Diagnostic markers include eosinophil granulocytes and granulomas in affected tissue, and antineutrophil cytoplasmic antibodies (ANCA) against neutrophil granulocytes. The American College of Rheumatology 1990 criteria for diagnosis of Churg–Strauss syndrome lists these criteria:

- Asthma

- Eosinophilia, i.e. eosinophil blood count greater than 500/microliter, or hypereosinophilia, i.e. eosinophil blood count greater than 1,500/microliter

- Presence of mononeuropathy or polyneuropathy

- Unfixed pulmonary infiltrates

- Presence of paranasal sinus abnormalities

- Histological evidence of extravascular eosinophils

For classification purposes, a patient shall be said to have Churg–Strauss syndrome (CSS) if at least four of these six criteria are positive. The presence of any four or more of the six criteria yields a sensitivity of 85% and a specificity of 99.7%.

The French Vasculitis Study Group has developed a five-point system ("five-factor score") that predicts the risk of death in Churg–Strauss syndrome using clinical presentations. These factors are:

- Reduced renal function (creatinine >1.58 mg/dl or 140 µmol/l)

- Proteinuria (>1 g/24h)

- Gastrointestinal hemorrhage, infarction, or pancreatitis

- Involvement of the central nervous system

- Cardiomyopathy

The lack of any of these factors indicates milder case, with a five-year mortality rate of 11.9%. The presence of one factor indicates severe disease, with a five-year mortality rate of 26%, and two or more indicate very severe disease: 46% five-year mortality rate.

Diagnosis is by complete blood count (CBC). However, in some cases, a more accurate absolute eosinophil count may be needed. Medical history is taken, with emphasis on travel, allergies and drug use. Specific test for causative conditions are performed, often including chest x-ray, urinalysis, liver and kidney function tests, and serologic tests for parasitic and connective tissue diseases. The stool is often examined for traces of parasites (i.e. eggs, larvae, etc.) though a negative test does not rule out parasitic infection; for example, trichinosis requires a muscle biopsy. Elevated serum B or low white blood cell alkaline phosphatase, or leukocytic abnormalities in a peripheral smear indicates a disorder of myeloproliferation. In cases of idiopathic eosinophilia, the patient is followed for complications. A brief trial of corticosteroids can be diagnostic for allergic causes, as the eosinophilia should resolve with suppression of the immune over-response. Neoplastic disorders are diagnosed through the usual methods, such as bone marrow aspiration and biopsy for the leukemias, MRI/CT to look for solid tumors, and tests for serum LDH and other tumor markers.

The diagnosis of EoE is typically made on the combination of symptoms and findings on diagnostic testing.

Prior to the development of the EE Diagnostic Panel, EoE could only be diagnosed if gastroesophageal reflux did not respond to a six-week trial of twice-a-day high-dose proton-pump inhibitors (PPIs) or if a negative ambulatory pH study ruled out gastroesophageal reflux disease (GERD).

Endoscopically, ridges, furrows, or rings may be seen in the esophageal wall. Sometimes, multiple rings may occur in the esophagus, leading to the term "corrugated esophagus" or "feline esophagus" due to similarity of the rings to the cat esophagus. Presence of white exudates in esophagus is also suggestive of the diagnosis. On biopsy taken at the time of endoscopy, numerous eosinophils can be seen in the superficial epithelium. A minimum of 15 eosinophils per high-power field are required to make the diagnosis. Eosinophilic inflammation is not limited to the esophagus alone, and does extend through the whole gastrointestinal tract. Profoundly degranulated eosinophils may also be present, as may microabcesses and an expansion of the basal layer.

Radiologically, the term "ringed esophagus" has been used for the appearance of eosinophilic esophagitis on barium swallow studies to contrast with the appearance of transient transverse folds sometimes seen with esophageal reflux (termed "feline esophagus").

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.

Treatment is directed toward the underlying cause. However, in primary eosinophilia, or if the eosinophil count must be lowered, corticosteroids such as prednisone may be used. However, immune suppression, the mechanism of action of corticosteroids, can be fatal in patients with parasitosis.

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.

Plasma cell gingivits is rare, and plasma cell cheilitis is very rare. Most people with plasma cell cheilitis have been elderly.

Histologically plasma cell gingivitis shows mainly plasma cells. The differential diagnosis is with acute leukemia and multiple myeloma. Hence, blood tests are often involved in ruling out other conditions. A biopsy is usually taken, and allergy testing may also be used. The histopathologic appearance is characterized by diffuse, sub-epithelial plasma cell inflammatory infiltration into the connective tissue. The epithelium shows spongiosis. Some consider that plasmoacanthoma (solitary plasma cell tumor) is part of the same spectrum of disease as plasma cell cheilitis.

In acquired angioedema, HAE types I and II, and nonhistaminergic angioedema, antifibrinolytics such as tranexamic acid or ε-aminocaproic acid may be effective. Cinnarizine may also be useful because it blocks the activation of C4 and can be used in patients with liver disease, while androgens cannot.

With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.

Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, one of various methods commonly known as allergy testing. The top three allergens found in patch tests from 2005–06 were: nickel sulfate (19.0%), Myroxylon pereirae (Balsam of Peru, 11.9%), and fragrance mix I (11.5%).

The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names, and do not always appear on labels.

The distinction between the various types of contact dermatitis is based on a number of factors. The morphology of the tissues, the histology, and immunologic findings are all used in diagnosis of the form of the condition. However, as suggested previously, there is some confusion in the distinction of the different forms of contact dermatitis. Using histology on its own is insufficient, as these findings have been acknowledged not to distinguish, and even positive patch testing does not rule out the existence of an irritant form of dermatitis as well as an immunological one.

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).

A detailed history allows physicians to determine whether the presenting symptoms are due to an allergen or another source. Diagnostic tests such as conjunctival scrapings to look for eosinophils are helpful in determining the cause of the allergic response. Antihistamines, medication that stabilizes mast cells, and NSAIDs are safe and usually effective. Corticosteroids are reserved for more severe cases of ocular allergy disease, and their use should be monitored by an eye care physician due to possible side-effects. When an allergen is identified, the person should avoid the allergen as much as possible.

If the allergen is encountered and the symptoms are mild, a cold compress can be used to provide relief.

Treatment strategies may include medication, dietary modification to exclude food allergens, and mechanical dilatation of the esophagus.

The current recommendation for first line treatment is PPI in lieu of diet as more than half of people with EOE respond to this, and it is a low risk, low cost treatment. The next step treatment is topical corticosteroids (topical viscous budesonide or fluticasone).

Dietary treatment can be effective, as there does appear to be a role of allergy in the development of EOE. Allergy testing is not particularly effective in predicting which foods are driving the disease process. Various approaches have been tried, where either six food groups (cow´s milk, wheat, egg, soy, nuts and fish/seafood), four groups (animal milk, gluten-containing cereals, egg, legumes) or two groups (animal milk and gluten-containing cereals) are excluded for a period of time, usually six weeks. Endoscopy is required to measure the response to the dietary measure. A "top down" (starting with six foods, then reintroducing) approach may be very restrictive. Four- or even two-group exclusion diets may be less difficult to follow and reduce the need for many endoscopies if the response to the limited restriction is good.

Endoscopic dilatation is sometimes required if there is significant narrowing of the esophagus. This is effective in 84% of people who require this procedure.

In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seem to decrease over time as people age. However, the biological reasons for these changes are not fully understood.

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.

Chronic ulcerative stomatitis is a recently discovered condition with specific immunopathologic features. It is characterized by erosions and ulcerations which relapse and remit. Lesions are located on the buccal mucosa (inside of the cheeks) or on the gingiva (gums). The condition resembles Oral lichen planus when biopsied.

The diagnosis is made with Immunofluorescence techniques, which shows circulating and tissue-bound autoantibodies (particulate stratified squamous-epithelium-specific antinuclear antibody) to DeltaNp63alpha protein, a normal component of the epithelium. Treatment is with hydroxychloroquine.

To confirm OAS, the suspected food is consumed in a normal way. The period of observation after ingestion and symptoms are recorded. If other co factors like combined foods are required, this is also replicated in the test. For example, if the individual always develops symptoms after eating followed by exercise, then this is replicated in the laboratory.

In an industrial setting the employer has a duty of care to its worker to provide the correct level of safety equipment to mitigate exposure to harmful irritants. This can take the form of protective clothing, gloves, or barrier cream, depending on the working environment.

Topical antibiotics should not be used to prevent infection in wounds after surgery. When they are used, it is inappropriate, and the person recovering from surgery is at significantly increased risk of developing contact dermatitis.

The diagnosis is made on the clinical picture. Routine blood tests (complete blood count, electrolytes, renal function, liver enzymes) are typically performed. Mast cell tryptase levels may be elevated if the attack was due to an acute allergic (anaphylactic) reaction. When the patient has been stabilized, particular investigations may clarify the exact cause; complement levels, especially depletion of complement factors 2 and 4, may indicate deficiency of "C1-inhibitor". HAE type III is a diagnosis of exclusion consisting of observed angioedema along with normal C1 levels and function.

The hereditary form (HAE) often goes undetected for a long time, as its symptoms resemble those of more common disorders, such as allergy or intestinal colic. An important clue is the failure of hereditary angioedema to respond to antihistamines or steroids, a characteristic that distinguishes it from allergic reactions. It is particularly difficult to diagnose HAE in patients whose episodes are confined to the gastrointestinal tract. Besides a family history of the disease, only a laboratory analysis can provide final confirmation. In this analysis, it is usually a reduced complement factor C4, rather than the C1-INH deficiency itself, that is detected. The former is used during the reaction cascade in the complement system of immune defense, which is permanently overactive due to the lack of regulation by C1-INH.

Angioedema is classified as either hereditary or acquired.

Although there are a multitude of varying appearances, the id reaction often presents with symmetrical red patches of eczema with papules and vesicles, particularly on the outer sides of the arms, face and trunk which occur suddenly and are intensely itchy occur a few days to a week after the initial allergic or irritant dermatitis. Most commonly, athletes foot can lead to localised vesicles on hands, bacterial infections to erythema nodosum and herpes simplex virus to erythema multiforme.

The diagnosis is frequently made by treating the initial triggering skin problem and observing the improvement in the eczematous rash. Both the initial skin problem and the id reaction must be observed to make the diagnosis.

All dyshidrotic rashes are not id reactions, but id reactions are often dishydrotic-like.

Initial tests may include isolating a fungus by taking a swab and sending it for culture. Patch testing may be considered if there is suspicion of allergic contact dermatitis.

A skin biopsy is rarely necessary, but if done mostly shows an interstitial granulomatous dermatitis, some lesions being spongiotic. Id reactions cannot be distinguished from other skin diseases by histopathology. However, they can be distinguished from other id reactions by histopathology.

There is no good evidence that a mother's diet during pregnancy, the formula used, or breastfeeding changes the risk. There is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use.

People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.

Diagnosis of eczema is based mostly on the history and physical examination. In uncertain cases, skin biopsy may be useful. Those with eczema may be especially prone to misdiagnosis of food allergies.

Patch tests are used in the diagnosis of allergic contact dermatitis.