Corticosteroids: For years, there was no treatment for atopic eczema. Atopy was believed to be allergic in origin due to the patients’ extremely high serum IgE levels, but standard therapies at the time did not help. Oral prednisone was sometimes prescribed for severe cases. Wet wraps (covering the patients with gauze) were sometimes used in hospitals to control itching. However, the discovery of corticosteroids in the 1950s, and their subsequent incorporation in topical creams and ointments, provided a significant advancement in the treatment of atopic eczema and other conditions. Thus, the use of topical steroids avoided many of the undesirable side-effects of systemic administration of corticosteroids. Topical steroids control the itching and the rash that accompany atopic eczema. Side-effects of topical steroid use are plentiful, and the patient is advised to use topical steroids in moderation and only as needed.

Immune modulators: Pimecrolimus and tacrolimus creams and ointments became available in the 1980s and are sometimes prescribed for atopic eczema. They act by interfering with T cells but have been linked to the development of cancer.

Avoiding dry skin: Dry skin is a common feature of patients with atopic eczema (see also eczema for information) and can exacerbate atopic eczema.

Avoiding allergens and irritants: See eczema for information.

Limited evidence suggests that acupuncture may reduce itching in those affected by atopic dermatitis. There is currently no scientific evidence for the claim that sulfur treatment relieves eczema.

It is unclear whether Chinese herbs help or harm. Dietary supplements are commonly used by people with eczema. Neither evening primrose oil nor borage seed oil taken orally have been shown to be effective. Both are associated with gastrointestinal upset. Probiotics do not appear to be effective. There is insufficient evidence to support the use of zinc, selenium, vitamin D, vitamin E, pyridoxine (vitamin B6), sea buckthorn oil, hempseed oil, sunflower oil, or fish oil as dietary supplements.

Chiropractic spinal manipulation lacks evidence to support its use for dermatitis. There is little evidence supporting the use of psychological treatments. While dilute bleach baths have been used for infected dermatitis there is little evidence for this practice.

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.

Oatmeal contains avenanthramide (anthranilic acid amides), which can have an anti-inflammatory effect.

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.

Several medications may be used to block the action of allergic mediators, or to prevent activation of cells and degranulation processes. These include antihistamines, glucocorticoids, epinephrine (adrenaline), mast cell stabilizers, and antileukotriene agents are common treatments of allergic diseases. Anti-cholinergics, decongestants, and other compounds thought to impair eosinophil chemotaxis, are also commonly used. Though rare, the severity of anaphylaxis often requires epinephrine injection, and where medical care is unavailable, a device known as an epinephrine autoinjector may be used.

Allergen immunotherapy is useful for environmental allergies, allergies to insect bites, and asthma. Its benefit for food allergies is unclear and thus not recommended. Immunotherapy involves exposing people to larger and larger amounts of allergen in an effort to change the immune system's response.

Meta-analyses have found that injections of allergens under the skin is effective in the treatment in allergic rhinitis in children and in asthma. The benefits may last for years after treatment is stopped. It is generally safe and effective for allergic rhinitis and conjunctivitis, allergic forms of asthma, and stinging insects.

The evidence also supports the use of sublingual immunotherapy for rhinitis and asthma but it is less strong. For seasonal allergies the benefit is small. In this form the allergen is given under the tongue and people often prefer it to injections. Immunotherapy is not recommended as a stand-alone treatment for asthma.

Topical corticosteroids, such as hydrocortisone have proven themselves effective in managing AD. If topical corticosteroids and moisturisers fail, short-term treatment with topical calcineurin inhibitors like tacrolimus or pimecrolimus may be tried, although they are usually avoided as they can increase the risk of developing skin cancer or lymphoma. Alternatively systemic immunosuppressants may be tried such as ciclosporin, methotrexate, interferon gamma-1b, mycophenolate mofetil and azathioprine. Antidepressants and naltrexone may be used to control pruritus (itchiness). In 2016 crisaborole was approved as a topical treatment for mild-to-moderate eczema. In 2017, the biologic agent dupilumab was approved to treat moderate-to-severe eczema.

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.

Other options for refractory symptoms of chronic hives include anti-inflammatory medications, omalizumab, and immunosuppressants.

Potential anti-inflammatory agents include dapsone, sulfasalazine, and hydroxychloroquine. Dapsone is a sulfone antimicrobial agent and is thought to suppress prostaglandin and leukotriene activity. It is helpful in therapy-refractory cases and is contraindicated in patients with G6PD deficiency. Sulfasalazine, a 5-ASA derivative, is thought to alter adenosine release and inhibit IgE mediated mast cell degranulation, Sulfasalazine is a good option for people with anemia who cannot take dapsone. Hydroxychloroquine is an antimalarial agent that suppresses T lymphocytes. It has a low cost however it takes longer than dapsone or sulfasalazine to work.

Omalizumab was approved by the FDA in 2014 for patients 12 years old and above with chronic hives. It is a monoclonal antibody directed against IgE. Significant improvement in pruritus and quality of life was observed in a phase III, multicenter, randomized control trial.

Immunosuppressants used for CU include cyclosporine, tacrolimus, sirolimus, and mycophenolate. Calcineurin inhibitors, such as cyclosporine and tacrolimus, inhibit cell responsiveness to mast cell products and inhibit T cell activity. They are preferred by some experts to treat severe symptoms. Sirolimus and mycophenolate have less evidence for their use in the treatment of chronic hives but reports have shown them to be efficacious. Immunosuppressants are generally reserved as the last line of therapy for severe cases due to their potential for serious adverse effects.

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.

A more novel form of treatment involves exposure to broad or narrow-band ultraviolet (UV) light. UV radiation exposure has been found to have a localized immunomodulatory effect on affected tissues and may be used to decrease the severity and frequency of flares. In particular, the usage of UVA1 is more effective in treating acute flares, whereas narrow-band UVB is more effective in long-term management scenarios. However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.

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.

External treatment should be oriented primarily according to the prevailing signs of illness. In the case of blister forming, drying treatments such as hand baths containing synthetic tannins or oily-moist preparations may hinder itching. If callus development exhibiting tear formation is present, the focus should be on softening the skin with preparations containing urea or salicylic acid. In order to reduce inflammation, creams and salves containing cortisone are often very effective. However, severe and chronic cases seldom respond sufficiently and require long periods of treatment which can increase the risk of side effects occurring. In individual cases, and especially in case of atopic hand eczema, the dermatologist may prefer to use cortisone-free, anti-inflammatory creams or salves, which include so-called "calcineurin inhibitors" tacrolimus or pimecrolimus.

Besides skin care, skin protection, and an external treatment, severe and chronic cases of hand eczema often also require systemic treatment. Various preparations are available for this. For acute, severe episodes exhibiting blister formation, internal cortisone preparations, sometimes in combination with certain antibiotics, may be helpful in the short term. The active agent ciclosporin, which is approved for treatment of severely pronounced neurodermitis, may also be used for severe, atopic hand eczema. Other substances that suppress the immune system have also shown effectiveness in some cases. However, these substances are not approved for hand eczema.

In the last couple of years an internal medicine has been approved for the first time for the treatment of chronic hand eczema. This involves a derivative of vitamin A, called alitretinoin, which is also naturally present in the human body. Alitretinoin can be used to treat all forms of severe chronic hand eczema which have not reacted to external cortisone preparations. The effectiveness of this form of treatment has been tested extensively in clinical study programs and proven prior to its approval. The trial results showed that two thirds of patients did not suffer a recurrence 6 months after application of the medication, and that re-treatment is effective if hand eczema reoccurs. The duration of alitretinoin treatment is 3 to 6 months. During treatment and one month prior to beginning and one month after completion, women of childbearing-age must use contraceptives and also test for pregnancy each month since, as with all derivatives of vitamin A, the substance involved is teratogenic. Side effects mainly include temporary headaches during the initial days of treatment, as well as a possible increase in blood fat and cholesterol values. Regular laboratory tests of blood values are recommended to monitor this.

Once a nickel allergy is detected, the best treatment is avoidance of nickel-releasing items. It is important to know the main items that can cause nickel allergy, which may be remembered using the mnemonic "BE NICKEL AWARE". The top 13 categories that contain nickel include beauty accessories, eyeglasses, money, cigarettes, clothes, kitchen and household, electronics and office equipment, metal utensils, aliment, jewelry, batteries, orthodontic and dental appliances, and medical equipment. Other than strict avoidance of items that release free nickel, there are other treatment options for reduction of exposure. The first step is to limit friction between skin and metallic items. Susceptible people may try to limit sweating while wearing nickel items, to reduce nickel release and thus decrease chances for developing sensitization and/or allergy. Another option is to shield electronics, metal devices, and tools with fabric, plastic, or acrylic coverings. Dermatological application tests has shown that barrier creams effectively prevent the symptoms of nickel allergy, such as the Nidiesque™.

There are test kits that can be very helpful to check for nickel release from items prior to purchasing. The ACDS providers can give a guidance list of safe items. In addition to avoidance, healthcare providers may prescribe additional creams or medications to help relieve the skin reaction.

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

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.

Treatment for accidental ingestion of milk products by allergic individuals varies depending on the sensitivity of the person. An antihistamine such as diphenhydramine (Benadryl) may be prescribed. Sometimes prednisone will be prescribed to prevent a possible late phase Type I hypersensitivity reaction. Severe allergic reactions (anaphalaxis) may require treatment with an epinephrine pen, i.e., an injection device designed to be used by a non-healthcare professional when emergency treatment is warranted. A second dose is needed in 16-35% of episodes.

There is active research on trying oral immunotherapy (OIT) to desensitize people to egg allergens. A Cochrane Review concluded that OIT can desensitize people, but it remains unclear whether long-term tolerance develops after treatment ceases, and 69% of the people enrolled in the trials had adverse effects. They concluded there was a need for standardized protocols and guidelines prior to incorporating OIT into clinical practice. A second review noted that allergic reactions, up to anaphylaxis, can occur during OIT, and recommends this treatment not be routine medical practice. A third review limited its scope to trials of baked egg-containing goods such as bread or cake as a means of resolving egg allergy. Again, there were some successes, but also some severe allergic reactions, and the authors came down on the side of not recommending this as treatment.

The need for a dairy-free diet should be reevaluated every six months by testing milk-containing products low on the "milk ladder", such as fully cooked, i.e., baked foods containing milk, in which the milk proteins have been denatured, and ending with fresh cheese and milk. Desensitization via oral immunotherapy holds some promise but is still being actively researched (see Research).

Treatment for accidental ingestion of milk products by allergic individuals varies depending on the sensitivity of the person. An antihistamine such as diphenhydramine (Benadryl) may be prescribed. Sometimes prednisone will be prescribed to prevent a possible late phase Type I hypersensitivity reaction. Severe allergic reactions (anaphalaxis) may require treatment with an epinephrine pen, i.e., an injection device designed to be used by a non-healthcare professional when emergency treatment is warranted. A second dose is needed in 16-35% of episodes.

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.

A number of medications speed up recovery including: tetracycline, doxycycline, and erythromycin. Erythromycin may be used as a cream. Doxycycline is most often the first antibiotic drug choice, given at a daily dosage of 100 mg for upto a month before considering tapering off or stopping. Sometimes, longer duration of low doses of doxycycline are required.

Metronidazole is less effective, is available in a gel and can be applied twice daily. If the perioral dermatitis was triggered by a topical steroid then pimecrolimus cream has been suggested as effective in improving symptoms. However, this has also been documented to cause the condition.

Multiple treatment regimes are available and treatment algorithms have been proposed.

Perioral dermatitis will usually resolve within a few months without medication and by limiting the use of cosmetics. This is called zero treatment. Topical corticosteroids should be stopped entirely if possible. If the flare proves intolerable, temporary use of a less potent topical corticosteroid can often be helpful.

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.