Treatments vary widely, and many different drugs have been documented as being successful. Some medications are successful in some patients, while unsuccessful in others. Below is a list of some medications used to treat GPP:

- Enbrel (Etanercept)

- Methotrexate

- PUVA

- Hydroxyurea

- Dapsone

- Systemic corticosteroids

- Cyclosporin A

- Adalimumab

- Etretinate

- Isotretinoin (Accutane)

- Acitretin (Neotigason)

Topical corticosteroid preparations are the most effective agents when used continuously for 8 weeks; retinoids and coal tar were found to be of limited benefit and may be no better than placebo. Greater benefit has been observed with very potent corticosteroids when compared to potent corticosteroids. Vitamin D analogues such as paricalcitol were found to be significantly superior to placebo. Combination therapy with vitamin D and a corticosteroid was superior to either treatment alone and vitamin D was found to be superior to coal tar for chronic plaque psoriasis.

Moisturizers and emollients such as mineral oil, petroleum jelly, calcipotriol, and decubal (an oil-in-water emollient) were found to increase the clearance of psoriatic plaques. Emollients have been shown to be even more effective at clearing psoriatic plaques when combined with phototherapy. However, certain emollients have no impact on psoriasis plaque clearance or may even decrease the clearance achieved with phototherapy. The emollient salicylic acid is structurally similar to para-aminobenzoic acid (PABA), commonly found in sunscreen, and is known to interfere with phototherapy in psoriasis. Coconut oil, when used as an emollient in psoriasis, has been found to decrease plaque clearance with phototherapy. Medicated creams and ointments applied directly to psoriatic plaques can help reduce inflammation, remove built-up scale, reduce skin turnover, and clear affected skin of plaques. Ointment and creams containing coal tar, dithranol, corticosteroids (i.e. desoximetasone), fluocinonide, vitamin D analogs (for example, calcipotriol), and retinoids are routinely used. The use of the finger tip unit may be helpful in guiding how much topical treatment to use.

Vitamin D analogues may be useful with steroids; however, alone have a higher rate of side effects. They may allow less steroids to be used.

Another topical therapy used to treat psoriasis is a form of balneotherapy, which involves daily baths in the Dead Sea. This is usually done for four weeks with the benefit attributed to sun exposure and specifically UVB light. This is cost-effective and it has been propagated as an effective way to treat psoriasis without medication. Decreases of PASI scores greater than 75% and remission for several months have commonly been observed. Side-effects may be mild such as itchiness, folliculitis, sunburn, poikiloderma, and a theoretical risk of nonmelanoma skin cancer or melanoma has been suggested. However, more recent studies have determined that there does not appear to be increased risk of melanoma in the long-term. Data are inconclusive with respect to nonmelanoma skin cancer risk, but support the idea that the therapy is associated with an increased risk of benign forms of sun-induced skin damage such as, but not limited to, actinic elastosis or liver spots. Dead Sea balneotherapy is also effective for psoriatic arthritis.

A case report published in the Journal of Dermatological Treatment documents the successful use of adalimumab to control symptoms and induce relapse for 72 weeks. “Adalimumab is ... approved for the treatment of moderate to severe rheumatoid arthritis ... and more recently for the treatment of psoriatic arthritis”

Psoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including medications by mouth or injectable treatments. People undergoing systemic treatment must have regular blood and liver function tests to check for medication toxicities. Pregnancy must be avoided for most of these treatments. The majority of people experience a recurrence of psoriasis after systemic treatment is discontinued.

Non-biologic systemic treatments frequently used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids. Methotrexate and ciclosporin are drugs that suppress the immune system; retinoids are synthetic forms of vitamin A. These agents are also regarded as first-line treatments for psoriatic erythroderma. Oral corticosteroids should not be used, for they can severely flare psoriasis upon their discontinuation.

Biologics are manufactured proteins that interrupt the immune process involved in psoriasis. Unlike generalised immunosuppressive drug therapies such as methotrexate, biologics target specific aspects of the immune system contributing to psoriasis. These medications are generally well-tolerated and limited long-term outcome data have demonstrated biologics to be safe for long-term use in moderate to severe plaque psoriasis. However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.

Guidelines regard biologics as third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments. The safety of biologics during pregnancy has not been assessed. European guidelines recommend avoiding biologics if a pregnancy is planned; anti-TNF therapies such as infliximab are not recommended for use in chronic carriers of the hepatitis B virus or individuals infected with HIV.

Several monoclonal antibodies target cytokines, the molecules that cells use to send inflammatory signals to each other. TNF-α is one of the main executor inflammatory cytokines. Four monoclonal antibodies (MAbs) (infliximab, adalimumab, golimumab, and certolizumab pegol) and one recombinant TNF-α decoy receptor, etanercept, have been developed to inhibit TNF-α signaling. Additional monoclonal antibodies, such as ixekizumab, have been developed against pro-inflammatory cytokines and inhibit the inflammatory pathway at a different point than the anti-TNF-α antibodies. IL-12 and IL-23 share a common domain, p40, which is the target of the recently FDA-approved ustekinumab. In 2017 the US FDA approved guselkumab for plaque psoriasis.

Two drugs that target T cells are efalizumab and alefacept. Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA-1. It also blocks the adhesion molecules on the endothelial cells that line blood vessels, which attract T cells. Efalizumab was voluntarily withdrawn from the European market in February 2009 and from the US market in June 2009 by the manufacturer due to the medication's association with cases of progressive multifocal leukoencephalopathy. Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even causes natural killer cells to kill T cells as a way of controlling inflammation. Apremilast may also be used.

Individuals with psoriasis may develop neutralizing antibodies against monoclonal antibodies. Neutralization occurs when an antidrug antibody prevents a monoclonal antibody such as infliximab from binding antigen in a laboratory test. Specifically, neutralization occurs when the antidrug antibody binds to infliximab's antigen binding site instead of TNF-α. When infliximab no longer binds tumor necrosis factor alpha, it no longer decreases inflammation, and psoriasis may worsen. Neutralizing antibodies have not been reported against etanercept, a biologic drug that is a fusion protein composed of two TNF-α receptors. The lack of neutralizing antibodies against etanercept is probably secondary to the innate presence of the TNF-α receptor, and the development of immune tolerance.

The treatments used for plaque psoriasis can also be used for guttate psoriasis. Few studies have specifically focused on guttate psoriasis management, so there is currently no firm guidelines for managing guttate psoriasis differently from plaque psoriasis. Due to the role streptococcal infection plays in the development of guttate psoriasis, systemic antibiotics have been considered as a potential treatment option. Although systemic antibiotics may be considered to treat the initial infection at its source, there is no support for their use in the management of subsequent guttate psoriasis itself. The condition often usually clears up on its own within weeks to months, and only about one third of patients will develop chronic plaques.

Acute GPP typically requires inpatient management including both topical and systemic therapy, and supportive measures. Systemic glucocorticoid withdrawal is a common causative agent. Withdrawal or administration of certain drugs in the patient's previous medication regimen may be required. Oral retinoids are the most effective treatment, and are considered first line. Cyclosporine or infliximab may be required for particularly acute cases.

Treatment differs according to what rash a patient has been diagnosed with. Common rashes can be easily remedied using steroid topical creams (such as hydrocortisone) or non-steroidal treatments. Many of the medications are available over the counter in the United States.

The problem with steroid topical creams i.e. hydrocortisone; is their inability to penetrate the skin through absorption and therefore not be effective in clearing up the affected area, thus rendering the hydrocortisone almost completely ineffective in all except the most mild of cases.

There are many treatments available for dyshidrosis. However, few of them have been developed or tested specifically on the condition.

- Barriers to moisture and irritants, including barrier creams and gloves.

- Topical steroids - while useful, can be dangerous long-term due to the skin-thinning side-effects, which are particularly troublesome in the context of hand dyshidrosis, due to the amount of toxins and bacteria the hands typically come in contact with.

- Potassium permanganate dilute solution soaks - also popular, and used to 'dry out' the vesicles, and kill off superficial "Staphylococcus aureus", but it can also be very painful. Undiluted it may cause significant burning.

- Dapsone (diamino-diphenyl sulfone), an antibacterial, has been recommended for the treatment of dyshidrosis in some chronic cases.

- Antihistamines: Fexofenadine up to 180 mg per day.

- Alitretinoin (9-cis-retinoic acid) has been approved for prescription in the UK. It is specifically used for chronic hand and foot eczema. It is made by Basilea of Switzerland (BAL 4079).

- Systemic steroids can be taken orally to treat especially acute and severe cases of dyshidrosis.

You have to treat the primary cause or the exacerbation may persisist and reincide.

Topical steroids are the primary category of medications used to treat exfoliative dermatitis (ED). A sedative antihistamine may be a useful adjunct for pruritic patients, since it helps patients to sleep at night, thus limiting nocturnal scratching and excoriations. Antimicrobial agents often are used if an infection is suspected to be precipitating or complicating exfoliative dermatitis. Other drugs specifically indicated for management of underlying cause of exfoliative dermatitis may be necessary.

There exist numerous treatments for nail psoriasis but there is little information concerning their effectiveness and safety.

Treatments include topical, intralesional, radiation, systemic, and combination therapies.

- Tacalcitol ointment obtains a significant improvement in all nail parameters, both of the matrix and of the bed.

- Clobetasol nail lacquer and tacalcitol ointment

- 5-fluorouracil. A reported side-effect is yellow nails

- Calcipotriol

- Calcipotriol plus betamethasone dipropionate ointment.

- Efalizumab

- Infliximab

- Golimumab

- Low dose methotrexate

- Intralesional corticosteroid injection

The mainstay of treatment for SSSS is supportive care along with eradication of the primary infection. Conservative measures include rehydration, antipyretics (e.g., ibuprofen, aspirin, and paracetamol), management of thermal burns, and stabilization. Parenteral antibiotics to cover "S. aureus" should be administered. Most strains of "S. aureus" implicated in SSSS have penicillinases, and are therefore penicillin resistant. Therefore, treatment with Nafcillin, oxacillin, or vancomycin is typically indicated. Clindamycin is sometimes also used because of its inhibition of exotoxins.

Topical preparations of immune suppressing medications including glucocorticoids (such as 0.05% clobetasol or 0.10% betamethasone) and calcineurin inhibitors (such as tacrolimus or pimecrolimus) are considered to be first-line vitiligo treatments.

Phototherapy is considered a second-line treatment for vitiligo. Exposing the skin to light from UVB lamps is the most common treatment for vitiligo. The treatments can be done at home with an UVB lamp or in a clinic. The exposure time is managed so that the skin does not suffer overexposure. Treatment can take a few weeks if the spots are on the neck and face and if they existed not more than 3 years. If the spots are on the hands and legs and have been there more than 3 years, it can take a few months. Phototherapy sessions are done 2–3 times a week. Spots on a large area of the body may require full body treatment in a clinic or hospital. UVB broadband and narrowband lamps can be used, but narrowband ultraviolet picked around 311 nm is the choice. It has been constitutively reported that a combination of UVB phototherapy with other topical treatments improves re-pigmentation. However, some vitiligo patients may not see any changes to skin or re-pigmentation occurring. A serious potential side effect involves the risk of developing skin cancer, the same risk as an over-exposure to natural sunlight.

Ultraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and ultraviolet A light (PUVA) treatment involves taking a drug that increases the skin's sensitivity to ultraviolet light, then exposing the skin to high doses of UVA light. Treatment is required twice a week for 6–12 months or longer. Because of the high doses of UVA and psoralen, PUVA may cause side effects such as sunburn-type reactions or skin freckling.

Narrowband ultraviolet B (NBUVB) phototherapy lacks the side-effects caused by psoralens and is as effective as PUVA. As with PUVA, treatment is carried out twice weekly in a clinic or every day at home, and there is no need to use psoralen.

Available studies lack sufficient power to extrapolate a standardized therapeutic regimen.

As of April 2009, an assessment of the evidence for the efficacy and safety of the treatments for nail psoriasis is in progress.

- Infliximab appears to be the most effective treatment for nail psoriasis to date.

- Results from low-dose acitretin therapy show NAPSI score reductions comparable with those studies evaluating biologic drugs for nail psoriasis and suggest that low-dose systemic acitretin should be considered in the treatment of nail psoriasis.

Dermographism can be treated by substances (i.e. an antihistamine) which prevent histamine from causing the reaction. These may need to be given as a combination of H antagonists, or possibly with an H-receptor antagonist such as cimetidine.

OTC Vitamin C, 1000 mg daily, increases histamine degradation and removal.

Not taking hot baths or showers may help if it is generalized (all over) and possibly for localized cases (in a specific area). If taking hot showers helps, it may be a condition called shower eczema. If it affects mainly the head, it may be psoriasis. In rare cases, allergy tests may uncover substances the patient is allergic to.

While cromoglycate, which prevents histamine from being released from mast cells, is used topically in rhinitis and asthma, it is not effective orally for treating chronic urticaria.

The 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 prognosis of SSSS in children is excellent, with complete resolution within 10 days of treatment, and without significant scarring. However, SSSS must be differentiated carefully from toxic epidermal necrolysis, which carries a poor prognosis. The prognosis in adults is generally much worse, and depends upon various factors such as time to treatment, host immunity, and comorbidities.

Initial treatments for minor erythrasma can begin with keeping the area clean and dry and with antibacterial soaps. The next level would be treated with topical fusidic acid, miconazole cream, and antibacterial solution such as clindamycin HCL to eradicate the bacteria. For aggressive types of Erythrasma, oral antibiotics like macrolides(erythromycin or azithromycin)can be prescribed. Below is a figure showing the different types and subtypes of therapies.

There is no current agreement on the most optimal treatment for this disease. There are plenty of limitations on these treatments such as more irritation, possible allergic reactions, and ulcerations. These treatments are suitable for most ages, but for young children it should be monitored very closely. Erythrasma if treated and found early on, is not fatal and the patient will live a full life. In more severe cases, it can be an indicator for another disease such as diabetes.

Reported treatments include topical agents, dermabrasion, cryotherapy, laser therapy, and surgical excision. These therapies have a high failure rate because of incomplete relief of symptoms, scarring, or recurrence .

Though similar in appearance, ILVEN will not respond to therapies known to affect psoriasis. ILVEN can be very difficult to live with but can be treated. The most effective method is full-thickness excision of the lesion. CO2 Laser Surgery can resurface the skin to give a flat, smoother and more normal appearance, but does not remove the lesion.

Tinea cruris is best treated with topical antifungal medications of the allylamine or azole type. The evidence is best for terbinafine and naftifine but other agents may also work.

The benefits of the use of topical steroids in addition to an antifungal is unclear. There might be a greater cure rate but no guidelines currently recommend its addition. The effect of Whitfield's ointment is also unclear.

Since most cases cause no symptoms, reassuring the person affected that the condition is entirely benign is usually the only treatment.

When symptoms are present, topical anesthetics can be used to provide temporary relief. Other medications that have been used to manage the symptoms include antihistamines, corticosteroids or anxiolytics, but these drugs have not been formally assessed for efficacy in geographic tongue. If some foods exacerbate or trigger the symptoms, then cutting these foods out of the diet may benefit. One uncontrolled trial has shown some benefit in controlling the symptoms of geographic tongue.

Medical professionals recommend a preventative based approach of stopping fungus before it occurs. Prevention is preferable over a reactive treatment approach. The preventative based approach involves removing heat and moisture to the groin area.

- Dry off with a clean towel immediately after showering, swimming or perspiring.

- Shower after physical activities.

- Wear underwear with high air and moisture permeability fabric, such as linen (flax).

The classification of exfoliative dermatitis into Wilson-Brocq (chronic relapsing), Hebra or pityriasis rubra (progressive), and Savill (self-limited) types may have had historical value, but it currently lacks pathophysiologic or clinical utility.

Treatment for fiddler’s neck is unnecessary if it is painless and shows minimal swelling, particularly since minor cases are taken as a mark of pride. But fiddler’s neck may lead to worse disorders. The primary methods of treatment involve adjustments to playing of the instrument:

- good hygiene for the affected area and for the instrument

- use of a clean cotton cloth that is changed frequently

- use of a shoulder rest to reduce pressure below the jaw

- a suitable chin rest, especially one carved or molded for the individual

- Covering or changing potentially allergenic materials on the instrument.

- shifting the chin rest to the center of the body over the tailpiece

- smoothing coarse surfaces to reduce abrasion

- for males, growing a beard to avoid folliculitis

Surgery is necessary for sialolithiasis, parotid tumors, and cysts. Cervical lymph nodes that are larger than 1 cm must be biopsied. Connective tissue can be removed by excision when a non-inflamed mass is large, and there is generally little recurrence. Infections should be treated conservatively, and causative species should be identified through smear and culture for appropriate antibiotic selection. Reduction of playing time may be helpful for cases without inflammation, but in 30% of cases this did not improve the symptoms.

The condition may disappear over time, but it is impossible to predict if or when this may happen.