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.

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.

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.

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 mainstay of therapy for both acute and chronic hives is patient education, avoiding triggers and using antihistamines.

Chronic hives can be difficult to treat and lead to significant disability. Unlike the acute form, 50–80% of people with chronic hives have no identifiable triggers. Fortunately, 50% of people with chronic hives will experience remission within 1 year. Overall, treatment is geared towards symptomatic management. Individuals with chronic hives may need other medications in addition to antihistamines to control symptoms. Patients who experience hives with angioedema require emergency treatment as this is a life-threatening condition.

Treatment guidelines for the management of chronic hives have been published. According to the 2014 American practice parameters, treatment involves a step wise approach. Step 1 consists of second generation, H1 receptor blocking antihistamines. Systemic glucocorticoids can also be used for episodes of severe disease but should not be used for long term due to their long list of side effects. Step 2 consists of increasing the dose of the current antihistamine, adding other antihistamines, or adding a leukotriene receptor antagonist such as montelukast. Step 3 consists of adding or replacing the current treatment with hydroxyzine or doxepin. If the individual doesn't respond to steps 1–3 then they are considered to have refractory symptoms. At this point, anti-inflammatory medications (dapsone, sulfasalazine), immunosuppressants (cyclosporin, sirolimus) or other medications like omalizumab can be used. These options are explained in more detail below.

Oral glucocorticoids are effective in controlling symptoms of chronic hives however they have an extensive list of adverse effects such as adrenal suppression, weight gain, osteoporosis, hyperglycemia, etc. Therefore, their use should be limited to a couple of weeks. In addition, one study found that systemic glucocorticoids combined with antihistamines did not hasten the time to symptom control compared with antihistamines alone.

There is no treatment that will rid the patient of symptoms of aquagenic urticaria. Most treatments are used to lessen the effects of the disease to promote more comfort when the body must come in contact with water.

- Oral antihistamine: Antihistamines such as hydrochloride, hydroxyzine, terfenadine and cyproheptadine have frequently been used to reverse or minimize the effects of aquagenic urticaria. The therapeutic response to these medications will vary from patient to patient and the benefits of applying a histamine antagonist to the skin has not been found to create a direct link to the minimization of water based urticaria effects.

- Topical corticosteroids: Parenteral corticosteroids have been used to help treat aquagenic uricaria in the past. The actual effect of this medication and its benefits are not clear at this time.

- Epinephrine: Patients with severe bouts of urticarial that appear to be acute will frequently use this medication to help decrease the appearance of cutaneous vasodilation. This can also help inhibit mast cell degranulation which may contribute to the presence of aquagenic urticaria.

- PUVA therapy: In one test a 21-year-old woman was given PUVA therapy four times a week in increased doses to help manage the symptoms of aquagenic urticaria. As the dosage was increased the lesions and itching caused by the disease disappeared.

- Ultraviolet radiation: Radiation is commonly used alongside antihistamines to help rid the patient of lesions and outbreaks caused by aquagenic urticaria. This therapy will cause thickening of the epidermis which can prevent water from penetrating this layer and interacting with the cells underneath. Ultraviolet therapy may also cause mast cells to limit their response to stimuli and immunosuppression which can help prevent these reactions.

- Stanazolol: Treatments for the human immunodeficiency virus or HIV have been found to help with the symptoms of aqugenic urticaria as well.

- Capsaicin: This medication is often used for producing Zostrix, a cream applied to lessen pain caused by aquagenic urticaria.

- Barrier methods: In some circumstances an oil in water solution or emulsion cream can be applied to the skin to protect it from water exposure while washing or performing aquatic activities. There does not appear to be a side effect to this method and the application is easier than many other options. Doctors will also recommend that these patients use physical barriers such as an umbrella or protective clothing to avoid contact with water to protect patients from potential outbreaks. Activities such as swimming or visiting a water park will also need to be avoided to minimize the risk of an outbreak.

Familial cold urticaria (also properly known as familial cold autoinflammatory syndrome, FCAS) is an autosomal dominant condition characterized by rash, conjunctivitis, fever/chills and arthralgias elicited by exposure to cold - sometimes temperatures below 22 °C (72 °F).

It has been mapped to CIAS1 and is a slightly milder member of the disease family including Muckle–Wells syndrome and NOMID. It is rare and is estimated as having a prevalence of 1 per million people and mainly affects Americans and Europeans.

FCAS is one of the cryopyrin-associated periodic syndromes (CAPS) caused by mutations in the CIAS1/NALP3 (aka NLRP3) gene at location 1q44. The disease was described in The Lancet Volume 364 by Hoffman H.M. et al.

The effect of FCAS on the quality of life of patients is far reaching. A survey of patients in the United States in 2008 found, "To cope with their underlying disease and to try to avoid symptomatic, painful, flares patients reported limiting their work, school, family, and social activities. Seventy-eight percent of survey participants described an impact of the disease on their work, including absenteeism and impaired job advancement; frequently, they quit their job as a consequence of their disease".

Treatment using anakinra (Kineret) has been shown effective for FCAS, although this does mean daily injections of the immunosuppressant into an area such as the lower abdomen. The monoclonal antibody canakinumab (Ilaris) is also used.

Histamines are proteins associated with many allergic reactions. When the UV radiation or light comes in contact with a person with solar urticaria, histamine is released from mast cells. When this occurs, the permeability of vessels near the area of histamine release is increased. This allows blood fluid to enter the vessels and cause inflammation. Antihistamines suppress the activity of the histamine.

Diphenhydramine, a first-generation H1 receptor antagonist or medicine that combats the H1 receptor that is associated with many allergic reactions, has been found to be the most potent antihistamine for this particular disease. Patients prescribed 50 milligrams four times per day have been able to sustain normal exposure to the sun without suffering a reaction.

Patients with less potent forms of solar urticaria such as fixed solar urticaria can be treated with the medication fexofenadine, which may also be used prophylactically to prevent recurrence.

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.

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.

Some patients and researchers have successfully treated solar urticaria with Omalizumab (trade name Xolair) which is commonly used to treat Idiopathic Urticaria. Omalizumab is a recombinant humanized monoclonal antibody against IgE. It acts by binding free IgE at the same site that IgE would bind to its high-affinity receptor (FcεRI) on mast cells, thereby reducing free IgE in the serum

There are no permanent cures for urticaria pigmentosa. However, treatments are possible. Most treatments for mastocytosis can be used to treat urticaria pigmentosa. Many common anti-allergy medications are useful because they reduce the mast cell's ability to react to histamine.

At least one clinical study suggested that nifedipine, a calcium channel blocker used to treat high blood pressure, may reduce mast cell degranulation in patients with urticaria pigmentosa. A 1984 study by Fairly et al. included a patient with symptomatic urticaria pigmentosa who responded to nifedipine at dose of 10 mg po tid. However, nifedipine has never been approved by the FDA for treatment of urticaria pigmentosa.

Another mast cell stabilizer Gastrocrom, a form of cromoglicic acid has also been used to reduce mast cell degranulation.

If the rash does not improve or continues to spread after 2–3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician. Medical treatment usually consists of lotions, creams, or oral medications.

- Corticosteroids. A corticosteroid medication similar to hydrocortisone may be prescribed to combat inflammation in a localized area. It may be applied to the skin as a cream or ointment. If the reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may be prescribed.

In severe cases, a stronger medicine like halobetasol may be prescribed by a dermatologist.

- Antihistamines. Prescription antihistamines may be given if non-prescription strengths are inadequate.

A rarely cited double-blind study in 1982 reported that a course of oral urushiol usually hyposensitized subjects.

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

A full recovery is expected with treatment. Recurrent id reactions are frequently due to inadequate treatment of the primary infection or dermatitis and often the cause of recurrence is unknown.

The clinical expression of the dermatitis can be mitigated by avoidance of the allergen. Through compliance with avoidance measures, the immune system can become less stimulated. The key to avoidance is proper evaluation and detection of the inciting allergen. However, once the immune system registers the allergen, the recognition is permanent.

The first step in treating the condition is appropriate recognition of the clinical problem, followed by identification of the culprit chemical and the source of that chemical. Corticosteroid creams should be used carefully and according to the prescribed directions because when overused over longer periods of time they can cause thinning of the skin. Also, in some instances such as poison ivy dermatitis calamine lotion and cool oatmeal baths may relieve itching.

Usually, severe cases are treated with systemic corticosteroids which may be tapered gradually, with various dosing schedules ranging from a total of 12 – 20 days to prevent the recurrence of the rash (while the chemical allergen is still in the skin, up to 3 weeks, as well as a topical corticosteroid. Tacrolimus ointment or pimecrolimus cream can also be used additionally to the corticosteroid creams or instead of these. Oral antihistamines such as diphenhydramine or hydroxyzine may also be used in more severe cases to relieve the intense itching. Topical antihistamines are not advised as there might be a second skin reaction (treatment associated contact dermatitis) from the lotion itself.

The other symptoms caused by allergic contact dermatitis may be eased with cool compresses to stop the itching. It is vital for treatment success that the trigger be identified and avoided. The discomfort caused by the symptoms may be relieved by wearing smooth-textured cotton clothing to avoid frictional skin irritation or by avoiding soaps with perfumes and dyes.

Commonly, the symptoms may resolve without treatment in 2 to 4 weeks but specific medication may hasten the healing as long as the trigger is avoided. Also, the condition might become chronic if the allergen is not detected and avoided.

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 consists of two phases: stopping the urushiol contact that is causing the reaction (this must be done within minutes) and, later, reducing the pain and/or itching.

Primary treatment involves washing exposed skin thoroughly with soap, water, and friction as soon as possible after exposure is discovered. Soap or detergent is necessary because urushiol is an oil; friction, with a washcloth or something similar, is necessary because urushiol adheres strongly to the skin. Commercial removal preparations, which are available in areas where poison ivy grows, usually contain surfactants, such as the nonionic detergent Triton X-100, to solubilize urushiol; some products also contain abrasives.

The U.S. Food and Drug Administration recommends applying a wet compress or soaking the affected area in cool water; topical corticosteroids (available over-the-counter) or oral corticosteroids (available by prescription); and topical skin protectants, such as zinc acetate, zinc carbonate, zinc oxide, and calamine. Baking soda or colloidal oatmeal can relieve minor irritation and itching. Aluminium acetate, sometimes known as Burow's solution, can also ease the rash.

Showers or compresses using hot (but not scalding) water can relieve itching for up to several hours, though this "also taxes the skin's integrity, opening pores and generally making it more vulnerable", and is only useful for secondary treatment (not for cleaning urushiol from the skin, which should be done with cold water). People who have had a prior systemic reaction may be able to prevent subsequent exposure from turning systemic by avoiding heat and excitation of the circulatory system and applying moderate cold to any infected skin with biting pain.

Antihistamine and hydrocortisone creams, or oral antihistamines in severe cases, can alleviate the symptoms of a developed rash. Nonprescription oral diphenhydramine (U.S. trade name Benadryl) is the most commonly suggested antihistamine. Topical formulations containing diphenhydramine are also available but may further irritate the skin.

In cases of extreme symptoms, steroids such as prednisone or triamcinolone are sometimes administered to attenuate the immune response and prevent long-term skin damage, especially if the eyes are involved. Prednisone is the most commonly prescribed systemic treatment but can cause serious adrenal suppression, so it must be taken carefully and tapered off slowly. If bacterial secondary infection of affected areas occurs, antibiotics may also be necessary.

Scrubbing with plain soap and cold water will remove urushiol from skin if it is done within a few minutes of exposure. Many home remedies and commercial products (e.g., Tecnu, Zanfel) also claim to prevent urushiol rashes after exposure. A study that compared Tecnu ($1.25/oz.) with Goop Hand Cleaner or Dial Ultra Dishwashing Soap ($0.07/oz.) found that differences among the three—in the range of 56–70% improvement over no treatment—were nonsignificant ("P" > 0.05), but that improvement over no treatment was significant at the same level of confidence.

Further observations:

- Ordinary laundering with laundry detergent will remove urushiol from most clothing but not from leather or suede.

- The fluid from the resulting blisters does "not" spread urushiol to others.

- Blisters should be left unbroken during healing.

- Poison ivy and poison oak are still harmful when the leaves have fallen off, as the toxic residue is persistent, and exposure to any parts of plants containing urushiol can cause a rash at any time of the year.

- Ice, cold water, cooling lotions, and cold air do "not" help cure poison ivy rashes, but cooling can reduce inflammation and soothe the itch.

- Results for jewelweed as a natural agent for treatment are conflicting. Some studies indicate that it "failed to decrease symptoms of poison ivy dermatitis" [1980] and had "no prophylactic effect" [1997]. The juice of the leaves and stems of Impatiens capensis is a traditional Native American remedy for skin rashes, including poison ivy and such use has been supported by at least one peer-reviewed study, as recently as 2012.

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.

Several factors can worsen the symptoms of urticaria pigmentosa:

- Emotional stress

- Physical stimuli such as heat, friction, and excessive exercise

- Bacterial toxins

- Venom

- Eye drops containing dextran

- NSAIDs

- Alcohol

- Morphine

The classification of NSAIDs can be disputed. Aspirin, for example, causes the mast cells to degranulate, releasing histamines and causing symptoms to flare. However, "daily" intake of 81 mg aspirin may keep the mast cells degranulated. Thus, while symptoms may be worsened at first, they can get better as the mast cells are unable to recharge with histamine.

In allergic angioedema, avoidance of the allergen and use of antihistamines may prevent future attacks. Cetirizine is a commonly prescribed antihistamine for angioedema. Some patients have reported success with the combination of a nightly low dose of cetirizine to moderate the frequency and severity of attacks, followed by a much higher dose when an attack does appear. Severe angioedema cases may require desensitization to the putative allergen, as mortality can occur. Chronic cases require steroid therapy, which generally leads to a good response. In cases where allergic attack is progressing towards airway obstruction, epinephrine may be life-saving.

It was noted that although antihistamines and anti-inflammatory drugs such as, colchicine, sulphasalazine, dapsone, and topical steroid are advocated for in the treatment of DPU, most if not all are unsatisfactory in relieving symptoms. Even a second generation antihistamine, ketotifen, was unable to efficiently and satisfactorily relieve symptoms of DPU

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.