolution was more likely if baseline serum IgE was lower, and if the baseline symptoms did not include anaphylaxis.

Peanut allergies tend to resolve in childhood less often than allergies to soy, milk, egg, and wheat. Accordingly, re-evaluation of peanut allergy is recommended on a yearly basis for young children with favorable previous test results, and every few years or longer for older children and adults.

Urinary cystyl-leukotriene or urinary LTE4 can be used after a supervised challenge with aspirin. In aspirin sensitivity, no change in N-methylhistamine is observed; while LTE4 levels are increased. This test however lacks sensitivity and has a 25 percent false negative rate among affected persons.

Diagnosis of egg allergy is based on the person's history of allergic reactions, skin prick test (SPT), patch test and measurement of egg-specific serum immunoglobulin E (IgE or sIgE). Confirmation is by double-blind, placebo-controlled food challenges. SPT and sIgE have sensitivity greater than 90% but specificity in the 50-60% range, meaning these tests will detect an egg sensitivity, but will also be positive for other allergens. For young children, attempts have been made to identify SPT and sIgE responses strong enough to avoid the need for a confirming oral food challenge.

Nickel allergy can be confirmed by a properly trained health care provider based on the medical history, physical exam and a painless specialized patch test— when necessary. A significant number of people may self-diagnose, and not contact medical professionals, which could result in massive underreporting of the problem by scientific researchers.

Confirming the diagnosis of Ni-ACD specifically involves inducing the skin to demonstrate a rash where the chemicals are applied (a delayed type hypersensitivity reaction), evidence that the patient is exposed to nickel, and establishing that the reaction and the exposure explain the current rash/symptoms under question. The patch test plays a significant role in diagnosing ACD.

The patch test evokes a delayed, Type IV hypersensitivity reaction, which is a cell-mediated, antibody independent, immune response. Patch testing is the "gold standard" diagnostic tool for Ni-ACD. In this sense, a positive patch test to nickel establishes that the subject has been previously exposed and is therefore sensitized to nickel. It does not necessarily indicate that the patch reaction is the cause of the current clinical disease. A negative test demonstrates that the patient is sub-threshold, either minimally or not sensitized. Cumulatively, clinical reasoning and a patch test help determine if nickel could be the cause of a current dermatitis reaction.

Diagnosing allergic contact dermatitis is primarily based on physical exam and medical history. In some cases doctors can establish an accurate diagnosis based on the symptoms that the patient experiences and on the rash's appearance. In the case of a single episode of allergic contact dermatitis, this is all that is necessary. Chronic and/or intermittent rashes which are not readily explained by history and physical exam often will benefit from further testing.

A patch test (contact delayed hypersensitivity allergy test) is a commonly used examination to determine the exact cause of an allergic contact dermatitis. According to the American Academy of Allergy, Asthma, and Immunology, "patch testing is the gold standard for contact allergen identification".

The patch test consists of applying small quantities of potential allergens to small patches and which are then placed on the skin. After two days, they are removed and if a skin reaction occurred to one of the substances applied, a raised bump will be noticeable underneath the patch. The tests are again read at 72 or 96 hours after application.

Patch testing is used for patients who have chronic, recurring contact dermatitis. Other tests that may be used to diagnose contact dermatitis and rule out other potential causes of the symptoms include a skin biopsy and culture of the skin lesion.

Diagnosis of soy allergy is based on the person's history of allergic reactions, skin prick test (SPT), patch test and measurement of soy protein specific serum immunoglobulin E (IgE or sIgE). A negative IgE test does not rule out non-IgE mediated allergy, also described as cell-mediated allergy. SPT and sIgE have sensitivities of 55% and 83% respectively, and specificities of 68% and 38%. These numbers mean that either test may miss diagnosing an existing soy allergy, and that both can also be positive for other food allergens. Confirmation is by double-blind, placebo-controlled food challenges, conducted by an allergy specialist.

Estimates of latex sensitivity in the general population range from 0.8% to 8.2%.

For some people, the sensitivity is so extreme that replacement of latex products with products made from alternative materials may still result in a reaction if the products are manufactured in the same facility as the latex-containing products, due to trace quantities of natural rubber latex on the non-latex products.

An allergy is different from an intolerance. Food allergies and food intolerances should not be confused because they do not contain the same risks and are not diagnosed the same way. Allergies can be fatal after only a small consumption, while intolerance, although uncomfortable, are not as deadly. An intolerance may lead to a nutrient deficiency which could cause death if untreated but the intolerance itself is not enough to cause rapid death. Allergies, with their varying symptoms, could cause instantaneous death if there is inflammation in the throat and causes suffocation.

Risk factors for drug allergies can be attributed to the drug itself or the characteristics of the patient. Drug-specific risk factors include the dose, route of administration, duration of treatment, repetitive exposure to the drug, and concurrent illnesses. Host risk factors include age, sex, atopy, specific genetic polymorphisms, and inherent predisposition to react to multiple unrelated drugs (multiple drug allergy syndrome).

A drug allergy is more likely to develop with large doses and extended exposure.

There are no laboratory or skin testing methods for testing salicylate sensitivity. Provocative challenge is one method of obtaining reliable diagnosis. Provocative challenge is intended to induce a controlled reaction as a means of confirming diagnosis. During provocative challenge, the person is given incrementally higher doses of salicylates, usually aspirin, under medical supervision, until either symptoms appear or the likelihood of symptoms appearing is ruled out.

Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids.

If the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.

Once a nickel allergy is detected, the best treatment is avoidance of nickel-releasing items. It is important to know the main items that can cause nickel allergy, which may be remembered using the mnemonic "BE NICKEL AWARE". The top 13 categories that contain nickel include beauty accessories, eyeglasses, money, cigarettes, clothes, kitchen and household, electronics and office equipment, metal utensils, aliment, jewelry, batteries, orthodontic and dental appliances, and medical equipment. Other than strict avoidance of items that release free nickel, there are other treatment options for reduction of exposure. The first step is to limit friction between skin and metallic items. Susceptible people may try to limit sweating while wearing nickel items, to reduce nickel release and thus decrease chances for developing sensitization and/or allergy. Another option is to shield electronics, metal devices, and tools with fabric, plastic, or acrylic coverings. Dermatological application tests has shown that barrier creams effectively prevent the symptoms of nickel allergy, such as the Nidiesque™.

There are test kits that can be very helpful to check for nickel release from items prior to purchasing. The ACDS providers can give a guidance list of safe items. In addition to avoidance, healthcare providers may prescribe additional creams or medications to help relieve the skin reaction.

Drug allergies are attributed to "drug hypersensitivity," otherwise known as objectively reproducible symptoms or signs initiated by exposure to a drug at a dose normally tolerated by non-hypersensitive persons. Drug hypersensitivity reactions are the mediators of a drug allergy.

There are two mechanisms for a drug allergy to occur: IgE or non-IgE mediated. In IgE-mediated reactions, also known as Immunoglobulin E mediated reactions, drug allergens bind to IgE antibodies, which are attached to mast cells and basophils, resulting in IgE cross-linking, cell activation and release of preformed and newly formed mediators.

Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. Sommer "et al." reported a multi-center prospective randomized cross-over trial with 30 patients following a low-salicylate diet for 6 weeks. This study demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet.

A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help. In a small study, aspirin-sensitive asthma patients taking 10 grams of fish oil daily reported relief of most symptoms after six weeks, however symptoms returned if the supplement was stopped.

Allergic inflammation is an important pathophysiological feature of several disabilities or medical conditions including allergic asthma, atopic dermatitis, allergic rhinitis and several ocular allergic diseases. Allergic reactions may generally be divided into two components; the early phase reaction, and the late phase reaction. While the contribution to the development of symptoms from each of the phases varies greatly between diseases, both are usually present and provide us a framework for understanding allergic disease.

The early phase of the allergic reaction typically occurs within minutes, or even seconds, following allergen exposure and is also commonly referred to as the immediate allergic reaction or as a Type I allergic reaction. The reaction is caused by the release of histamine and mast cell granule proteins by a process called degranulation, as well as the production of leukotrienes, prostaglandins and cytokines, by mast cells following the cross-linking of allergen specific IgE molecules bound to mast cell FcεRI receptors. These mediators affect nerve cells causing itching, smooth muscle cells causing contraction (leading to the airway narrowing seen in allergic asthma), goblet cells causing mucus production, and endothelial cells causing vasodilatation and edema.

The late phase of a Type 1 reaction (which develops 8–12 hours and is mediated by mast cells) should not be confused with delayed hypersensitivity Type IV allergic reaction (which takes 48–72 hours to develop and is mediated by T cells). The products of the early phase reaction include chemokines and molecules that act on endothelial cells and cause them to express Intercellular adhesion molecule (such as vascular cell adhesion molecule and selectins), which together result in the recruitment and activation of leukocytes from the blood into the site of the allergic reaction. Typically, the infiltrating cells observed in allergic reactions contain a high proportion of lymphocytes, and especially, of eosinophils. The recruited eosinophils will degranulate releasing a number of cytotoxic molecules (including Major Basic Protein and eosinophil peroxidase) as well as produce a number of cytokines such as IL-5. The recruited T-cells are typically of the Th2 variety and the cytokines they produce lead to further recruitment of mast cells and eosinophils, and in plasma cell isotype switching to IgE which will bind to the mast cell FcεRI receptors and prime the individual for further allergic responses.