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.

Non-sedating antihistamines that block the histamine H1 receptors are the first line of therapy. First generation antihistamines such as diphenhydramine or hydroxyzine block both central and peripheral H1 receptors and can be sedating. Second generation antihistamines such as loratadine, cetirizine, or desloratadine selectively antagonize the peripheral H1 receptors and are less sedating, less anticholinergic, and generally preferred over the first generation antihistamines.

People who don’t respond to the maximum dose of H1 antihistamines may benefit from increasing the dose, then to switching to another non-sedating antihistamine, then to adding a leukotriene antagonist, then to using an older antihistamine, then to using systemic steroids and finally to using ciclosporin or omalizumab.

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.

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

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.

Doctors will sometimes prescribe immunosuppressive drugs such as prednisolone and ciclosporin if the patient is suffering from an intense form of solar urticaria. However, the side effects of these medicines can be severe which is why they are reserved for the most extreme of cases.

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.

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.

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.

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.

Id reactions are frequently unresponsive to corticosteroid therapy, but clear when the focus of infection or infestation is treated. Therefore, the best treatment is to treat the provoking trigger. Sometimes medications are used to relieve symptoms.These include topical corticosteroids, and antihistamines. If opportunistic bacterial infection occurs, antibiotics may be required.

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.

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.

In hereditary angioedema, specific stimuli that have previously led to attacks may need to be avoided in the future. It does not respond to antihistamines, corticosteroids, or epinephrine. Acute treatment consists of C1-INH (C1-esterase inhibitor) concentrate from donor blood, which must be administered intravenously. In an emergency, fresh frozen blood plasma, which also contains C1-INH, can also be used. However, in most European countries, C1-INH concentrate is only available to patients who are participating in special programmes. The medications ecallantide and icatibant may be used to treat attacks. In 2017 these medications cost between 5,700 and 14,000 per dose in the United States, prices that tripled in two years.

Future attacks of hereditary angioedema can be prevented by the use of androgens such as danazol, oxandrolone or methyltestosterone. These agents increase the level of aminopeptidase P, an enzyme that inactivates kinins; kinins (especially bradykinin) are responsible for the manifestations of angioedema.

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.

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.

Since the cause of the condition cannot be fully avoided in all cases, treatment is usually focused on topical itch management. This can be effected by the application of antipruritic lotions or creams, using phototherapy, or the application of hot or cold packs to the skin after water contact. Paradoxically, hot baths or showers help many patients, possibly because heat causes mast cells in the skin to release their supply of histamine and to remain depleted for up to 24 hours afterward. However, the itching associated with aquagenic pruritus is not clearly caused by histamine; other neurotransmitters, such as substance P, may be involved.

H1 and H2 blockers, such as loratadine, doxepin, or cimetidine, have historically been the first line of pharmacological treatment, but not all sufferers find relief with these medications. When antihistamines do work, loratadine seems to be the most effective for mild cases and doxepin most effective for more severe cases.

Naltrexone, hydrocortisone, or propranolol may relieve itching for some people.

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.

There is currently no cure for mastocytosis, but there are a number of medicines to help treat the symptoms:

- Antihistamines block receptors targeted by histamine released from mast cells. Both H and H blockers may be helpful.

- Leukotriene antagonists block receptors targeted by leukotrienes released from mast cells.

- Mast cell stabilizers help prevent mast cells from releasing their chemical contents. Cromoglicic acid is the only medicine specifically approved by the FDA for the treatment of mastocytosis. Ketotifen is available in Canada and Europe, but is only available in the U.S. as eyedrops (Zaditor).

- Proton pump inhibitors help reduce production of gastric acid, which is often increased in patients with mastocytosis. Excess gastric acid can harm the stomach, esophagus, and small intestine.

- Epinephrine constricts blood vessels and opens airways to maintain adequate circulation and ventilation when excessive mast cell degranulation has caused anaphylaxis.

- Salbutamol and other beta-2 agonists open airways that can constrict in the presence of histamine.

- Corticosteroids can be used topically, inhaled, or systemically to reduce inflammation associated with mastocytosis.

Antidepressants are an important and often overlooked tool in the treatment of mastocytosis. Depression and other neurological symptoms have been noted in mastocytosis. Some antidepressants, such as doxepin, are themselves potent antihistamines and can help relieve physical as well as cognitive symptoms.

Calcium channel blockers of the dihydropyridine type are sometimes used to treat high blood pressure. At least one clinical study suggested nifedipine, one of the dihydropyridines, may reduce mast cell degranulation in patients who exhibit "urticaria pigmentosa". A 1984 study by Fairly et al. included a patient with symptomatic "urticaria pigmentosa" who responded to nifedipine. However, nifedipine has not been approved by the FDA for treatment of mastocytosis.

In rare cases in which mastocytosis is cancerous or associated with a blood disorder, the patient may have to use steroids and/or chemotherapy. The agent imatinib (Glivec or Gleevec) has been found to be effective in certain types of mastocytosis.

The laboratory AB Science filed a new drug application for its molecule masitinib at the EMA, as its clinical trials are progressing. In spite of the refusal of the EMA, AB Science decided to restart its clinical trial.

There are clinical trials currently underway testing stem cell transplants as a form of treatment.

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

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.

Generous application of bland emollients can improve the rash. However, complete resolution will not occur until the lip licking stops. Breaking the cycle of dryness then licking followed by more dryness is key to treatment. Sometimes, unlike in perioral dermatitis, topical steroids may be used for few days only.

Antihistamines are not effective in treating the hives in this condition. It may respond to immunosuppressant drugs such as corticosteroids, cyclooxygenase inhibitors, interferon alpha, interleukin 1 receptor antagonists (Anakinra), perfloxacin, colchicine, cyclosporine or thalidomide. The hives may respond to treatment with PUVA, and the bone pain may respond to bisphosphonates.

Because Schnitzler's syndrome is so rare, the efficacy of different treatments cannot be compared using statistics. Nevertheless, case studies provide evidence that anakinra (otherwise known as kineret) is much more effective for Schnitzler's syndrome than any other drug, and that the improvement in symptoms associated with this treatment is dramatic. For example, Beseda and Nossent (2010) reviewed the literature concerning IL1-RA treatment (i.e. anakinra) for Schnitzler's syndrome. They concluded that, “Twenty-four patients with Schnitzler's syndrome... have been successfully treated with anakinra.” They add that “seven out of seven patients [with Schnitzler’s syndrome], that either interrupted or used anakinra every other day, had relapse of their symptoms within 24-48 h; anakinra was restarted in all patients with the same clinical efficiency.” Kluger et al. (2008) investigated the effectiveness of anakinra for a range of conditions. They searched MEDLINE for English-language trials of anakinra and abstracts from rheumatologial scientific meetings. They conclude that, “Over the last few years it has become increasingly evident that anakinra is highly effective and safe in patients with ... Schnitzler’s syndrome”. The year before, De Koning et al. (2007) reviewed the disease characteristics of Schnitzler syndrome and collected follow-up information to gain insight into long-term prognosis and treatment efficacy. They used data from 94 patients, and their conclusions about treatment for the condition are that, “There have been promising developments in therapeutic options, especially antiinterleukin-1 treatment, which induced complete remission in all 8 patients treated so far.”

Reports of individual patients treated with anakinra illustrate its effectiveness. Beseda and Nossent (ibid.) report treating a longstanding multidrug resistant Schnitzler’s syndrome patient with anakinra: “Within 24 h after the first injection, both the urticaria and the fever disappeared and have not recurred. For the past 6 months, the patient has been in clinical and biochemical remission.” Other authors report “a complete resolution of symptoms” (Dybowski et al., 2008). Crouch et al. (2007) report the effective treatment of a 52-year-old man who had been diagnosed with Schnitzler’s syndrome 8 years earlier: “On review, one week later, the patient’s systemic symptoms had resolved, and his previously elevated white cell count and inflammatory markers had normalised. The use of anakinra in our patient resulted in resolution of symptoms and has enabled cessation of oral prednisolone. Our patient remains symptom free on anakinra after 14 months of follow-up”. Similar stories are reported by Frischmeyer-Guerrerio et al. (2008), Wastiaux et al. (2007), and Eiling et al. (2007), Schneider et al. (2007). De Koning et al. (2006) treated three patients with Schnitzler’s syndrome with thalidomide and anakinra. Thalidomide was only effective for one of the three patients and was discontinued because of polyneuropathy. In contrast, for all three patients, anakinra “led to disappearance of fever and skin lesions within 24 hours. After a follow-up of 16-18 months, all patients are free of symptoms”. The authors concluded that anakinra as a treatment for Schnitzler’s syndrome “is preferable to thalidomide... as it has fewer side effects”.

As well as being more effective, anakinra is safer than the other treatments available for Schnitzler's syndrome. The Cochrane review entitled, ‘Anakinra for rheumatoid arthritis’ (Mertens and Singh, 2009 ) evaluates the (clinical effectiveness and) safety of anakinra in adult patients with rheumatoid arthritis, using data from 2876 patients, from five trials which constituted 781 randomized to placebo and 2065 to anakinra. The authors conclude, “There were no statistically significant differences noted in most safety outcomes with treatment with anakinra versus placebo - including number of withdrawals, deaths, adverse events (total and serious), and infections (total and serious). Injection site reactions were significantly increased, occurring in 1235/1729 (71%) versus 204/729 (28%) of patients treated with anakinra versus placebo, respectively”. These injection site reactions last for no more than four months, and are trivial compared to the very debilitating symptoms of Schnitzler's syndrome.

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