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.

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.

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

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.

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 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.

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.

This form of treatment is meant to reduce the intensity or altogether eliminate the allergic reactions people have by gradually increasing exposure to the form of radiation that brings about the reaction. In the case of solar urticaria, phototherapy and photochemotherapy are the two major desensitization treatments.

Phototherapy can be used for prevention. Exposure to a certain form of light or UV radiation enables the patient to build up a tolerance and outbreaks can be reduced. This type of treatment is generally conducted in the spring. However, the benefits of this therapy only last for two to three days.

Photochemotherapy, or PUVA, is considered superior to phototherapy because it produces a longer-lasting tolerance of the radiation that initiates the outbreak. When treatment first begins, the main goal is to build up the patient's tolerance to UVA radiation enough so that they can be outdoors without suffering an episode of solar urticaria. Therefore, treatments are regulated at three per week while constantly increasing the exposure to UVA radiation. Once the patient has reached an adequate level of desensitization, treatments are reduced to once or twice per week.

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.

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.

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.

Urticaria pigmentosa is a rare disease, affecting fewer than 200,000 people in the United States.

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

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.

Due to the delayed appearance of wheals, plausible causes are hard to establish; the natural course and/or clinical pattern is variable and inconclusive.

National Institute of Allergy and Infectious Diseases scientists have been studying and treating patients with mastocytosis for several years at the National Institutes of Health (NIH) Clinical Center.

Some of the most important research advances for this rare disorder include improved diagnosis of mast cell disease and identification of growth factors and genetic mechanisms responsible for increased mast cell production. Researchers are currently evaluating approaches to improve ways to treat mastocytosis.

Scientists also are focusing on identifying disease-associated mutations (changes in genes). NIH scientists have identified some mutations, which may help researchers understand the causes of mastocytosis, improve diagnosis, and develop better treatments.

Clinical development of several new active substances, which intervene in the disease process in different ways, is currently ongoing.

Pharming Group NV announced on 24 June 2010 that the European Medicines Agency has adopted a positive opinion on conestat alfa (trade name Ruconest), a C1-inhibitor for the treatment of acute angioedema attacks.

Ecallantide, a peptide inhibitor of kallikrein, has received orphan status for HAE and has shown positive results in phase III trials.

Icatibant (marketed as Firazyr) is a selective bradykinin receptor antagonist, which has been approved in Europe and was approved in the USA by the FDA in Aug 2011. After initial borderline results this drug was shown to be effective in phase III trials. Cinryze has been approved by the FDA in October 2008.

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.

Most patients with hyper IgE syndrome are treated with long-term antibiotic therapy to prevent staphylococcal infections. Good skin care is also important in patients with hyper IgE syndrome. High-dose intravenous gamma-globulin has also been suggested for the treatment of severe eczema in patients with HIES and atopic dermatitis.

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.

Acne treatment may require oral tetracycline antibiotics or isotretinoin. Treatments directed at tumor necrosis factor (TNF) (infliximab, etanercept) and interleukin-1 (anakinra) have shown a good response in resistant arthritis and pyoderma gangrenosum. Other traditional immunosuppressant treatments for arthritis or pyoderma gangrenosum may also be used.

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).

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.

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.

Since interleukin 1β plays a central role in the pathogenesis of the disease, therapy typically targets this cytokine in the form of monoclonal antibodies (such as canakinumab), binding proteins/traps (such as rilonacept), or interleukin 1 receptor antagonists (such as anakinra). These therapies are generally effective in alleviating symptoms and substantially reducing levels of inflammatory indices. Case reports suggest that thalidomide and the anti-IL-6 receptor antibody tocilizumab may also be effective.