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.

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.

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)

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”

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

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.

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.

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 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.

Shampoos use a combination of special ingredients to control dandruff.

Antifungal treatments including ketoconazole, zinc pyrithione and selenium disulfide have been found to be effective. Ketoconazole appears to have a longer duration of effect.

Ketoconazole is a broad spectrum antimycotic agent that is active against "Candida" and "M. furfur". Of all the antifungals of the imidazole class, ketoconazole has become the leading contender among treatment options because of its effectiveness in treating seborrheic dermatitis as well.

Ciclopirox is widely used as an anti-dandruff agent in most preparations.

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.

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.

Treatment is aimed at reducing itching and minimizing existing lesions because rubbing and scratching exacerbate LSC. The itching and inflammation may be treated with a lotions or steroid cream (such as triamcinolone or Betamethasone) applied to the affected area of the skin. Nighttime scratching can be reduced with sedatives and antihistamines. SSRIs can effectively reduce the scratching associated with obsessive psychosomatic behaviors.

Typically the medications first prescribed for psoriatic arthritis are NSAIDs such as ibuprofen and naproxen, followed by more potent NSAIDs like diclofenac, indomethacin, and etodolac. NSAIDs can irritate the stomach and intestine, and long-term use can lead to gastrointestinal bleeding. Coxibs (COX-2 inhibitors) e.g. Celecoxib or Etoricoxib, are associated with a statistically significant 50 to 66% relative risk reduction in gastrointestinal ulcers and bleeding complications compared to traditional NSAIDs, but carry an increased rate of cardiovascular events such as myocardial infarction (MI) or heart attack, and stroke. Both COX-2 inhibitors and other non-selective NSAIDS have potential adverse effects that include damage to the kidneys.

These are used in persistent symptomatic cases without exacerbation. Rather than just reducing pain and inflammation, this class of drugs helps limit the amount of joint damage that occurs in psoriatic arthritis. Most DMARDs act slowly and may take weeks or even months to take full effect. Drugs such as methotrexate or leflunomide are commonly prescribed; other DMARDS used to treat psoriatic arthritis include cyclosporin, azathioprine, and sulfasalazine. These immunosuppressant drugs can also reduce psoriasis skin symptoms but can lead to liver and kidney problems and an increased risk of serious infection.

Intertrigo is treated by addressing associated infections, by removing moisture from the site, and by using substances at the site to help maintain skin integrity. If the individual is overweight, losing weight may also help. Relapses of intertrigo are common.

Keeping the area of the intertrigo dry and exposed to the air can help prevent recurrences, as can removing moisture from the area using absorbent fabrics or body powders, including plain cornstarch and judiciously used antiperspirants.

Greases, oils, and barrier ointments, may help by protecting skin from moisture and from friction. Antifungal powders, most commonly clotrimazole 1%, may also be used in conjunction with a barrier ointment. Diaper rash ointment can also help.

Fungal infections associated with intertrigo may be treated with prescription antifungals applied directly to the skin (in most cases) or systemic antifungals, including fluconazole, nystatin, and griseofulvin.

Intertrigo is also a known symptom of vitamin B6 deficiency.

Most treatments are topical or oral antifungal medications.

Topical agents include ciclopirox nail paint, amorolfine or efinaconazole. Some topical treatments need to be applied daily for prolonged periods (at least 1 year). Topical amorolfine is applied weekly. Topical ciclopirox results in a cure in 6% to 9% of cases; amorolfine might be more effective. Ciclopirox when used with terbinafine appears to be better than either agent alone.

Oral medications include terbinafine (76% effective), itraconazole (60% effective) and fluconazole (48% effective). They share characteristics that enhance their effectiveness: prompt penetration of the nail and nail bed, persistence in the nail for months after discontinuation of therapy. Ketoconazole by mouth is not recommended due to side effects. Oral terbinafine is better tolerated than itraconazole. For superficial white onychomycosis, systemic rather than topical antifungal therapy is advised.

No treatment is usually needed as they usually go away anywhere from months to years. The lesions may last from anywhere between 4 weeks to 34 years with an average duration of 11 months. If caused by an underlying disease or malignancy, then treating and removing the disease or malignancy will stop the lesions. It usually doesn't require treatment, but topical corticosteroids may be helpful in reducing redness, swelling and itchiness.

Some supported and not supported methods of having an effect on EAC include:

- Photosensitive so it can be moved/reduced with appropriate sunlight.

- Vitamin D

- Immune system - hence it will increase in size/number when the immune system is low or overloaded.

- Hormone Drugs

- Disulone

- Stress reduction

- Topical calcipotriol - a topical vitamin D derivative has been known to be beneficial

Madarosis has different possible treatments and can be reversed if treated early enough. The treatments for madarosis are completely dependent upon the pre-existing condition. When suffering from blepheritis, antibiotics are used to combat the bacterial infection. People who are suffering from trichotillomania need to seek behavioral and psychological help. Many people look to hair transplant surgeries, especially in non-scarring cases. These surgeries are mainly used as a cosmetic reason rather than a medical one. There are also other treatments that can be used for cosmetic purposes.

Chemical (keratolytic) or surgical debridement of the affected nail appears to improve outcomes.

As of 2014 evidence for laser treatment is unclear as the evidence is of low quality and varies by type of laser.

As of 2013 tea tree oil has failed to demonstrate benefit in the treatment of onychomycosis. A 2012 review by the National Institutes of Health found some small and tentative studies on its use.

Minoxidil is a common topical treatment of eyebrow hair loss due to alopecia areata. There are other topical treatments (latanprost or bimatroprost) that are mainly used to treat glaucoma that can also be used to lengthen, thicken, and change the pigments of the lashes.

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.

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.

Subacute cutaneous lupus erythematosus (SCLE) is a clinically distinct subset of cases of lupus erythematosus that is most often present in white women aged 15 to 40, consisting of skin lesions that are scaly and evolve as polycyclic annular lesions or plaques similar to those of plaque psoriasis.

Characteristically the lesions appear in sun-exposed areas such as the vee of the neckline or the forearms, but not the face. It may be brought on by sun-sensitizing medications, but is usually associated with autoimmune disorders such as rheumatoid arthritis and Sjögren's syndrome.

Treatment generally involves sun avoidance and protection and topical corticosteroids. Sometimes systemic drug treatment is necessary. Besides corticosteroids other immunosuppressants such as methotrexate are also used.

Lesions of SCLE may have an annular configuration, with raised red borders and central clearing.