Schematic of<unk>  treatment ladder While no cure is available for<unk> , many treatment options exist. Topical agents are typically used for mild disease, phototherapy for moderate disease, and systemic agents for severe disease. There is no evidence to support the effectiveness of conventional topical and systemic drugs, biological therapy, or phototherapy for acute guttate<unk>  or an acute guttate flare of chronic<unk> . Topical agents Topical corticosteroid preparations are the most effective agents when used continuously for eight 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 are superior to placebo. Combination therapy with vitamin D and a corticosteroid are superior to either treatment alone and vitamin D is superior to coal tar for chronic plaque<unk> . For<unk>  of the scalp, a 2016 review found dual therapy (vitamin D analogues and topical corticosteroids) or corticosteroid monotherapy to be more effective and safer than topical vitamin D analogues alone. Due to their similar safety profiles and minimal benefit of dual therapy over monotherapy, corticosteroid monotherapy appears to be an acceptable treatment for short-term treatment. Moisturizers and emollients such as mineral oil, petroleum jelly, calcipotriol, and decubal (an oil-in-water emollient) were found to increase the clearance of<unk> oriatic plaques. Some emollients have been shown to be even more effective at clearing<unk> oriatic plaques when combined with phototherapy. Certain emollients, though, have no impact on<unk>  plaque clearance or may even decrease the clearance achieved with phototherapy, e.g. the emollient salicylic acid is structurally similar to para-aminobenzoic acid, commonly found in sunscreen, and is known to interfere with phototherapy in<unk> . Coconut oil, when used as an emollient in<unk> , has been found to decrease plaque clearance with phototherapy. Medicated creams and ointments applied directly to<unk> oriatic 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 D3 analogues (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; steroids alone have a higher rate of side effects. Vitamin D analogues may allow less steroids to be used. Another topical therapy used to treat<unk>  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<unk>  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 cancer or melanoma has been suggested. Some studies indicate no 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<unk> oriatic arthritis. Tentative evidence indicates that balneophototherapy, a combination of salt bathes and exposure to ultraviolet B-light (UVB), in chronic plaque<unk>  is better than UVB alone. UV phototherapy Phototherapy in the form of sunlight has long been used for<unk> . UVB wavelengths of 311–313 nanometers are most effective, and special lamps have been developed for this application. The exposure time should be controlled to avoid overexposure and burning of the skin. The UVB lamps should have a timer that turns off the lamp when the time ends. The amount of light used is determined by a person's skin type. Increased rates of cancer from treatment appear to be small. Narrowband UVB therapy has been demonstrated to have similar efficacy to<unk> oralen and ultraviolet A phototherapy (PUVA). A 2013 meta-analysis found no difference in efficacy between NB-UVB and PUVA in the treatment of<unk> , but NB-UVB is usually more convenient. One of the problems with clinical phototherapy is the difficulty many people have gaining access to a facility. Indoor tanning resources are almost ubiquitous today and could be considered as a means for people to get UV exposure when dermatologist-provided phototherapy is not available. Indoor tanning is already used by many people as a treatment for<unk> ; one indoor facility reported that 50% of its clients were using the center for<unk>  treatment; another reported 36% were doing the same thing. However, a concern with the use of commercial tanning is that tanning beds that primarily emit UVA might not effectively treat<unk> . One study found that plaque<unk>  is responsive to erythemogenic doses of either UVA or UVB, as exposure to either can cause dissipation of<unk> oriatic plaques. It does require more energy to reach erythemogenic dosing with UVA. UV light therapies all have risks; tanning beds are no exception, being listed by the World Health Organization as carcinogens. Exposure to UV light is known to increase the risks of melanoma and squamous cell and basal cell carcinomas; younger people with<unk> , particularly those under age 35, are at increased risk from melanoma from UV light treatment. A review of studies recommends that people who are susceptible to skin cancers exercise caution when using UV light therapy as a treatment. A major mechanism of NBUVB is the induction of DNA damage in the form of pyrimidine dimers. This type of phototherapy is useful in the treatment of<unk>  because the formation of these dimers interferes with the cell cycle and stops it. The interruption of the cell cycle induced by NBUVB opposes the characteristic rapid division of skin cells seen in<unk> . The activity of many types of immune cells found in the skin is also effectively suppressed by NBUVB phototherapy treatments. The most common short-term side effect of this form of phototherapy is redness of the skin; less common side effects of NBUVB phototherapy are itching and blistering of the treated skin, irritation of the eyes in the form of conjunctival inflammation or inflammation of the cornea, or cold sores due to reactivation of the herpes simplex virus in the skin surrounding the lips. Eye protection is usually given during phototherapy treatments. PUVA combines the oral or topical administration of<unk> oralen with exposure to ultraviolet A (UVA) light. The mechanism of action of PUVA is unknown, but probably involves activation of<unk> oralen by UVA light, which inhibits the abnormally rapid production of the cells in<unk> oriatic skin. There are multiple mechanisms of action associated with PUVA, including effects on the skin's immune system. PUVA is associated with nausea, headache, fatigue, burning, and itching. Long-term treatment is associated with squamous cell carcinoma (but not with melanoma). A combination therapy for moderate to severe<unk>  using PUVA plus acitretin resulted in benefit, but acitretin use has been associated with birth defects and liver damage. Systemic agents Pictures of a person with<unk>  (and<unk> oriatic arthritis) at baseline and eight weeks after initiation of infliximab therapy<unk>  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<unk>  after systemic treatment is discontinued. Non-biologic systemic treatments frequently used for<unk>  include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids. Methotrexate and ciclosporin are medications that suppress the immune system; retinoids are synthetic forms of vitamin A. These agents are also regarded as first-line treatments for<unk> oriatic erythroderma. Oral corticosteroids should not be used, for they can severely flare<unk>  upon their discontinuation. Biologics are manufactured proteins that interrupt the immune process involved in<unk> . Unlike generalized immunosuppressive medical therapies such as methotrexate, biologics target specific aspects of the immune system contributing to<unk> . 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<unk> . 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<unk>  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,
Psoriasis
Onychomycosis
Parapsoriasis
Basal-cell carcinoma
Lupus vulgaris
Dermatitis
Vitiligo
Dandruff