Editing Psoriasis (section)

==Management==
[[Image:Psoriasis treatment ladder.svg|thumb|upright=1.3|Schematic of psoriasis treatment ladder]]
While no cure is available for psoriasis,<ref name=Weller2008 /> many treatment options exist. [[Topical medication|Topical agents]] are typically used for mild disease, [[Light therapy|phototherapy]] for moderate disease, and systemic agents for severe disease.<ref name=Lancet07>{{cite journal | vauthors = Menter A, Griffiths CE | title = Current and future management of psoriasis | journal = Lancet | volume = 370 | issue = 9583 | pages = 272–284 | date = July 2007 | pmid = 17658398 | doi = 10.1016/S0140-6736(07)61129-5 | s2cid = 7907468 }}</ref> There is no evidence to support the effectiveness of conventional topical and systemic drugs, biological therapy, or phototherapy for acute guttate psoriasis or an acute guttate flare of chronic psoriasis.<ref>{{cite journal | vauthors = Maruani A, Samimi M, Stembridge N, Abdel Hay R, Tavernier E, Hughes C, Le Cleach L | title = Nonantistreptococcal interventions for acute guttate psoriasis or an acute guttate flare of chronic psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | pages = CD011541 | date = April 2019 | issue = 4 | pmid = 30958563 | pmc = 6452774 | doi = 10.1002/14651858.CD011541.pub2 | collaboration = Cochrane Skin Group }}</ref>

===Topical agents===
Topical [[corticosteroid]] preparations are the most effective agents when used continuously for eight weeks; [[retinoid]]s and [[coal tar]] were found to be of limited benefit and may be no better than [[placebo]].<ref name="Samarasekera2013">{{cite journal | vauthors = Samarasekera EJ, Sawyer L, Wonderling D, Tucker R, Smith CH | title = Topical therapies for the treatment of plaque psoriasis: systematic review and network meta-analyses | journal = The British Journal of Dermatology | volume = 168 | issue = 5 | pages = 954–967 | date = May 2013 | pmid = 23413913 | doi = 10.1111/bjd.12276 | s2cid = 21979785 }}</ref> Very potent topical corticosteroids may be helpful in some cases, however, it is suggested to only use them for four weeks at a time and only if other less potent topical treatment options are not working.<ref>{{cite journal | vauthors = Kleyn EC, Morsman E, Griffin L, Wu JJ, Cm van de Kerkhof P, Gulliver W, van der Walt JM, Iversen L | title = Review of international psoriasis guidelines for the treatment of psoriasis: recommendations for topical corticosteroid treatments | journal = The Journal of Dermatological Treatment | volume = 30 | issue = 4 | pages = 311–319 | date = June 2019 | pmid = 31138038 | doi = 10.1080/09546634.2019.1620502 | s2cid = 169036303 | doi-access = free }}</ref>

[[Vitamin D analogue]]s (such as [[paricalcitol]], [[calcipotriol]], [[tacalcitol]], and [[calcitriol]]) are superior to placebo. Combination therapy with vitamin D and a corticosteroid is superior to either treatment alone and [[vitamin D]] is superior to coal tar for chronic plaque psoriasis.<ref name="Mason2013">{{cite journal | vauthors = Mason AR, Mason J, Cork M, Dooley G, Hancock H | title = Topical treatments for chronic plaque psoriasis | journal = The Cochrane Database of Systematic Reviews | issue = 3 | pages = CD005028 | date = March 2013 | volume = 2015 | pmid = 23543539 | doi = 10.1002/14651858.CD005028.pub3 | pmc = 11227123 | url = http://dro.dur.ac.uk/20582/1/20582.pdf | id = CD005028 | access-date = 6 November 2019 | archive-date = 28 April 2021 | archive-url = https://web.archive.org/web/20210428101001/https://dro.dur.ac.uk/20582/1/20582.pdf | url-status = live }}</ref>

For psoriasis of the scalp, a 2016 review found dual therapy (vitamin D analogs and topical corticosteroids) or corticosteroid monotherapy to be more effective and safer than topical vitamin D analogs alone.<ref name=Schlager2016>{{cite journal | vauthors = Schlager JG, Rosumeck S, Werner RN, Jacobs A, Schmitt J, Schlager C, Nast A | title = Topical treatments for scalp psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2016 | issue = 2 | pages = CD009687 | date = February 2016 | pmid = 26915340 | doi = 10.1002/14651858.CD009687.pub2 | pmc = 8697570 | id = CD009687 }}</ref> 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.<ref name=Schlager2016 />

[[Moisturizer]]s and emollients such as [[mineral oil]], [[petroleum jelly]], and [[decubal]] (an oil-in-water emollient) were found to increase the clearance of psoriatic plaques. Some emollients are even more effective at clearing psoriatic plaques when combined with [[Light therapy|phototherapy]].<ref name="Asztalos2013">{{cite journal | vauthors = Asztalos ML, Heller MM, Lee ES, Koo J | title = The impact of emollients on phototherapy: a review | journal = Journal of the American Academy of Dermatology | volume = 68 | issue = 5 | pages = 817–24 | date = May 2013 | pmid = 23399460 | doi = 10.1016/j.jaad.2012.05.034 | url = https://zenodo.org/record/897997 | access-date = 30 June 2019 | archive-date = 29 August 2021 | archive-url = https://web.archive.org/web/20210829015357/https://zenodo.org/record/897997/preview/article.pdf | url-status = live }}</ref> Certain emollients, though, have no impact on psoriasis 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 psoriasis. [[Coconut oil]], when used as an emollient in psoriasis, has been found to decrease plaque clearance with phototherapy.<ref name="Asztalos2013"/> 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<sub>3</sub> analogues (for example, calcipotriol), and [[retinoid]]s are routinely used. (The use of the [[finger tip unit]] may be helpful in guiding how much topical treatment to use.)<ref name="Clarke2011"/><ref>{{cite journal | vauthors = Menter A, Korman NJ, Elmets CA, Feldman SR, Gelfand JM, Gordon KB, Gottlieb A, Koo JY, Lebwohl M, Lim HW, Van Voorhees AS, Beutner KR, Bhushan R | title = Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies | journal = Journal of the American Academy of Dermatology | volume = 60 | issue = 4 | pages = 643–59 | date = April 2009 | pmid = 19217694 | doi = 10.1016/j.jaad.2008.12.032 }}</ref>

Vitamin D analogs may be useful with [[steroid]]s; steroids alone have a higher rate of side effects.<ref name="Mason2013" /> Vitamin D analogs may allow lower doses of steroids to be used.<ref>{{cite journal | vauthors = Soleymani T, Hung T, Soung J | title = The role of vitamin D in psoriasis: a review | journal = International Journal of Dermatology | volume = 54 | issue = 4 | pages = 383–92 | date = April 2015 | pmid = 25601579 | doi = 10.1111/ijd.12790 | s2cid = 1688553 }}</ref>

Another topical therapy used to treat psoriasis is a form of [[balneotherapy]], which involves daily baths in [[Saline water|saltwater]], such as the [[Dead Sea]], combined with sun exposure. This is usually done for four weeks in which exposure time is gradually increased. The primary benefit is 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.<ref name="Halverstam2008">{{cite journal | vauthors = Halverstam CP, Lebwohl M | title = Nonstandard and off-label therapies for psoriasis | journal = Clinics in Dermatology | volume = 26 | issue = 5 | pages = 546–53 | date = September–October 2008 | pmid = 18755374 | doi = 10.1016/j.clindermatol.2007.10.023 }}</ref> Decreases of PASI scores greater than 75% and [[Remission (medicine)|remission]] for several months have commonly been observed.<ref name="Halverstam2008"/> Side effects may be mild such as itchiness, [[folliculitis]], [[sunburn]], [[poikiloderma]], and a theoretical risk of nonmelanoma cancer or melanoma has been suggested.<ref name="Halverstam2008"/> Some studies indicate no increased risk of melanoma in the long term.<ref name="Katz2012"/> Data are inconclusive concerning 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 [[solar lentigines|liver spots]].<ref name="Katz2012">{{cite journal | vauthors = Katz U, Shoenfeld Y, Zakin V, Sherer Y, Sukenik S | title = Scientific evidence of the therapeutic effects of dead sea treatments: a systematic review | journal = Seminars in Arthritis and Rheumatism | volume = 42 | issue = 2 | pages = 186–200 | date = October 2012 | pmid = 22503590 | doi = 10.1016/j.semarthrit.2012.02.006 }}</ref> Dead Sea balneotherapy is also effective for psoriatic arthritis.<ref name="Katz2012"/> Tentative evidence indicates that balneophototherapy, a combination of [[balneotherapy|salt bath]]es and exposure to [[ultraviolet]] B-light (UVB), in chronic plaque psoriasis is better than UVB alone.<ref>{{cite journal | vauthors = Peinemann F, Harari M, Peternel S, Chan T, Chan D, Labeit AM, Gambichler T | title = Indoor salt water baths followed by artificial ultraviolet B light for chronic plaque psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | issue = 5 | pages = CD011941 | date = May 2020 | pmid = 32368795 | doi = 10.1002/14651858.CD011941.pub2| pmc = 7199317 }}</ref> [[Glycerin]] is also an effective treatment for Psoriasis.<ref>Medical College of Georgia at Augusta University. "Glycerin is safe, effective in psoriasis model." ScienceDaily. [www.sciencedaily.com/releases/2021/10/211004104229.htm] (accessed 9 July 2023).</ref>

===UV phototherapy===
[[Phototherapy]] in the form of [[sunlight]] has long been used for psoriasis.<ref name=Lancet07/> UVB [[wavelength]]s of 311–313&nbsp;[[nanometer]]s are most common. [[UV-B lamps]] have been developed for this treatment.<ref name=Lancet07/> 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 dose is increased in every treatment to let the skin get used to the light.<ref name=Lancet07/> Increased rates of cancer from treatment appear to be small.<ref name=Lancet07/> [[Narrowband UVB therapy]] has been demonstrated to have similar efficacy to [[psoralen and ultraviolet A phototherapy]] (PUVA).<ref name="Dogra2010"/> A 2013 meta-analysis found no difference in efficacy between NB-UVB and PUVA in the treatment of psoriasis, but NB-UVB is usually more convenient.<ref>{{cite journal | vauthors = Chen X, Yang M, Cheng Y, Liu GJ, Zhang M | title = Narrow-band ultraviolet B phototherapy versus broad-band ultraviolet B or psoralen-ultraviolet A photochemotherapy for psoriasis | journal = The Cochrane Database of Systematic Reviews | issue = 10 | pages = CD009481 | date = October 2013 | volume = 2016 | pmid = 24151011 | doi = 10.1002/14651858.CD009481.pub2 | pmc = 11076274 }}</ref>

<!-- Tanning bed benefits and limited effectiveness with UVA -->
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 psoriasis; one indoor facility reported that 50% of its clients were using the center for psoriasis 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 psoriasis. One study found that plaque psoriasis is responsive to [[erythema|erythemogenic]] doses of either UVA or UVB, as exposure to either can cause dissipation of psoriatic plaques. It does require more energy to reach erythemogenic dosing with UVA.<ref name="radack">{{cite journal | vauthors = Radack KP, Farhangian ME, Anderson KL, Feldman SR | title = A review of the use of tanning beds as a dermatological treatment | journal = Dermatology and Therapy | volume = 5 | issue = 1 | pages = 37–51 | date = March 2015 | pmid = 25735439 | pmc = 4374067 | doi = 10.1007/s13555-015-0071-8 }}</ref>

<!-- Risks of UV light therapy -->
UV light therapies all have risks; tanning beds are no exception, being listed by the [[World Health Organization]] as [[carcinogen]]s.<ref>{{cite book | vauthors=((World Health Organization)) | title=Artificial tanning devices: public health interventions to manage sunbeds | publisher=[[World Health Organization]] (WHO) | date=15 June 2017 | hdl=10665/255695 | isbn=978-92-4-151259-6 }}</ref> Exposure to UV light is known to increase the risks of melanoma and squamous cell and basal cell carcinomas; younger people with psoriasis, 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.<ref name="radack" />

A major mechanism of NB-UVB is the induction of [[DNA]] damage in the form of [[pyrimidine dimer]]s. This type of phototherapy is useful in the treatment of psoriasis because the formation of these dimers interferes with the [[cell cycle]] and stops it. The interruption of the cell cycle induced by NB-UVB opposes the characteristic rapid division of skin cells seen in psoriasis.<ref name="Dogra2010">{{cite journal | vauthors = Dogra S, De D | title = Narrowband ultraviolet B in the treatment of psoriasis: the journey so far! | journal = Indian Journal of Dermatology, Venereology and Leprology | volume = 76 | issue = 6 | pages = 652–61 | date = November–December 2010 | pmid = 21079308 | doi = 10.4103/0378-6323.72461 | doi-access = free | title-link = doi }}</ref> The activity of many types of immune cells found in the skin is also effectively suppressed by NB-UVB phototherapy treatments.<ref>{{cite journal | vauthors = Rácz E, Prens EP, Kurek D, Kant M, de Ridder D, Mourits S, Baerveldt EM, Ozgur Z, van IJcken WF, Laman JD, Staal FJ, van der Fits L | title = Effective treatment of psoriasis with narrow-band UVB phototherapy is linked to suppression of the IFN and Th17 pathways | journal = The Journal of Investigative Dermatology | volume = 131 | issue = 7 | pages = 1547–1558 | date = July 2011 | pmid = 21412260 | doi = 10.1038/jid.2011.53 | doi-access = free | title-link = doi | oclc = 6757253389 }}</ref> The most common short-term side effect of this form of phototherapy is redness of the skin; less common side effects of NB-UVB phototherapy are itching and [[blister]]ing of the treated skin, irritation of the eyes in the form of [[conjunctivitis|conjunctival inflammation]] or [[keratitis|inflammation of the cornea]], or [[Herpes labialis|cold sores]] due to reactivation of the [[herpes simplex virus]] in the skin surrounding the lips. Eye protection is usually given during phototherapy treatments.<ref name="Dogra2010"/>

PUVA combines the oral or topical administration of psoralen with exposure to ultraviolet A (UVA) light. The [[mechanism of action]] of PUVA is unknown but probably involves activation of psoralen by UVA light, which inhibits the abnormally rapid production of the cells in psoriatic 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 (physical)|fatigue]], burning, and itching. Long-term treatment is associated with [[squamous cell carcinoma]] (but not with [[melanoma]]).<ref name="Richard2013"/><ref name="Lapolla2011">{{cite journal | vauthors = Lapolla W, Yentzer BA, Bagel J, Halvorson CR, Feldman SR | title = A review of phototherapy protocols for psoriasis treatment | journal = Journal of the American Academy of Dermatology | volume = 64 | issue = 5 | pages = 936–49 | date = May 2011 | pmid = 21429620 | doi = 10.1016/j.jaad.2009.12.054 }}</ref> A combination therapy for moderate to severe psoriasis using PUVA plus [[acitretin]] resulted in benefit, but acitretin use has been associated with [[birth defect]]s and [[hepatotoxicity|liver damage]].<ref name="Dunn2011">{{cite journal | vauthors = Dunn LK, Gaar LR, Yentzer BA, O'Neill JL, Feldman SR | title = Acitretin in dermatology: a review | journal = Journal of Drugs in Dermatology | volume = 10 | issue = 7 | pages = 772–82 | date = July 2011 | pmid = 21720660 }}</ref>

===Systemic agents===
[[Image:Psoriasis infliximab ar1182-2.gif|thumb|Pictures of a person with psoriasis (and [[psoriatic arthritis]]) at baseline and eight weeks after initiation of [[infliximab]] therapy]]
Psoriasis resistant to [[topical|topical treatment]] and [[light therapy|phototherapy]] may be treated with systemic therapies including [[medication]]s by mouth or [[Injection (medicine)|injectable treatments]].<ref name="Dogra2013">{{cite journal | vauthors = Dogra S, Mahajan R | title = Systemic methotrexate therapy for psoriasis: past, present and future | journal = Clinical and Experimental Dermatology | volume = 38 | issue = 6 | pages = 573–88 | date = August 2013 | pmid = 23837932 | doi = 10.1111/ced.12062 | s2cid = 11207097 }}</ref> People undergoing systemic treatment must have regular [[Blood test|blood]] and [[liver function tests]] to check for medication toxicities.<ref name="Dogra2013"/> [[Pregnancy]] must be avoided for most of these treatments.{{medical citation needed|date=July 2023}} The majority of people experience a [[Recrudescence|recurrence]] of psoriasis after systemic treatment is discontinued.{{medical citation needed|date=July 2023}}

<!-- First line treatments -->
Non-biologic systemic treatments frequently used for psoriasis include [[methotrexate]], [[ciclosporin]], [[hydroxycarbamide]], [[fumarate]]s such as [[dimethyl fumarate]], and [[retinoids]].<ref name="Rustin2012">{{cite journal | vauthors = Rustin MH | title = Long-term safety of biologics in the treatment of moderate-to-severe plaque psoriasis: review of current data | journal = The British Journal of Dermatology | volume = 167 | issue = Suppl 3 | pages = 3–11 | date = November 2012 | pmid = 23082810 | doi = 10.1111/j.1365-2133.2012.11208.x | s2cid = 22462278 }}</ref> Methotrexate and ciclosporin are [[immunosuppressive drug|medications that suppress the immune system]]; retinoids are synthetic forms of [[vitamin A]]. These agents are also regarded as first-line treatments for [[psoriatic erythroderma]].<ref name="Zattra2012"/> Oral [[corticosteroid]]s should not be used as they can severely flare psoriasis upon their discontinuation.<ref>{{cite web|url=https://www.aad.org/education/basic-derm-curriculum/suggested-order-of-modules/psoriasis|title=Learning module: Psoriasis {{!}} American Academy of Dermatology|website=www.aad.org|access-date=26 March 2017|url-status=live|archive-url=https://web.archive.org/web/20170327075847/https://www.aad.org/education/basic-derm-curriculum/suggested-order-of-modules/psoriasis|archive-date=27 March 2017}}</ref>

<!-- Biologics -->
[[biologic medical product|Biologics]] are manufactured proteins that interrupt the immune process involved in psoriasis. Unlike generalized immunosuppressive medical therapies such as methotrexate, biologics target specific aspects of the immune system contributing to psoriasis.<ref name="Rustin2012"/> 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.<ref name="Rustin2012"/><ref name="Griffiths2012"/> However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.<ref name="Rustin2012"/>

Guidelines regard biologics as a third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments.<ref name="Griffiths2012">{{cite journal | vauthors = Griffiths CE | title = Biologics for psoriasis: current evidence and future use | journal = The British Journal of Dermatology | volume = 167 | issue = Suppl 3 | pages = 1–2 | date = November 2012 | pmid = 23082809 | doi = 10.1111/j.1365-2133.2012.11207.x | s2cid = 42598571 }}</ref> The safety of biologics during pregnancy has not been assessed. European guidelines recommend avoiding biologics if a pregnancy is planned; [[TNF inhibitor|anti-TNF]] therapies such as infliximab are not recommended for use in chronic carriers of the [[hepatitis B virus]] or individuals infected with [[HIV]].<ref name="Rustin2012"/>

<!-- Monoclonal antibiodies -->
Several monoclonal [[Antibody|antibodies]] target cytokines, the molecules that cells use to send inflammatory signals to each other. [[tumor necrosis factor α|TNF-α]] is one of the main executor inflammatory cytokines. Four [[monoclonal antibody|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]],<ref>{{cite journal | vauthors = Farahnik B, Beroukhim K, Zhu TH, Abrouk M, Nakamura M, Singh R, Lee K, Bhutani T, Koo J | title = Ixekizumab for the Treatment of Psoriasis: A Review of Phase III Trials | journal = Dermatology and Therapy | volume = 6 | issue = 1 | pages = 25–37 | date = March 2016 | pmid = 26910853 | pmc = 4799032 | doi = 10.1007/s13555-016-0102-0 }}</ref> have been developed against pro-inflammatory cytokines<ref>{{cite journal | vauthors = Hueber W, Patel DD, Dryja T, Wright AM, Koroleva I, Bruin G, Antoni C, Draelos Z, Gold MH, Durez P, Tak PP, Gomez-Reino JJ, Foster CS, Kim RY, Samson CM, Falk NS, Chu DS, Callanan D, Nguyen QD, Rose K, Haider A, Di Padova F | title = Effects of AIN457, a fully human antibody to interleukin-17A, on psoriasis, rheumatoid arthritis, and uveitis | journal = Science Translational Medicine | volume = 2 | issue = 52 | pages = 52ra72 | date = October 2010 | pmid = 20926833 | doi = 10.1126/scitranslmed.3001107 | doi-access =  | title-link = doi | s2cid = 10132276 }}</ref> and inhibit the inflammatory pathway at a different point than the anti-TNF-α antibodies.<ref name=Nestle/> IL-12 and IL-23 share a common domain, [[interleukin-12 subunit beta|p40]], which is the target of the [[Food and Drug Administration|FDA-approved]] [[ustekinumab]].<ref name="Prieto2013">{{cite journal | vauthors = Prieto-Pérez R, Cabaleiro T, Daudén E, Ochoa D, Roman M, Abad-Santos F | title = Genetics of psoriasis and pharmacogenetics of biological drugs | journal = Autoimmune Diseases | volume = 2013 | issue = 613086 | pages = 613086 | date = August 2013 | pmid = 24069534 | pmc = 3771250 | doi = 10.1155/2013/613086 | doi-access = free | title-link = doi }}</ref> In 2017 the [[US FDA]] approved [[guselkumab]] for plaque psoriasis.<ref name=FDA-n-2017>[https://www.fda.gov/drugs/developmentapprovalprocess/druginnovation/ucm537040.htm Novel Drug Approvals for 2017] {{webarchive|url=https://web.archive.org/web/20170629124028/https://www.fda.gov/Drugs/DevelopmentApprovalProcess/DrugInnovation/ucm537040.htm |date=29 June 2017 }}</ref> There have been few studies of the efficacy of anti-TNF medications for psoriasis in children. One randomized control study suggested that 12 weeks of etanercept treatment reduced the extent of psoriasis in children with no lasting adverse effects.<ref>{{cite journal | vauthors = Sanclemente G, Murphy R, Contreras J, García H, Bonfill Cosp X | title = Anti-TNF agents for paediatric psoriasis | journal = The Cochrane Database of Systematic Reviews | issue = 11 | pages = CD010017 | date = November 2015 | volume = 2019 | pmid = 26598969 | pmc = 6493213 | doi = 10.1002/14651858.CD010017.pub2 }}</ref>

<!-- Others -->
Two medications that target T cells are [[efalizumab]] and [[alefacept]]. Efalizumab is a monoclonal antibody that specifically targets the [[CD11a]] subunit of [[LFA-1]].<ref name="Rustin2012"/> 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 U.S. market in June 2009, by the manufacturer due to the medication's association with cases of [[progressive multifocal leukoencephalopathy]].<ref name="Rustin2012"/> Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even causes [[natural killer cell]]s to kill T cells as a way of controlling inflammation.<ref name=Nestle/> [[Apremilast]] may also be used.<ref name="Palfreeman2013"/>

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 anti-drug 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 medication 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]].<ref>{{cite journal | vauthors = Harding FA, Stickler MM, Razo J, DuBridge RB | title = The immunogenicity of humanized and fully human antibodies: residual immunogenicity resides in the CDR regions | journal = mAbs | volume = 2 | issue = 3 | pages = 256–65 | date = 2010 | pmid = 20400861 | pmc = 2881252 | doi = 10.4161/mabs.2.3.11641 }}</ref>

There is strong evidence to indicate that infliximab, [[bimekizumab]], ixekizumab, and [[risankizumab]] are the most effective biologics for treating moderate to severe cases of psoriasis.<ref name=":5">{{cite journal | vauthors = Sbidian E, Chaimani A, Guelimi R, Garcia-Doval I, Hua C, Hughes C, Naldi L, Kinberger M, Afach S, Le Cleach L | title = Systemic pharmacological treatments for chronic plaque psoriasis: a network meta-analysis | journal = The Cochrane Database of Systematic Reviews | volume = 2023 | issue = 7 | pages = CD011535 | date = July 2023 | pmid = 37436070 | pmc = 10337265 | doi = 10.1002/14651858.CD011535.pub6 }}</ref> There is also some evidence to support use of [[secukinumab]], [[brodalumab]], [[guselkumab]], certolizumab, and ustekinumab.<ref name="pmid26714681">{{cite journal | vauthors = Campa M, Mansouri B, Warren R, Menter A | title = A Review of Biologic Therapies Targeting IL-23 and IL-17 for Use in Moderate-to-Severe Plaque Psoriasis | journal = Dermatology and Therapy | volume = 6 | issue = 1 | pages = 1–12 | date = March 2016 | pmid = 26714681 | pmc = 4799039 | doi = 10.1007/s13555-015-0092-3 }}</ref><ref name=":5" /> In general, anti-IL17, anti-IL12/23, anti-IL23, and anti-TNF alpha biologics were found to be more effective than traditional systemic treatments.<ref name=":5" /> The [[Immunology|immunologic]] pathways of psoriasis involve [[Th 9 cell|Th9]], [[Th17]], [[Th1 cell|Th1]] lymphocytes, and [[Interleukin 22|IL-22]]. The aforementioned biologic agents hinder different aspects of these pathways.{{citation needed|date=January 2020}}

Another set of treatments for moderate to severe psoriasis are [[fumaric acid esters]] (FAE), which may be similar in effectiveness to [[methotrexate]].<ref>{{cite journal | vauthors = Atwan A, Ingram JR, Abbott R, Kelson MJ, Pickles T, Bauer A, Piguet V | title = Oral fumaric acid esters for psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2015 | issue = 8 | pages = CD010497 | date = August 2015 | pmid = 26258748 | pmc = 6464505 | doi = 10.1002/14651858.CD010497.pub2 }}</ref>

[[Apremilast]] (Otezla, Celgene) is an oral small-molecule inhibitor of the enzyme [[phosphodiesterase 4]], which plays an important role in chronic inflammation associated with psoriasis.<ref>{{cite journal |last1=Papp |first1=K |last2=Reich |first2=K |last3=Leonardi |first3=CL |last4=Kircik |first4=L |last5=Chimenti |first5=S |last6=Langley |first6=RG |last7=Hu |first7=C |last8=Stevens |first8=RM |last9=Day |first9=RM |last10=Gordon |first10=KB |last11=Korman |first11=NJ |last12=Griffiths |first12=CE |title=Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, in patients with moderate to severe plaque psoriasis: Results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis [ESTEEM] 1). |journal=Journal of the American Academy of Dermatology |date=July 2015 |volume=73 |issue=1 |pages=37–49 |doi=10.1016/j.jaad.2015.03.049 |pmid=26089047 |url=https://pubmed.ncbi.nlm.nih.gov/26089047/ |access-date=17 September 2024|doi-access=free }}</ref>

It has been theorized that [[Streptococcus|antistreptococcal]] medications may improve guttate and chronic plaque psoriasis; however, limited studies do not show that [[antibiotic]]s are effective.<ref>{{cite journal | vauthors = Dupire G, Droitcourt C, Hughes C, Le Cleach L | title = Antistreptococcal interventions for guttate and chronic plaque psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | pages = CD011571 | date = March 2019 | issue = 3 | pmid = 30835819 | pmc = 6400423 | doi = 10.1002/14651858.cd011571.pub2 }}</ref>

===Surgery===
Limited evidence suggests [[tonsillectomy|removal of the tonsils]] may benefit people with chronic plaque psoriasis, guttate psoriasis, and [[Pustulosis palmaris et plantaris|palmoplantar pustulosis]].<ref name="Wu2014">{{cite journal | vauthors = Wu W, Debbaneh M, Moslehi H, Koo J, Liao W | title = Tonsillectomy as a treatment for psoriasis: a review | journal = The Journal of Dermatological Treatment | volume = 25 | issue = 6 | pages = 482–6 | date = December 2014 | pmid = 24283892 | pmc = 4620715 | doi = 10.3109/09546634.2013.848258 }}</ref><ref>{{cite journal | vauthors = Sigurdardottir SL, Thorleifsdottir RH, Valdimarsson H, Johnston A | title = The role of the palatine tonsils in the pathogenesis and treatment of psoriasis | journal = The British Journal of Dermatology | volume = 168 | issue = 2 | pages = 237–42 | date = February 2013 | pmid = 22901242 | doi = 10.1111/j.1365-2133.2012.11215.x | url = https://deepblue.lib.umich.edu/bitstream/2027.42/96289/1/bjd11215.pdf | hdl = 2027.42/96289 | s2cid = 11572308 | hdl-access = free | access-date = 3 September 2019 | archive-date = 29 August 2021 | archive-url = https://web.archive.org/web/20210829015354/https://deepblue.lib.umich.edu/bitstream/handle/2027.42/96289/bjd11215.pdf;jsessionid=582C9DAE0038517119D12BA23A3404DF?sequence=1 | url-status = live }}</ref>

===Diet===
Uncontrolled studies have suggested that individuals with psoriasis or psoriatic arthritis may benefit from a diet supplemented with [[fish oil]] rich in [[eicosapentaenoic acid]] (EPA) and [[docosahexaenoic acid]] (DHA).<ref name="Kaimal2010">{{cite journal | vauthors = Kaimal S, Thappa DM | title = Diet in dermatology: revisited | journal = Indian Journal of Dermatology, Venereology and Leprology | volume = 76 | issue = 2 | pages = 103–15 | year = 2010 | pmid = 20228538 | doi = 10.4103/0378-6323.60540 | doi-access = free | title-link = doi }}</ref> A low-calorie diet appears to reduce the severity of psoriasis.<ref name=Shu2019/> Diet recommendations include consumption of cold water fish (preferably wild fish, not [[Fish farming|farmed]]) such as [[salmon]], [[herring]], and [[mackerel]]; extra virgin olive oil; legumes; vegetables; fruits; and whole grains; and avoid consumption of alcohol, red meat, and dairy products (due to their saturated fat). The effect of caffeine consumption (including from coffee, [[black tea]], mate, and dark chocolate) remains to be determined.<ref name=BarreaNappi2016>{{cite journal | vauthors = Barrea L, Nappi F, Di Somma C, Savanelli MC, Falco A, Balato A, Balato N, Savastano S | title = Environmental Risk Factors in Psoriasis: The Point of View of the Nutritionist | journal = International Journal of Environmental Research and Public Health | volume = 13 | issue = 5 | pages = 743 | date = July 2016 | pmid = 27455297 | pmc = 4962284 | doi = 10.3390/ijerph13070743 | doi-access = free | title-link = doi }}</ref>

Many patients report improvements after consuming less tobacco, caffeine, sugar, [[nightshades]] (tomatoes, eggplant, peppers, [[paprika]] and white potatoes) and taking [[probiotic]]s and oral Vitamin D.<ref name=AfifiDanesh2017>{{cite journal | vauthors = Afifi L, Danesh MJ, Lee KM, Beroukhim K, Farahnik B, Ahn RS, Yan D, Singh RK, Nakamura M, Koo J, Liao W | title = Dietary Behaviors in Psoriasis: Patient-Reported Outcomes from a U.S. National Survey | journal = Dermatology and Therapy | volume = 7 | issue = 2 | pages = 227–242 | date = 19 May 2017 | pmid = 28526915 | pmc = 5453925 | doi = 10.1007/s13555-017-0183-4 | doi-access = free | title-link = doi }}</ref>

There is a higher rate of [[celiac disease]] among people with psoriasis.<ref name=BarreaNappi2016 /><ref name=NiChiu2014>{{cite journal | vauthors = Ni C, Chiu MW | title = Psoriasis and comorbidities: links and risks | journal = Clinical, Cosmetic and Investigational Dermatology | volume = 7 | pages = 119–32 | year = 2014 | pmid = 24790463 | pmc = 4000177 | doi = 10.2147/CCID.S44843 | type = Review | doi-access = free }}</ref> When adopting a [[gluten-free diet]], disease severity generally decreases in people with celiac disease and those with [[anti-gliadin antibodies]].<ref name="Kaimal2010"/><ref name=LefflerGreen2015>{{cite journal | vauthors = Leffler DA, Green PH, Fasano A | title = Extraintestinal manifestations of coeliac disease | journal = Nature Reviews. Gastroenterology & Hepatology | volume = 12 | issue = 10 | pages = 561–71 | date = October 2015 | pmid = 26260366 | doi = 10.1038/nrgastro.2015.131 | s2cid = 15561525 | type = Review }}</ref><ref name=BhatiaMillsop2014>{{cite journal | vauthors = Bhatia BK, Millsop JW, Debbaneh M, Koo J, Linos E, Liao W | title = Diet and psoriasis, part II: celiac disease and role of a gluten-free diet | journal = Journal of the American Academy of Dermatology | volume = 71 | issue = 2 | pages = 350–8 | date = August 2014 | pmid = 24780176 | pmc = 4104239 | doi = 10.1016/j.jaad.2014.03.017 }}</ref>