Chronic plaque psoriasis is a skin disease with erythematosus, thick, silvery scale plaque lesions with sharp demarcation from normal skin.

It is now thought to be a systemic condition, and not just a skin disease, with obesity, diabetes, major cardiovascular events, and a life expectancy of five years less than that of persons without psoriasis.

A systemic inflammatory autoimmune disease.

Affects approximately 3.2% of adults, and 0.13% of children.
The incidence is approximately 80 new cases per 100,000 person-years.
Worldwide approximately 60-125 million people have psoriasis, and its prevalence is variable across regions ranging from 0.5% in parts of Asia to as high as 8% in Norway.
Affects about 2% of the world’s population.
Women and men are equally affected.
A bimodal age distribution exists at age is 18-39 and also age is 50-69 years.
Risk factors include genetic, environmental, and behavioral factors, with genetic factors being the largest contributor.
Genetic and environmental factors influence the age of onset of disease, as the presence of HLA C *06 allele is associated with early onset of disease.
One study revealed that the risk of psoriasis is approximately 40% if both parents are affected, 14% if one parent is affected and 6% of the sibling is affected.
Environmental and behavioral factors associated with psoriasis include skin trauma, infections, smoking, certain medications such as lithium and Interferon and possibly stress.

A chronic skin disease characterized by infiltration of inflammatory cells into the skin and excessive keratinocyte proliferation resulting in well demarcated erythematous lesions.

The  IL-23/IL-17 pathway plays a major role in the autoimmune disorder psoriasis.

In psoriasis immune cells react to inflammatory molecules released within the skin around the joints and scalp.

This response causes the epidermal cells to recycle more rapidly than usual, which leads to the formation of red, scaly lesions and chronic skin inflammation.

Analysis of biopsies taken from lesions of psoriasis patients show an enrichment of cytotoxic T cells and neutrophils containing IL-17.

A heterogeneous disease with the skin being the most commonly affected organ, but joints, nails, eyes and the cardiovascular system may also be involved.

Plaque psoriasis has a disproportionate effect on quality of life when it involves the face, palms, soles, nails, intertriginous areas of the axilla, inframammary, and genital regions.

Any area of the skin can be affected with the scalp, genitals, palms, and soles being especially involved.

Involvement of the intertriginous areas, which are moist and therefore lesions lack the typical scales,  makes it more likely to misdiagnose it as a fungal infection.

Genital psoriasis is seen in approximately 1/3 of patients.

Psoriatic involvement of the palms and soles limit the function of the hands and feet.

Associated with increased cardiometabolic comorbidities.

About 20% of patients have moderate to severe cutaneous involvement, and among these patients, inflammatory arthritis develops in approximately 30%.

Has a genetic overlap with rheumatoid arthritis and Crohn’s disease.

More than 40 genetic mutation’s have been implicated in the development of psoriasis including mutations to: IL36 RN, AP1S3, CARD1, KLRC2, LNPEP, LCE3B, Lce3C, TRAF3IP2, MTHFR, and ZNF750.

Psoriatic skin inflammation and atherosclerosis share pathways including those involving neutrophils and T cells.

Patients with psoriasis have elevated levels of pro inflammatory markers-C reactive protein, leptin, tumor necrosis  factor-alpha and interleukin-6 related to clinical severity and duration of the dermatological disease.
Patient with psoriasis have hyperleptinemia,  even in patients who are not obese.
Increased serum levels associated with psoriasis.
Leptin expression is enhanced in the skin of patients with active psoriasis, as it induces pro inflammatory response in dermal fibroblasts, keratinocytes, and leptin deficiency ameliorates psoriasis.
Leptin, an adipokine promotes inflammation in keratinocytes and dermal fibroblasts and probably accounts for the fact that obesity  adversely affects the course of psoriasis.
Patient with obesity tend to be resistant to anti-inflammatory treatments for psoriasis.

Activated T cells migrate to and infiltrate affected areas, releasing interferon-gamma, interleukin-two, and tumor necrosis factor-alpha.

Other factors involved including natural killer T cells, the T helper 17, dendritic cell overproduction and secretion of IL-23, activated macrophages, and T regulatory cells.

Dysregulation of AhR is one of the hallmarks of psoriasis, as psoriasis patients have a higher serum concentration of AhR compared to healthy individuals.

A systemic inflammatory disease with increased inflammation to take your skin, joints, and blood vessels.

Inflammation results in hyperproliferation of keratinocytes whose migration time from the basal layer to the corneal layer is reduced from 20-30 days to 3 to 5 days

In individuals with darker skin psoriasis plaques may appear violaceous or hyper pigmented.

Beta hemolytic streptococci and human immunodeficiency virus are associated with the development of psoriasis, either as a causal or incidental association.

Stress, tobacco exposure, infections, alcohol use, hormones, skin trauma and possible medications have been implicated triggers for the first occurrence or subsequent outbreaks of psoriasis.

Pathogenesis involves environmental factors and immune dysregulation in patients with a genetic predisposition.

Psoriatic skin lesions are a focus of T cell mediated immunity with dendritic cells and macrophages in the presence of inflammatory cytokines and other mediators.

Activation of parts of the adaptive immune system is thought to be central to its pathogenesis: A variety of cell types including plasmacytoid dendritic cells, keratinocytes, natural killer T cells and macrophages, secrete cytokines to activate myeloid dendritic cells.
Activated myeloid dendritic cells induce native T cells to TH1 cells and secrete IL-12 and I L-23.
IL-23 mediated activation of T cell pathways predominant and signals pathways which lead to transcription of key inflammatory mediators.

The cytokines lead to downstream Keratinocyte proliferation, increased expression of angiogenic mediators and endothelial adhesion molecules, and infiltration of immune cells into skin lesions.

High production of inflammatory elements within the psoriatic plaque can migrate systemically and expose other tissues, such as the arterial circulation to high levels of inflammation leading to a pro atherosclerotic state.

Patients with psoriasis have accelerated coronary artery disease and increased risk of myocardial infarction.
Patients with psoriasis have a 40-80% increase in the risk of coronary ischemic events.
The risk of coronary artery disease is markedly increased in younger patients with early onset and clinically severe or prolonged  psoriasis.
The risk of coronary artery disease in patients with psoriasis is increased 3-9 fold.
Increase coronary artery disease in psoriasis  cannot be explained by changes in body weight, blood pressure, lipids, or glucose and coronary plaques exhibit high risk features for plaque rupture.
Coronary artery plaques regress following the use of anti-cytokine agents for psoriasis and also reduce the risk of myocardial infarction.
Antagonist of pro inflammatory cytokines commonly used for the treatment of psoriasis ameliorates coronary artery disease and aortic vascular inflammation, and a reduction in the risk of myocardial infarction.(similar benefits are not observed with topical therapies).
Patients with psoriasis have a 50% increase the incidence of atrial myopathy leading to atrial fibrillation.
Patients with psoriasis have a 30-60% increase in the incidence of heart failure.
Patients with psoriasis often have increased circulating levels of natriuretic peptides and impaired diastolic filling: Hallmarks of heart failure with preserved ejection fraction.

Plaque psoriasis is the most common form of psoriasis, experienced by 80-90 percent of patients with psoriasis.

Plaque psoriasis has a predilection for the hairy scalp, the extensor surfaces of the elbows, knees, and gluteal cleft.

Lesions in plaque psoriasis can range from small erythematous and scaly papules to large thick plaques.

Areas of plaque psoriasis characteristically are well demarcated in often symmetric.

Plaque lesions present with thick erythematous sharply marginated plaques with characteristic silvery scale.

Psoriasis typically appears as raised, red patches covered with a silvery white buildup of dead skin cells or scale. 


On skin of color, the discoloration is darker and thicker, more of a purple or grayish color or darker brown.


Such  patches or plaques most often appear on the scalp, knees, elbows and lower back. 


They range from coin-size to palm-size, and are often itchy and painful.


The lesions can crack and bleed.


Plaque psoriasis is most often located on the outside of knees and elbows, the scalp, the lower back, the face, the palms and soles of feet. 

In general, psoriasis is asymptomatic, but in some cases may be pruriticd or tender.

Other types of psoriasis are less frequent and have a different distribution and

characteristics of lesions.

Psoriasis vulgaris, plaque psoriasis: is frequently painful and often debilitating.

Worldwide prevalence 0.1 to 3%.

The burden of disease is directly related to its prevelence: ranges from 0.5-11.4% in adult, and 0%-1.4% and children worldwide.

Chronic, relapsing inflammatory process of the skin affecting 2-3% of global adult population.

More than 125 million patients suffer with psoriasis worldwide.

Affects more than 7.4 million Americans and 2% of the world’s population.

Prevalence in US ranges from 0.5-4.6%.

Seen mostly in adults.

79% of patients with severe disease have adverse affects on their lives and activities of daily living.

Disease ranges from just a few spots on the elbows, knees, or scalp to severe systemic involvement.

Most frequent symptoms include scaling, itching and burning sensation.

Pustular variants are rare.

Pustular psoriasis can develop independently or in association with pre-existing psoriasis.

Pustular psoriasis is most often seen in middle aged adults but can occur in children.

Pustular psoriasis has been linked to URI, pregnancy, withdrawal of steroids, hypocalcemia, and medications such as interferon, lithium, penicillin, cyclosporine, salicylates, and tumor necrosis factor alpha inhibitors.

Pustular psoriasis can be localized

Pustular psoriasis characterized by acute, subacute or chroniic eruption of sterile pustules associated with erythema and inflammation.

Pustular psoriasis can be generalized and is associated with interleukin 36 receptor antagonist sequence variation.

Commonly associated with depression, anxiety and suicidal ideation.

Up to 10% of patients consider suicidal ideation.

US estimated prevalence estimated at 3%, with approximately 17% having moderate-severe plaque disease.

Psoriasis vulgaris is the most common form of the disease, accounting for 80-90% of cases.

Psoriasis vulgaris characterized by papulosquamous plaques of varying size and number.

Onset at any age, but usually between ages 18-35 years.

Affects men and women equally and adults more than children.

Bimodal onset is suggested with initial peak 16-22 years and a second peak 57-60 years.

Characterized by inflammatory changes and keratinocyte hyper proliferation, probably a consequence of T cell mediated immunity to a presently unidentified auto antigen.

An immune-mediated inflammatory process of the skin that affects up to 3% of the population.

Alters the skin barrier, and is associated with T-cell driven immune responses with involvement of the skin and other sites such as joints.

Pro-inflammatory interleukin-12-mediated type 1 helper T (Th1) cell and interleukin-23-mediated type 17 helper T (Th17) cell signaling pathways are upregulated in psoriatic lesions.

Antibodies that inhibit interleukin-12 and interleukin-23 and interleukin-17 inhibit the expression of molecular and clinical disease characteristics associated with psoriasis.

Interleukin-12 induces the development of Th1 cells.

IL-17 essential to the formation of psoriatic skin lesions.

Interleukin-23 is required for terminal differentiation of Th17 cells, and the maintenance of Th

17 phenotype.

Th17 cells produce interleukin17 and interleukin22 which have pro inflammatory effects in skin and are related to the pathogenesis of psoriasis

Caused by an immune response driven by Th1 cells, which secrete high levels of interferon-gammaanf by Th17 cells which secrete interleukin 17A, interleukin 17F, and interleukin 22.

T-helper 1 cells of adaptive cellular immune system are essential to plaque development and inflammation propagates psoriasis and atherosclerosis.

Activated T-helper cells release proinflammatory cytokines interferon-gamma, IL-2and TNF-alpha.

Released cytokines activate macrophages, keratinocytes and vascular cells, which further release cytokines.

Downstream cytokine molecules including IL-6 and acute phase reactants are produced in also result in up regulation vascular adhesion molecules with recruitment of more leukocytes.

Upregulated genes in atherosclerosis include recognizable psoriasis pro inflammatory cytokines including IL-8 IL-36 and chemokine ligand.

The biology of psoriasis mirrors that of atherosclerosis.

Plaque psoriasis is a chronic skin disease that can cause patches of a person’s skin to become inflamed and thicken.

Plaque psoriasis accounts for more than 80% of psoriasis cases.
Plaque psoriasis occurs commonly on extensive surfaces, but it can also affect intertriginous  areas, palms, souls, and nails.
Clinical variants include plaque, guttate, erythrodermic, and pustular psoriasis.
All psoriasis variants share three  clinical features: erythema, thickening, and scale.

One variant typically predominates in an individual, different variants make coexist in a person at any single point in time.

These patches can be covered with slivery scales, and can cause pain, itching, and discomfort.

Most people with plaque psoriasis experience cycles of the disease.

Avoiding psoriasis triggers is an important part of managing the disease, reducing its symptoms, and improving quality of life.

Each person with plaque psoriasis has a different set of triggers.

Some patients have more triggers than others.

Some triggers affect certain people but not others.

Some triggers that are common among people with plaque psoriasis include:


Skin injuries


Lifestyle and environmental triggers: stress, smoking, drinking alcohol heavily, diet, allergies and weather.

Any type of infection in the body can be a trigger for plaque psoriasis or other types of psoriasis, in particular, guttate psoriasis.

Cuts, scrapes, and scratches, vaccinations, surgeries, bug bites, or sunburns other common types of skin injury that can trigger psoriasis.

Skin injury psoriatic trigger is known as the Koebner phenomenon.

In the Koebner phenomenon new psoriasis lesions can develop at the site of trauma, such as from scratching, cuts, or pressure.
Lifting plaque psoriasis scale is associated with pinpoint bleeding and may create Auspitz sign.

Plaque psoriasis patients can experience substantial pruritud  with moderate to severe psoriasis or during exacerbation.

Medications may be triggers for psoriasis and include:

Beta blockers

Antimalarial medicines




Seasonal allergies and weather changes that dry out the skin can trigger their psoriasis symptoms.

Approximate 30% of patients will develop psoriatic arthritis (Gladdman DD).

In approximately 85% of patients with psoriatic arthritis, psoriasis either precedes or occurs concurrently with psoriatic arthritis.

Psoriatic  arthritis is characterized by stiffness, pain, and swelling of joints and can progress to debilitating joint destruction

Affects nails and joints in 5-20% of cases.

Nail changes are present in up to 50% of patients with skin psoriasis.

Psoriatic arthritis may precede nail changes by 15 years.

Both finger and toe nail changes may be present and changes based on the location involved within the nail unit.

Most commonly, irregular nail pitting, nail plate thickening, and onycholysis are present.

Nail pathognomonic features include the presence of oil stains there is diagnostically useful for distinguishing nail psoriasis from a fungal infection.

Psoriatic arthritis affects peripheral and axial joints, entheses, or tendon insertions.

Axial involvement which is related to the prevalence of HLA-B27 which is higher in individuals of the White race, especially of northern European descent.

Predisposes patients to arthritis, metabolic syndrome, cardiovascular disease, insulin resistance, hypertension, and other diseases that involve endothelial dysfunction, atherosclerosis depression, malignancy, and inflammatory bowel disease.

Psoriasis associated with a four times greater prevalence of inflammatory bowel disease.

Patients with severe psoriasis will those who develop psoriasis at a young age are at a higher risk for cardiometabolic comorbidities in the general population.

psoriasis is associated with vascular inflammation and high risk coronary atherosclerotic plaques.

The proportion of psoriasis patients with moderate to severe coronary artery calcification is similar to those with type two diabetes.

Severe psoriasis is associated with a high risk coronary atherosclerotic plaques, increased risk of myocardial infarction, stroke, and cardiovascular mortality.

It targets adipose tissue depots especially around the heart and blood vessels resulting in adipocyte dysfunction and insulin resistance manifested as the metabolic syndrome, which is present in about 20-40% of patients with psoriasis.

The metabolic syndrome is especially seen in patients with early onset or severe disease or with accompaning arthropathy.

Chronic T cell mediated immune disease.

Studies show a subgroup of CD4+ T cells and 17 helper T (Th17) cells, has a role in the pathogenesis of psoriasis.

Type 17 helper T cells secrete pro-inflammatory cytokines including interleukin-17A.

Interleukin-17 levels elevated in skin lesions and blood of patients with psoriasis and correlates with disease severity.

Interleukin-17A is the primary effector of the Th17 cells and is also produced by other cell types in psoriatic lesions including neutrophils, possibly mast cells and gamma/delta T cells.

Interleukin-17A stimulates keratinocytes to secrete chemokines and other pro-inflammatory mediators that recruit additional inflammatory cells including neutrophils, dendritic cells, lymphoid cells and Th17 cells.

Interleukin-17 cytokine family has 6 cytokines, interleukins A-F and 5 receptors, interleukins 17RA to 17RE.

Patients may develop co-morbidities such as metabolic syndrome, coronary artery disease, diabetes, and cerebral vascular disease along with psoriatic arthritis.

Associated with adverse cardiovascular outcomes that is most pronounced among young patients with severe psoriasis.

Patients with psoriasis demonstrate an expansion of epicardial adipose tissue bass, related to systemic inflammation and is associated with the presence in severity of coronary artery disease.

59% increase in prevalence and 27% increase incidence of diabetes.

Studies show an 18% increased risk of developing cancer with psoriasis.

Patients with severe psoriasis have a 22% increase in the risk of developing cancer.

Psoriasis associated with cancer risk: oral cancer three times higher, esophageal cancer two times higher, squamous cell carcinoma risk doubled, risk of liver cancer 83% higher, laryngeal cancer 79% higher, skin cancer 71% higher, and the risk of developing kidney pancreatic and colon rectal cancer as well as lymphoma or non-Hodgkin’s lymphoma are also is elevated (JAMA Dec , 2019).

Patients increase risk of chronic kidney disease, and the more severe psoriasis associated with a higher risk.

TNF Inhibitors associated with a significant reduction in MI risk compared with topical agents and associated with a non-statistically significant lower MI incident rate compared with treatments with oral agents or phototherapy.

Obesity a risk factor for the development of psoriasis, and is associated with increased the severity of psoriasis (Wilson FC).

Weight loss can ameliorate the severity of psoriasis, and it also reduces epicardial fat volume, improves atrial and ventricular geometry, and reduces the risk of both atrial fibrillation  and heart failure.

The use of anti-diabetic medications have favorable clinical responses in psoriasis, presumably because of amelioration of adipose tissue dysfunction that minimizes at the adipocytokine promoted dermal inflammation.

Generalized pustular psoriasis is a life-threatening, multi-systemic inflammatory disease with repeated flareups with diffuse erythematosus, pustular rash with high-grade fever, malaise and extra cutaneous organ involvement.

Generalized pustular psoriasis is often observed in the presence of psoriasis vulgaris and involves recruitment of T cells and neutrophils.

Ethnic factors influence the prevalence with black Americans having a prevalence of 0.45-0.7% compared to 1.4-4.6% among the remainder of the U.S. population.

Compelling evidence for genetic predisposition but inheritance pattern is not clear.

The disease follows mendelian transmission in a small minority of families.

As many as half the siblings of parents that both have psoriasis have the disease.

The prevalence of psoriasis is 16% in children with one parent with the disease.

The prevalence of psoriasis is 8% when neither parent has psoriasis.

One third of adults have onset at or before age 16.

Compelling evidence for genetic predisposition but inheritance pattern is not clear.

As many as half the siblings of parents that both have psoriasis have the disease.

The prevalence of psoriasis is 16% in children with one parent with the disease.

The prevalence of psoriasis is 8% when neither parent has psoriasis.

Concordance rate for monozygotic twins is about 70% compared to 20% for dizygotic twins.

Children with psoriasis have a positive family history in up to 71% of cases.

Plaques commonly occur on areas of the skin exposed to mechanical trauma.

Plaque severity and extent of affected body surface area varies throughout lifetime.

Skin lesions of psoriasis or try sharply demarcated, red, scaly plaques with variable patterns and body distribution and commonly affects the scalp, the extensor surfaces of the elbows and knees, the emboli kiss, the gluteal cleft and the nails.

May be more common in obese individuals.

Associated with increased serum leptin levels and is independent of female sex, obesity and metabolic syndrome.

Associated with depression, myocardial infarction, inflammatory bowel disease, arthritis , malignancy, and metabolic syndrome.

Patients with psoriasis more likely than controls to have increased cardiovascular risks, hypertension, diabetes, hyperlipidemia and obesity.

Higher prevalence of cardiovascular atherosclerotic diease, CHF, peripheral vascular disease and cerebrovascular disease compared with controls.

Psoriasis and atopic dermatitis are associated with increased prevalence of coronary artery disease.

Patients with psoriasis of increased prevalence of severe coronary artery disease.

Immune mechanisms results in plaques in the skin and in arteries.

Classical distribution includes the elbows, knees and scalp, umbilicus and lumbar area.

About 70% to 90% of patients suffer from pruritus.

Nail involvement is common and up to 30% have psoriatic arthritis.

The finger nails are affected more frequently than the toenails with 50% and 35% involvement, respectively.

Nail changes range from pitted areas to yellowish discoloration and severe onchodystrophy.

A psoriatic diaper rash is the most common type of lesions in children under the age of two years.

A lifelong illness with periods of exacerbation and quiescence.

Joint involvement occurs in 15 to 30% of patients with involvement of the distal intenrphalangeal joint in a symmetric fashion.

Diagnosis is based on physical examination and laboratory or histopathology confirmation is rarely required.

If adherent scale is removed, pinpoint bleeding may be evident and referred to Auspitz sign.

Guttate psoriasis accounts with 2% of cases and is characterized by multiple confetti like,  pink scaly patches.

Approximately 2/3 of the new onset guttate psoriasis is proceeded by a upper respiratory tract infection such as a streptococcal infection, and in most cases resolve in weeks to months but can become chronic.

Erythrodermic psoriasis is uncommon: patients have coalescent erythema, scales or exfoliation involving at least 75% of the body.

Erythrodermic psoriasis occurs in 2 to 3% of psoriasis cases.

Erythrodermic psoriasis Is a medical emergency as it can be associated with electrolyte disturbances and life-threatening desquamation.

Differential diagnosis includes Inflammatory, infectious, and neoplastic conditions: atopic  dermatitis,  seborrheic  dermatitis,  pityriasis rosacea, syphilis, cutaneous T-cell lymphoma, eczema, and systemic lupus.

Patients with mild disease can be managed with topical therapies such as vitamin D analogues, retinoids, corticosteroids, and tar.

First treatment is to address and treat psychological concerns.

The overall treatment for psoriasis begins with evaluation of psoriatic arthritis, regardless of the extent of the psoriasis.

The presence of active psoriatic arthritis may alter the treatment choices in favor of options that affect both psoriasis and psoriatic arthritis.

Patients with localized lesions usually are treated with topical agents and possibly localized ultraviolet phototherapy.

Treatment choices of usually depends on disease.

The definition of mild psoriasis typically involves less than 3 to 5% of the affected body surface area.

For mild psoriasis treatment options include topical corticosteroids, vitamin D analogues, calcineurin inhibitors, keratolytics, and targeted phototherapy.

Topical vitamin D analogues bind to vitamin D receptors on T cells and vitamin D receptors on keratinocytes to block keratinocyte proliferation and boost keratinocyte differentiation.

Topical vitamin D analogues have modest benefit in psoriasis when used alone.

Vitamin D analogues primary adverse effect is burning and irritation which occurs in up to 35% of patients and typically lessen overtime..

Topical therapies remain the mainstay of treatment for most patients regardless of disease severity.

Topical therapies are associated with poor adherence to treatment and patient satisfactory due to the properties of the formulation and vehicle and difficulty of application.

Topical Treatments slow down skin cell growth and reduce inflammation.

Topical corticosteroids are anti-inflammatory, anti-proliferative, and locally vasoconstrictive by down regulating genes coding pro inflammatory cytokines.

Topical calcineurin and inhibitors block T cell activation by inhibiting the synthesis of IL-2  and interferon-gamma.

Topical calcineuron inhibitors include tacrolimus and pimecrolimus, frequently used to treat psoriasis in facial and intertriginous  areas without the adverse effect of skin atrophy.

Woth topical calcineurin inhibitors is many is 71% of patients experience clear almost clear psoriasis after eight weeks.

Common adverse effects of calcineurin topical inhibitors include skin irritation.

Topical keratolytics includes topical tazarotene and salicylic acid.

Tazarotene is a retinoid that inhibits proliferation of keratinocytes and breaks down the thick scales on the plaque.

Topical salicylic acid is a keratolytic that reduces scaling but is associated with irritation.

Phototherapy involves exposing the skin to ultraviolet light on a regular basis.

Phototherapy delivers specific wavelengths in a therapeutic for psoriasis and minimizes emission of wavelengths responsible for carcinogenesis.

The use the photo therapy has decreased since the advance of biologic agents.

Systemic medications are taken orally, by injection or infusion, and include biologics.

There are four classes of biologics used to treat psoriasis: TNF inhibitors, IL-12/23 inhibitor, IL-17 inhibitors, and IL-23 inhibitors.

IL-17 inhibitors have fast onet of action, robust response, and sustainability in treating plaque psoriasis.

All biologics used to treat psoriasis are administered subcutaneously, except infliximab.

There are no increased rates of serious infections or internal malignancies in patients with psoriasis treated with biologics.

Adverse effects that occur include injection site reactions, nasal pharyngitis, and URIs.

Patients with extensive disease may require phototherapy or systemic agents along with topical treatment of the worst lesions.

The main types of phototherapy used to treat psoriasis include UV B narrow or broadband psoralen and UVA.

Narrowband UV B is preferred over broadband form because it is more efficacious, and has a better safety profile.

Psoralen’s intercalate into DNA.

Topical corticosteroids are the first agents for localized lesions with good efficacy in the treatment of mild to moderate disease.

Topical glucocorticoids are effective in the treatment of psoriasis, but use is  limited to no more than 2-8 weeks, and may be associated with adverse events that resolve slowly such as skin atrophy, or that are irreversible with long-term use such as striae.

Topical corticosteroids can vary from low potency agents such as hydrocortisone, to medium potency such is triamcinolone, to high potency betamethasone and ultra high potency clobetasol.

UV B decreases DNA synthesis call, leading to keratinocyte apoptosis and decreased production of pro-inflammatory cytokines by T cells.

UV-B consists of 290 to 320nm and narrowband 311 bandwidths.

Photo therapy adverse effects include erythema, pruritis, blistering, photoaging, and photo  carcinogenesis.

PUVA involves the use of psotpsoralen administered orally or topically prior to UV A radiation.

Psoralens are used to Intercal lead into DNA to suppress DNA synthesis.

The use of PUVA is associated with the development of skin cancer with long-term use, and known adverse effects include gastrointestinal upset burning, pruritus, hypotrichosis, and photo aging.

Topical PUVA typically is used for palmoplanter psoriasis and involves soaking hands and feet in the water with psoralen and then being irradiated by UV-A.

Low potency corticosteroids are utilized for the face and genitalia areas, while higher potency agents are used for thicker plaques on the body and scalp.

Topical corticosteroids maybe utilized in combination with other measures.

Targeted phototherapy/laser therapy is effective but less convenient than topical treatment.

Laser therapy is preferred over whole body therapy for localized psoriasis, since it spares uninvolved skin from UV radiation and allows higher doses to be used, speeds the response to treatment and reduces the risks.

Formulation such as foams and sprays are available to improve ease of use.

Patients treated with topical corticosteroids should be monitored for adverse affects such as skin atrophy and the rare event of hypothalamic-pituitary-adrenal axis suppression.

Possible skin reactions to topical steroids include telangiectasia, acne exacerbation, skin hypopigmentation, hyperpigmentation, or secondary skin infections.

The vitamin D analogues calcipotriene and calcitriol can be effective, but tends to work very slowly.

Topical Treatments for Chronic Plaque Psoriasis

Vitamin D analogs are safe and effective in the treatment of psoriasis; however, corticosteroids are as effective with less skin irritation.

Chronic plaque psoriasis is the most common type of psoriasis and is characterized by redness, thickness, and scaling.

First-line management of chronic plaque psorias is with topical treatments.

Corticosteroids were more effective than vitamin D for treating psoriasis of the scalp.

For both body and scalp psoriasis, potent corticosteroids were less likely than vitamin D to cause skin irritation.

Vitamin D preparations in combination with topical corticosteroids speed the rate of disease improvement and reduce the risks of skin irritation from the former and dosage of the latter.

Tazarotene is a topical retinoid that can be used in combination with topical corticosteroids.

Tazarotene is less effective and more irritating agent than topical vitamin D, and must be avoided in pregnancy.

Topical ((roflumilast)) cream is effective for psoriasis for chronic plaque psoriasis.

Some define psoriasis as moderate when it covers 3 to 10% of the body surface area,, whereas others define it as coverage of 5 to 10% of the body surface area.

Severe psoriasis is typically considered body surface area coverage of 10% or greater.

Systemic treatments are the mainstay of moderate and severe psoriasis: biologics, oral agents, and phototherapy.

Treatment of moderate to severe psoriasis usually requires phototherapy and systemic therapy such a cyclosporine, methotrexate, retinoids, on biological drugs to include TNF-alpha blocking agents.

Drugs for treating plaque psoriasis: advances in treatment include a use of monoclonal antibodies, tumor metachrosis factor alpha inhibitors, agents that target Interleukin 12 and Interleukin 23, Interleukin 17 A and 17 F.

Most studies that show drug improvement in skin findings do not, however, affectcardiovascular and metabolic risks.

Methotrexate and cyclosporine have equal efficacy in the treatment of moderate to severe psoriasis.

Use of oral methoxasalen and ultraviolet A radiation in the treatment of psoriasis is associated with elevated risk of squamous cell carcinoma of the skin.

Topical immunomodulator tacrolimus and pimecrolimus are used in sensitive skin sites such as the face of genital areas.

Unlike topical corticosteroids, immunomodulators do not have adverse skin changes such as atrophy, telangiectasia, or permanent purple striae.

Utilized to treat psoriasis in adults and reduces severity of disease in children and adolescents with moderate to severe plaque psoriasis.

Cytokines such as a tumor necrosis factor-alpha, play a central role in the inflammation seen in psoriasis and agents that block TNF-alpha are effective in treatment.

Cytokines IL-12 and IL-23 induce CD4+ lymphocytes to differentiate into type 1 helper T cells and type 17 helper T cells, respectively, and are mediators of this process.

Inhibition of interleukin-17A is a targeted approach to management of psoriasis.

Brodalumab, a human, anti-interleukin-17RA monoclonal antibody that antagonizes the intereukin-17 pathway.

Brodalumab binds with high affinity to human interleukin-17RA.

Brodalumab blocks biologic activity of IL_ 17A, 17F, and 17E.

Brodalumab significantly improves plaque psoriasis (Papp KA et al).

Anti-interleukin-17 monoclonal antibody Ixekizumab in chronic/psoriasis improves clinical symptoms (Leonardi C et al).

Efalizumab reduces frequency and severity of psoriasis symptoms.

In a randomized trial of 903 patients with moderate to severe disease comparing ustekinumab an agent that blocks IL-12 and IL-23, to etanercept a TNF-alpha inhibitor: ustekinumab is superior to etanercept over a 12 week perod in improving psoriasis (Griffiths GEM).

Adalimumab more effective in psoriasis, in direct comparison to methotrexate, 16 weeks after initiating treatment(Saurat JH).

Spesilimab an interleukin-36 receptor inhibitor impatient with generalized pustular psoriasis results in a higher incidence of lesion clearance at one week then placebo buddies associate with infections in systemic drug reactions.

Clinical trials rely on the Psoriasis Area and Severity Index (PASI): scores range from 0 to 72 with higher scores, indicating greater extent of severity of psoriasis. A 75% reduction in the PASI score is the primary endpoint and the 90% reduction is similar to a result of clear or early clear skin.


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