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.

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.

Afamelanotide is being studied as a hives treatment.

Opioid antagonists such as naltrexone have tentative evidence to support their use.

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

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.

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.

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.

Treatments include class I topical steroids (clobetasol, halobetasol, etc.) which in some studies have proven to be equally effective as systemic, or pill, therapy and somewhat safer. However, in difficult-to-manage or widespread cases, systemic prednisone and powerful steroid-free immunosuppressant medications, such as methotrexate, azathioprine or mycophenolate mofetil, may be appropriate. Antibiotics such as tetracycline or erythromycin may also control the disease, particularly in patients who cannot use corticosteroids. The anti-CD20 monoclonal antibody rituximab has been found to be effective in treating some otherwise refractory cases of bullous pemphigoid.

IgA-mediated pemphigoid can often be difficult to treat even with usually effective medications such as rituximab.

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.

The culprit can be both a prescription drug or an over-the-counter medication.

Examples of common drugs causing drug eruptions are antibiotics and other antimicrobial drugs, sulfa drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), biopharmaceuticals, chemotherapy agents, anticonvulsants, and psychotropic drugs. Common examples include photodermatitis due to local NSAIDs (such as piroxicam) or due to antibiotics (such as minocycline), fixed drug eruption due to acetaminophen or NSAIDs (Ibuprofen), and the rash following ampicillin in cases of mononucleosis.

Certain drugs are less likely to cause drug eruptions (rates estimated to be ≤3 per 1000 patients exposed). These include: digoxin, aluminum hydroxide, multivitamins, acetaminophen, bisacodyl, aspirin, thiamine, prednisone, atropine, codeine, hydrochlorothiazide, morphine, insulin, warfarin, and spironolactone.

The most accepted way to treat PG is with the use of corticosteroids, i.e. prednisone; and/or topical steroids, i.e. clobetasol and betamethasone. Suppressing the immune system with corticosteroids helps by decreasing the number of antibodies attacking the skin. Treating PG can be difficult and can take several months. Some cases of PG persist for many years. In the" post partum" period, if necessary, the full range of immunosuppressive treatment may be administered for cases unresponsive to corticosteroid treatments, such as tetracyclines, nicotinamide, cyclophosphamide, ciclosporin, goserelin, azathioprine, dapsone, rituximumab, or plasmaphoresis, or intravenous immunoglobulin may sometimes be considered when the symptoms are severe.

There is no cure for PG. Women who have PG are considered in remission if they are no longer blistering. Remission can last indefinitely, or until a subsequent pregnancy. PG usually occurs in subsequent pregnancies; however, it often seems more manageable because it is anticipated.

There is no effective treatment for this condition. It has been reported that clearance of lesions can be done with melphalan and cyclophosphamide alone or in combination with prednisone. Both isotretinoin and etretinate have also been shown to improve the conditions. All medications listed can cause adverse symptoms, with isotretinoin and etretinate particularly dangerous since they are both teratogens. Other attempted treatments include interferon-alpha, cyclosporine, PUVA photochemotherapy, electron-beam therapy, IVIg, and dermabrasion. However, the overall prognosis for the disease is poor. There are reported instances of remission of the disease when treated with a combination of Revlimid and Dexamethasone over a 24-month period.

Treatment may include corticoids, astringents, and keratolytics. Dermatoses tend to be recurrent unless the use or contact can be avoided. Discontinuation of the instrument is curative in almost all cases, but usually impractical.

Sweating causes lesions to form, but lesions aggravated by sweat usually return to "normal" fairly quicklyavoiding sweat is not a reason to avoid exercise. Minor outbreaks can be controlled with prescription strength topical cortisone creams. More severe eruptions usually clear up after treatment for one to three months with Accutane or tetracycline. If these fail or the outbreak is severe, PUVA phototherapy treatments, antifungal pills and cortisone injections are alternatives.

Some research has suggested a correlation of Grover's disease with mercury toxicity in which case Dimercaptosuccinic acid might help.

The treatment of Majocchi's disease can be difficult because the condition can slowly progress and is chronic in nature. After a period of time, the lesions can reoccur. Even though the condition has improved, there is always the possibility of reoccurrence. There are treatments available to help improve the symptoms, however, there is no absolute cure for the disease. Some of these treatments include the application of topical steroids and lotions and ultraviolet therapy. The use of narrowband UVB and psoralen plus UVA have shown to be effective treatments for some patients with pigmented purpuric dermatoses. Majocchi granuloma also commonly occurs as a result of the use of potent topical steroids on unsuspected tinea. Historically, antifungal therapy has been successful in controlling MG in most instances. Therapies that have been used, included oral potassium iodide, mildly filtered local X-radiation, and topical applications of Asterol as a fungicide in both tincture and ointment forms. In modern medicine, systemic antifungals, such as griseofulvin, ketoconazole, and itraconazole, are the pillars of therapy, as they are safe and effective. The duration of therapy should be at least 4–8 weeks, and treatment should be continued until all lesions are cleared. Currently, no data about relapse rates or the complications of not treating Majocchi granuloma exist.

Soothing mild cases during pregnancy consists mainly of the application of topical moisturising creams or aqueous/emollient ointments. Class I or II corticosteroid creams and ointments are used in more aggressive cases, and oral (systemic) corticosteroids can be used to treat very severe cases—although the benefits of a pregnant woman's ingesting high-potency corticosteroids must be weighed carefully against possible (and mostly unknown) risks to the developing fetus or fetuses. Rarely, in unusually persistent and distressing cases, some women have had their labor induced as soon as they are considered to be at term (37 weeks).

Antihistamine tablets may be prescribed to provide relief from the itch, although they are generally considered much less effective than corticosteroid treatments, and may act as little more than a sleep aid.

Pine tar soap/body wash can bring relief as can keeping the skin chilled such as through a cold shower or iced cloths.

In the majority of cases, PUPPP resolves spontaneously within a week of delivery. However, a few women continue to experience symptoms long into the postpartum period.

Bullous pemphigoid may be self-resolving in a period ranging from several months to many years even without treatment. Poor general health related to old age is associated with a poorer prognosis.

Imiquimod is a topical immune-enhancing agent licensed for the treatment of genital warts. Imiquimod stimulates the immune system through the release and up-regulation of cytokines. Treatment with Imiquimod cream applied 2–3 times per week for 12 to 16 weeks was found to result in complete resolution of AKs in 50% of people, compared to 5% of controls. The Imiquimod 3.75% cream has been validated in a treatment regimen consisting of daily application to entire face and scalp for two 2-week treatment cycles, with a complete clearance rate of 36%. While the clearance rate observed with the Imiquimod 3.75% cream was lower than that observed with the 5% cream (36 and 50 percent, respectively), there are lower reported rates of adverse reactions with the 3.75% cream: 19% of individuals using Imiquimod 3.75% cream reported adverse reactions including local erythema, scabbing, and flaking at the application site, while nearly a third of individuals using the 5% cream reported the same types of reactions with Imiquimod treatment. However, it is ultimately difficult to compare the efficacy of the different strength creams directly, as current study data varies in methodology (e.g. duration and frequency of treatment, and amount of skin surface area covered).

Topical diclofenac sodium gel is a nonsteroidal anti-inflammatory drug that is thought to work in the treatment of AK through its inhibition of the arachidonic acid pathway, thereby limiting the production of prostaglandins which are thought to be involved in the development of UVB-induced skin cancers. Recommended duration of therapy is 60 to 90 days with twice daily application. Treatment of facial AK with diclofenac gel led to complete lesion resolution in 40% of cases. Common side effects include dryness, itching, redness, and rash at the site of application.

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

The underlying mechanism can be immunological (such as in drug allergies) or non-immunological (for example, in photodermatitis or as a side effect of anticoagulants). A fixed drug eruption is the term for a drug eruption that occurs in the same skin area every time the person is exposed to the drug. Eruptions can occur frequently with a certain drug (for example, with phenytoin), or be very rare (for example, Sweet's syndrome following the administration of colony-stimulating factors).

The exact cause of Majocchi's granuloma is not well established however a dysfunctinoal immune system may be a causative factor. The first form of MG, the superficial perifollicular form occurs predominately on the legs of otherwise healthy young women who repeatedly shave their legs and develop hair follicle occlusions that directly or indirectly disrupt the follicle and allow for passive introduction of the organism into the dermis. Hence, the physical barrier of the skin is important because it prevents the penetration of microorganisms. Physical factors that play a major role in inhibiting dermal invasion include the interaction among keratin production, the rate of epidermal turnover, the degree of hydration and lipid composition of the stratum corneum, CO levels, and the presence or absence of hair. Keratin and/or necrotic material can also be introduced into the dermis with an infectious organism to further enhance the problem. In immunocompromised individuals, the use of topical corticosteroids may lead to a dermatophyte infection due to local immunosuppression.

Urticarial allergic eruption is a cutaneous condition characterized by annular or gyrate urticarial plaques that persist for greater than 24 hours.

Autoimmune estrogen dermatitis presents as a cyclic skin disorder, that may appear eczematous, papular, bullous, or urticarial. with pruritus typically present, skin eruptions that may be chronic but which are exacerbated premenstrually or occur immediately following menses.

Cutaneous disorders in musicians include frictional injury ("fiddler's neck"), hyperhidrosis, acne mechanica and vascular compromise. Other agents of irritant and allergic contact dermatitis may be rosewood, Makassar ebony, cocobolo wood, African blackwood, nickel, reed, propolis (bee glue), chromium and paraphenylenediamine. Patch testing can be performed for identification of the cause.