The cause of chronic hives can rarely be determined. In some cases regular extensive allergy testing over a long period of time is requested in hopes of getting new insight. No evidence shows regular allergy testing results in identification of a problem or relief for people with chronic hives. Regular allergy testing for people with chronic hives is not recommended.

This very rare form of angioedema develops in response to contact with vibration. In vibratory angioedema, symptoms develop within two to five minutes after contact with a vibrating object, and abate after about an hour. Patients with this disorder do not suffer from dermographism or pressure urticaria. Vibratory angioedema is diagnosed by holding a vibrating device such as a laboratory vortex machine against the forearm for four minutes. Speedy swelling of the whole forearm extending into the upper arm is also noted later. The principal treatment is avoidance of vibratory stimulants. Antihistamines have also been proven helpful.

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.

Diagnosis is typically obtained by an allergist or other licensed practitioner performing a cold test. During the cold test, a piece of ice is held against the forearm, typically for 3–4 minutes. A positive result is a specific looking mark of raised red hives. The hives may be the shape of the ice, or it may radiate from the contact area of the ice." However, while these techniques assist in diagnosis, they do not provide information about temperature and stimulation time thresholds at which patients will start to develop symptoms."which is essential because it can establish disease severity and monitor the effectiveness of treatment.

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.

Antihistamine agents are the typically prescribed drug for the treatment of physical urticaria. They block the effect of histamine, a compound produced by the body which forms a part of the local immune response consequently causing inflammation. Some research has suggested that the use antihistamines and antagonist in synergy are better for the treatment of physical urticarias.

The cascade of events that link the autoantibody-antigen reaction with the production and release of histamine is not well characterized. Therefore, the focus of treatment for physical urticaria has been on characterizing the effectiveness of antihistamines rather than analysis of receptor binding or the pathomechanisms.

Solar urticaria can be difficult to diagnose, but its presence can be confirmed by the process of phototesting. There are several forms of these tests including photopatch tests, phototests, photoprovocation tests, and laboratory tests. All of these are necessary to determine the exact infliction that the patient is suffering from. Photopatch tests are patch tests conducted when it is believed that a patient is experiencing certain symptoms due to an allergy that will only occur when in contact with sunlight. After the procedure, the patient is given a low dosage of UVA radiation.

Another test known as a phototest is the most useful in identifying solar urticaria. In this test, one centimeter segments of skin are subject to varying amounts of UVA and UVB radiation in order to determine the specific dosage of the certain form of radiation that causes the urticaria to form. When testing for its less intense form (fixed solar urticaria), phototesting should be conducted only in the areas where the hives have appeared to avoid the possibility of getting false-negative results.

A third form of testing is the photoprovocation test which is used to identify disorders instigated by sun burns. The process of this test involves exposing one area of a patient's arm to certain dosage of UVB radiation and one area on the other arm to a certain dosage of UVA radiation. The amount of radiation that the patient is exposed to is equal to that "received in an hour of midday summer sun." If the procedure produces a rash, then the patient will undergo a biopsy. Finally, there are laboratory tests which generally involve procedures such as blood, urine, and fecal biochemical tests. In some situations, a skin biopsy may be performed.

Diagnosis of aquagenic urticaria will begin with an evaluation of the patient's clinical history looking for any signs of what might be causing this severe reaction. The patient will then be put to a water treatment test where water will be applied to the upper body for 30 minutes. Water may be placed directly on the skin or a soaked paper towel may be applied. In many cases distilled water, tap water and saline will be used to check for a difference in reaction. After this is removed the skin will be checked for a reaction for the next 10–15 minutes. Because aqugenic urticaria frequently accompanies other types of physical urticaraia, the doctor may perform tests to check for these other conditions. An ice cube may be placed on the forearm for a few minutes to check for cold urticarial, exposure to a hot bath will be used to check for Cholinergis uticaria and the lesions will be inspected to determine the root cause of their appearance.

Evaluations for aquagenic urticaria consist of a clinical history and water challenge test. The standard test for aquagenic urticaria is application of a 35 °C water compress to the upper body for 30 minutes. Water of any temperature can provoke aquagenic urticaria; however, keeping the compress at a similar temperature to that of the human body (37 °C) avoids confusion with cold-induced or local heat urticaria. In addition, a forearm or hand can be immersed in water of varying temperatures. A diagnosis of aquagenic urticaria requires exclusion of other types of physical urticaria, so an exercise test and ice cube test should be performed to rule out other types of physical urticarial. aquagenic urticaria should be distinguished from aquagenic pruritus, in which brief contact with water evokes intense itching without wheals or erythema. The pathogenesis of aquagenic urticaria is not fully known; however, several mechanisms have been proposed. Interaction with water with a component in or on the stratum corneum or sebum, generating a toxic compound, has been suggested. Absorption of this substance would exert an effect of perifollicular mast cell degranulation with release of histamine.

Dermographism can be treated by substances (i.e. an antihistamine) which prevent histamine from causing the reaction. These may need to be given as a combination of H antagonists, or possibly with an H-receptor antagonist such as cimetidine.

OTC Vitamin C, 1000 mg daily, increases histamine degradation and removal.

Not taking hot baths or showers may help if it is generalized (all over) and possibly for localized cases (in a specific area). If taking hot showers helps, it may be a condition called shower eczema. If it affects mainly the head, it may be psoriasis. In rare cases, allergy tests may uncover substances the patient is allergic to.

While cromoglycate, which prevents histamine from being released from mast cells, is used topically in rhinitis and asthma, it is not effective orally for treating chronic urticaria.

The cause of physical urticaria is unknown but it has been suggested to be an autoimmune disease. Suggesting that antibodies, which are produced by the immune system to protect humans from foreign microbes, are binding to body tissue; damaging body tissue.

In some cases physical urticaria can be a symptom of an underlying health issue such as:

- thyroid disease

- hepatitis

- infection

- cancer.

Or can also be due to:

- food allergies

- atopy

The disease is most often diagnosed as an infant, when parents take their baby in for what appears to be bug bites. The bug bites are actually the clumps of mast cells. Doctors can confirm the presence of mast cells by rubbing the baby's skin. If hives appear, it most likely signifies the presence of urticaria pigmentosa.

The first-line therapy in ColdU, as recommended by EAACI/GA2 LEN/EDF/WAO guidelines, is symptomatic relief with second-generation H1- antihistamines. if standard doses are ineffective increasing up to 4-fold is recommended to control symptoms.

The second-generation H1-antihistamine, rupatadine, was found to significantly reduce the development of chronic cold urticaria symptom without an increase in adverse effects using 20 and 40 mg.

Allergy medications containing antihistamines such as diphenhydramine (Benadryl), cetirizine (Zyrtec), loratidine (Claritin), cyproheptadine (Periactin), and fexofenadine (Allegra) may be taken orally to prevent and relieve some of the hives (depending on the severity of the allergy). For those who have severe anaphylactic reactions, a prescribed medicine such as doxepin, which is taken daily, should help to prevent and/or lessen the likelihood of a reaction and thus, anaphylaxis. There are also topical antihistamine creams which are used to help relieve hives in other conditions, but there is not any documentation stating it will relieve hives induced by cold temperature.

Cold hives can result in a potentially serious, or even fatal, systemic reaction (anaphylactic shock). People with cold hives may have to carry an injectable form of epinephrine (like Epi-pen or Twinject) for use in the event of a serious reaction.

The best treatment for this allergy is avoiding exposure to cold temperature.

Studies have found that Omalizumab (Xolair) may be an effective and safe treatment to cold urticaria for patient who do not sufficiently respond to standard treatments.

Ebastine has been proposed as an approach to prevent acquired cold urticaria.

The more poignant part of this disorder is the lack of desensitization for water and aqua intile injection as allergen even on repeated exposure. Avoidance of allergen as a general principle in any allergic disorder necessitates the evasion of water exposure. Topical application of antihistamines like 1% diphenhydramine before water exposure is reported to reduce the hives. Oil in water emulsion creams, petrolatum as barrier agents for water can be used prior to shower or bath with good control of symptoms. Therapeutic effectiveness of various classes of drugs differs from case to case.

Solar urticaria, due to its particular features, is considered to be a type of physical urticaria or light sensitivity. Physical urticaria arises from physical factors in the environment, which in the case of solar urticaria is UV radiation or light. SU may be classified based on the wavelength of the radiative energy that causes the allergic reaction; known as Harber's classification, six types have been identified in this system. Type I solar urticaria is caused by UVB (ultraviolet B) radiation, with wavelengths ranging from 290–320 nm. Type II is induced by UVA (ultraviolet A) radiation with wavelengths that can range from 320–400 nm. The wavelength range of type III and IV spans from 400 to 500 nm, while type V can be caused by UVB radiation to visible light (280–600 nm). Type VI has only been known to occur at 400 nm.

Another classification distinguishes two types. The first is a hypersensitivity caused by a reaction to photoallergens located only in people with SU; while the second is caused by photoallergens that can be found in both people with SU and people without it.

A subgroup of solar urticaria, fixed solar urticaria, has also been identified. It is a rare, less intense form of the disease with wheals (swollen areas of the skin) that affect certain, fixed areas of the body. Fixed solar urticaria is induced by a broad spectrum of radiative energy with wavelengths ranging from 300–700 nm.

Diagnosis of autoimmune disorders largely rests on accurate history and physical examination of the patient, and high index of suspicion against a backdrop of certain abnormalities in routine laboratory tests (example, elevated C-reactive protein). In several systemic disorders, serological assays which can detect specific autoantibodies can be employed. Localised disorders are best diagnosed by immunofluorescence of biopsy specimens. Autoantibodies are used to diagnose many autoimmune diseases. The levels of autoantibodies are measured to determine the progress of the disease.

Prevention measures include avoidance of the irritant through its removal from the workplace or through technical shielding by the use of potent irritants in closed systems or automation, irritant replacement or removal and personal protection of the workers.

Doctors can diagnose "urticaria pigmentosa" (cutaneous mastocytosis, see above) by seeing the characteristic lesions that are dark-brown and fixed. A small skin sample (biopsy) may help confirm the diagnosis.. To check whether the mastocytosis is cutaneous only or systemic, the level of serum tryptase in the blood is also checked. If the level is elevated, this most probably implies that the mastocytosis is systemic and can only be confirmed by undergoing a bone marrow biopsy.

By taking a biopsy from a different organ, such as the bone marrow, the doctor can diagnose systemic mastocytosis. Using special techniques on a bone marrow sample, the doctor looks for an increase in mast cells. Another sign of this disorder is high levels of certain mast-cell chemicals and proteins in a person's blood and sometimes in the urine. Serum tryptase level is the initial screening test for suspected systemic mastocytosis.

Diagnoses of wheat allergy may deserve special consideration. Omega-5 gliadin, the most potent wheat allergen, cannot be detected in whole wheat preparations; it must be extracted and partially digested (similar to how it degrades in the intestine) to reach full activity. Other studies show that digestion of wheat proteins to about 10 amino acids can increase the allergic response 10 fold. Certain allergy tests may not be suitable to detect all wheat allergies, resulting in cryptic allergies. Because many of the symptoms associated with wheat allergies, such as sacroiliitis, eczema and asthma, may be related or unrelated to a wheat allergy, medical deduction can be an effective way of determining the cause. If symptoms are alleviated by immunosuppressant drugs, such as Prednisone, an allergy-related cause is likely. If multiple symptoms associated with wheat allergies are present in the absence of immunosuppressants then a wheat allergy is probable.

Clinical examination alone cannot distinguish between a response caused by infection, such as cellulitis, and skeeter syndrome. However, skeeter syndrome usually progresses over the course of hours versus cellulitis, which typically will evolve over the course of several days. As such, accurate history is imperative when making the diagnosis. Since IgE and IgG are key players in mosquito allergy, diagnosis can be confirmed by an immunosorbent assay measuring IgE and IgG to mosquito saliva antigens.

Symptoms are thought to be the result of histamine being released by mast cells on the surface of the skin. Due to the lack of antigens, histamine causes the skin to swell in affected areas. If the membrane that surrounds the mast cells is too weak it will easily and rapidly break down under physical pressure, which will therefore cause an allergic-like reaction.

Symptoms can be caused or induced by

- stress

- tight or abrasive clothing

- watches

- glasses

- heat

- cold

- anything placing pressure on exposed skin

- infection

The underlying cause of dermatographism is not known, and can last for many years without relief. The condition may subside and be effectively cured; however, it is often a lifelong ailment. It is not a life-threatening disease and is not contagious.

Dermographism may occur in Mastocytosis (systemic mast cell proliferation).

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.

Other types of mast cell disease include:

- Monoclonal mast cell activation, defined by the World Health Organisation definitions 2010, also has increased mast cells but insufficient to be systemic mastocytosis (in World Health Organisation Definitions)

- Mast cell activation syndrome – has normal number of mast cells, but all the symptoms and in some cases the genetic markers of systemic mastocytosis.

- Other known but rare mast cell proliferation diseases are mast cell leukemia and mast cell sarcoma.

A literature review of 2014 found that non-coeliac gluten sensitivity diagnosis can be reached only by excluding celiac disease (CD) and wheat allergy.

Persons suspected of having celiac disease may undergo serological testing for IgA anti-tissue transglutaminase antibodies (abbreviated anti-tTG antibodies or anti-TG2 antibodies) and anti-endomysial antibodies (abbreviated EMA) provided the IgA-level is high, and if IgA is low, testing for certain IgG antibodies; in case of positive serological indication, a duodenal biopsy may confirm active celiac disease.

Eliminating the possibility of CD can generally also be done by adding HLA-DQ typing. The absence of HLA-DQ2 and HLA-DQ8 has a very high negative predictive value for CD, and the predictive value can be further enhanced by including HLA-DQ7.5 (HLA-DQ2 and HLA-DQ8 are found in coeliac disease 98% of the time in Caucasians, HLA-DQ7.5 present in the remaining 1.6% and only 0.4% of Caucasians are missed with the combination of these 3). Without serological or HLA-DQ2/8 positivity, celiac disease is likely not present. HLA-DQ typing has a practical advantage in that it is the only diagnostic test that allows to exclude CD when a patient is already on a gluten-free diet; however, as not only celiacs are HLA-DQ2/HLA-DQ8 positive, this method has a higher false positive rate than anti-TG2 and EMA antibody testing.

A four-of-five rule was proposed 2010 for confirming celiac disease, with the disease confirmed if at least four of the following five criteria are satisfied:

- typical symptoms of celiac disease;

- positivity of serum celiac disease immunoglobulin, A class autoantibodies at high titer;

- human leukocyte antigen (HLA)-DQ2 or DQ8 genotypes;

- celiac enteropathy at the small bowel biopsy; and

- response to the gluten-free diet.

For diagnosis of wheat allergy, allergy tests are available.

A sweat allergy is the exacerbation of atopic dermatitis associated with an elevated body temperature and resulting increases in the production of sweat. It appears as small reddish wheals that become visible in response to increased temperature and resulting production of sweat. It can effect all ages. Sweating can trigger intense itching or cholinergic urticaria. The protein MGL_1304 secreted by mycobiota present on the skin such as "Malassezia globosa" acts as a histamine or antigen. People can be desensitized using using their own samples of sweat that have been purified that contains small amounts of the allergen. The allergy is not due to the sweat itself but instead to an allergy-producing protein secreted by baceria found on the skin.

Cholinergic urticaria (CU) is one of the physical urticaria which is provoked during sweating events such as exercise, bathing, staying in a heated environment, or emotional stress. The hives produced are typically smaller than classic hives and are generally shorter-lasting.

Multiple subtypes have been elucidated, each of which require distinct treatment.

Tannic-acid has been found to suppress the allergic response along with showering.

Urticarial dermatoses are distinct from urticaria, which examples being drug-induced urticaria, eosinophilic cellulitis and bullous pemphigoid. It is important to distinguish urticaria from urticarial dermatoses. The individual wheals of urticaria are ‘here today and gone tomorrow’ (i.e. they last less than 24 hours), whereas with urticarial dermatoses, the individual lesions last for days or longer.