Psoriasis is a complex, chronic, multifactorial, inflammatory disease that involves hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell turnover rate (see the image below). Environmental, genetic, and immunologic factors appear to play a role. The disease most commonly manifests on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans penis. In up to 30% of patients, the joints are also affected.
Treatment is based on surface areas of involvement, body site(s) affected, the presence or absence of arthritis, and the thickness of the plaques and scale.
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Plaque psoriasis is raised, roughened, and covered with white or silver scale with underlying erythema. Contributed by Randy Park, MD.
See Psoriasis: Manifestations, Management Options, and Mimics, a Critical Images slideshow, to help recognize the major psoriasis subtypes and distinguish them from other skin lesions.
Signs and symptoms
Signs and symptoms of psoriasis may include the following:
Worsening of a long-term erythematous scaly area
Sudden onset of many small areas of scaly redness
Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma
Pain (especially in erythrodermic psoriasis and in some cases of traumatized plaques or in the joints affected by psoriatic arthritis)
Pruritus (especially in eruptive, guttate psoriasis)
Afebrile (except in pustular or erythrodermic psoriasis, in which the patient may have high fever)
Dystrophic nails, which may resemble onychomycosis
Long-term, steroid-responsive rash with recent presentation of joint pain
Joint pain (psoriatic arthritis) without any visible skin findings
Conjunctivitis or blepharitis
See Clinical Presentation for more detail.
Diagnosis
The diagnosis of psoriasis is clinical, and the type of psoriasis present affects the physical examination findings.
Types of psoriasis
Common types of psoriasis include the following:
Chronic stationary psoriasis (psoriasis vulgaris): Most common type of psoriasis; involves the scalp, extensor surfaces, genitals, umbilicus, and lumbosacral and retroauricular regions
Plaque psoriasis: Most commonly affects the extensor surfaces of the knees, elbows, scalp, and trunk
Guttate psoriasis: Presents predominantly on the trunk; frequently appears suddenly, 2-3 weeks after an upper respiratory tract infection with group A beta-hemolytic streptococci; this variant is more likely to itch, sometimes severely
Inverse psoriasis: Occurs on the flexural surfaces, armpit, and groin; under the breast; and in the skin folds; this is often misdiagnosed as a fungal infection
Pustular psoriasis: Presents on the palms and soles or diffusely over the body
Erythrodermic psoriasis: Typically encompasses nearly the entire body surface area with red skin and a diffuse, fine, peeling scale
Scalp psoriasis: Affects approximately 50% of patients
Nail psoriasis: May be indistinguishable from, and more prone to developing, onychomycosis
Psoriatic arthritis: Affects approximately 10-30% of those with skin symptoms; usually in the hands and feet and, occasionally, the large joints
Oral psoriasis: May present as severe cheilosis, with extension onto the surrounding skin, crossing the vermillion border
Eruptive psoriasis: Involves the upper trunk and upper extremities; most often seen in younger patients
Napkin psoriasis: Presence of psoriasis in children's diaper region
Linear psoriasis: Psoriasis that occurs within a dermatome
Examination in patients with psoriasis includes the following:
Dermatologic: Most commonly, scaling erythematous macules, papules, and plaques; area of skin involvement varies with the form of psoriasis
Ocular: Ectropion and trichiasis, conjunctivitis and conjunctival hyperemia, and corneal dryness with punctate keratitis and corneal melt[1] ; blepharitis
Musculoskeletal: Stiffness, pain, throbbing, swelling, or tenderness of the joints; distal joints most often affected (eg, fingers, toes, wrists, knees, ankles); may progress to a severe and mutilating arthritis of the hands, especially if treatment has been suboptimal
Testing
There is no specific or diagnostic blood test for psoriasis. Laboratory studies and findings for patients with psoriasis may include the following:
Rheumatoid factor level: Negative
Erythrocyte sedimentation rate: Usually normal, except in pustular and erythrodermic psoriasis, where it may be elevated along with the white blood cell count
Uric acid level: May be elevated in psoriasis (especially in pustular psoriasis)
Examination of fluid from pustules: Sterile bacterial culture with neutrophilic infiltrate
Fungal studies: Especially important in cases of hand and foot psoriasis that seem to be worsening with the use of topical steroids or to determine if psoriatic nails are also infected with fungus
Conjunctival impression cytology: Increased incidence of squamous metaplasia, neutrophil clumping, and snakelike chromatin
The differentiation of psoriatic arthritis from rheumatoid arthritis and gout can be facilitated by the absence of the typical laboratory findings of those conditions.
Consider obtaining the following baseline laboratory studies in patients being initiated on systemic therapies (eg, immunologic inhibitors):
CBC count
BUN and creatinine levels
Liver function tests
Hepatitis panel
TB screening
HIV testing
Pregnancy test
Other studies
Radiographs of affected joints: Can be helpful in differentiating types of arthritis
Joint radiographs: Can facilitate the diagnosis of psoriatic arthritis
Bone scans: Can identify joint involvement early
Dermatologic biopsy: Can be used to make the diagnosis when some cases of psoriasis are difficult to recognize (eg, pustular forms)
See Workup for more detail.
Management
Pharmacotherapy
Medications used in the management of psoriasis include the following:
Intramuscular corticosteroids (eg, triamcinolone): Requires caution because the patient may have a significant flare as the medication wears off; 3 months should elapse between injections
Intralesional corticosteroids: May be useful for resistant plaques and for the treatment of psoriatic nails
Coal tar 0.5-33%
Keratolytic agents (eg, anthralin, urea): Use of these medications may facilitate more direct steroid contact with the skin
Vitamin D analogs (eg, calcitriol ointment, calcipotriene, calcipotriene and betamethasone topical ointment)
Topical retinoids (eg, tazarotene aqueous gel and cream 0.05% and 0.1%)
The American Academy of Dermatology (AAD) guidelines recommend treatment with methotrexate, cyclosporine, and acitretin, with consideration of contraindications and drug interactions.[6]
A 2013 international consensus report on treatment optimization and transitioning for moderate-to-severe plaque psoriasis include the following recommendations[7] :
Methotrexate, for as long as it remains effective and well-tolerated
Cyclosporine, generally used intermittently for inducing a clinical response with one or several courses over 3-6 months
Transition from conventional systemic therapy to a biologic agent, either directly or with an overlap if transitioning is needed due to lack of efficacy, or with a treatment-free interval if transitioning is needed for safety reasons
Combination therapy
Continuous therapy for patients receiving biologic agents
Switching biologic agents: If due to lack of efficacy, perform without a washout period; if for safety reasons, a treatment-free interval may be required
Combinations of multiple agents (eg, methotrexate and a biologic) are necessary in some patients but the long-term safety and optimal laboratory monitoring have yet to be defined
Other therapies
Management of psoriasis may also involve the following nondrug therapies:
Light therapy with solar or ultraviolet radiation
Stress reduction
Biofeedback
Climatotherapy
Adjuncts, such as sunshine, sea bathing, moisturizers, oatmeal baths
Punctal occlusion (and ocular lubricants): For keratoconjunctivitis sicca
Bandage contact lens: To retard corneal melting
Surgical option
Ocular manifestations such as trichiasis and cicatricial ectropion usually require surgical treatment. Progression of corneal melting, inflammation, and vascularization may require lamellar or penetrating keratoplasty.
Psoriasis is a chronic, noncontagious, multisystem, inflammatory disorder. Patients with psoriasis have a genetic predisposition for the illness, which most commonly manifests itself on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans penis. The joints are also affected by psoriasis in up to 30% of patients with the disease. (See Pathophysiology and Etiology.)
Psoriasis has a tendency to wax and wane with flares related to systemic or environmental factors, including life stress events and infection. It impacts quality of life and potentially long-term survival. There should be a higher clinical suspicion for depression in the patient with psoriasis. (See Prognosis.)
Multiple types of psoriasis are identified, with plaque-type psoriasis, also known as discoid psoriasis, being the most common type. Plaque psoriasis usually presents with plaques on the scalp, trunk, and limbs (see the image below). These plaques appear as focal, raised, inflamed, edematous lesions covered with silvery-white “micaceous” scales. (See Clinical Presentation.)
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Plaque psoriasis is most common on the extensor surfaces of the knees and elbows. Contributed by Randy Park, MD.
Ocular signs occur in approximately 10% of psoriasis patients, and they are more common in men than in women. Patients with ocular findings almost always have psoriatic skin disease; however, it is rare for the eye to become involved before the skin.[8]
The diagnosis of psoriasis is clinical. (See Workup.) Management of psoriasis may involve topical or systemic medications, light therapy, stress reduction, climatotherapy, and various adjuncts such as sunshine, moisturizers, and salicylic acid. (See Treatment and Management.)
Psoriasis is a complex, multifactorial disease that appears to be influenced by genetic and immune-mediated components. This is supported by the successful treatment of psoriasis with immune-mediating, biologic medications.
The pathogenesis of this disease is not completely understood. Multiple theories exist regarding triggers of the disease process including an infectious episode, traumatic insult, and stressful life event. In many patients, no obvious trigger exists at all. However, once triggered, there appears to be substantial leukocyte recruitment to the dermis and epidermis resulting in the characteristic psoriatic plaques.
Specifically, the epidermis is infiltrated by a large number of activated T cells, which appear to be capable of inducing keratinocyte proliferation. This is supported by histologic examination and immunohistochemical staining of psoriatic plaques revealing large populations of T cells within the psoriasis lesions. One report calculated that a patient with 20% body surface area affected with psoriasis lesions has around 8 billion blood circulating T cells compared with approximately 20 billion T cells located in the dermis and epidermis of psoriasis plaques.[9]
Ultimately, a ramped-up, deregulated inflammatory process ensues with a large production of various cytokines (eg, tumor necrosis factor-α [TNF-α], interferon-gamma, interleukin-12). Many of the clinical features of psoriasis are explained by the large production of such mediators. Interestingly, elevated levels of TNF-α specifically are found to correlate with flares of psoriasis.
One study adds further support that T-cell hyperactivity and the resulting proinflammatory mediators (in this case IL-17/23) play a major role in the pathogenesis of psoriasis.[10]
Key findings in the affected skin of patients with psoriasis include vascular engorgement due to superficial blood vessel dilation and altered epidermal cell cycle. Epidermal hyperplasia leads to an accelerated cell turnover rate (from 23 d to 3-5 d), leading to improper cell maturation.
Cells that normally lose their nuclei in the stratum granulosum retain their nuclei, a condition known as parakeratosis. In addition to parakeratosis, affected epidermal cells fail to release adequate levels of lipids, which normally cement adhesions of corneocytes. Subsequently, poorly adherent stratum corneum is formed leading to the flaking, scaly presentation of psoriasis lesions, the surface of which often resembles silver scales.
Conjunctival impression cytology demonstrated a higher incidence of squamous metaplasia, neutrophil clumping, and nuclear chromatin changes in patients with psoriasis.[11]
Psoriasis involves hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell turnover rate. (See Pathophysiology.) The cause of the loss of control of keratinocyte turnover is unknown. However, environmental, genetic, and immunologic factors appear to play a role.
Environmental factors
Many factors besides stress have also been observed to trigger exacerbations, including cold, trauma, infections (eg, streptococcal, staphylococcal, human immunodeficiency virus), alcohol, and drugs (eg, iodides, steroid withdrawal, aspirin, lithium, beta-blockers, botulinum A, antimalarials). One study showed an increased incidence of psoriasis in patients with chronic gingivitis. Satisfactory treatment of the gingivitis led to improved control of the psoriasis but did not influence longterm incidence, highlighting the multifactorial and genetic influences of this disease.[12]
Hot weather, sunlight, and pregnancy may be beneficial, although the latter is not universal. Perceived stress can exacerbate psoriasis. Some authors suggest that psoriasis is a stress-related disease and offer findings of increased concentrations of neurotransmitters in psoriatic plaques.
Genetic factors
Patients with psoriasis have a genetic predisposition for the disease. The gene locus is determined. The triggering event may be unknown in most cases, but it is likely immunologic. The first lesion commonly appears after an upper respiratory tract infection.
Psoriasis is associated with certain human leukocyte antigen (HLA) alleles, the strongest being human leukocyte antigen Cw6 (HLA-Cw6). In some families, psoriasis is an autosomal dominant trait. Additional HLA antigens that have shown associations with psoriasis and psoriatic subtypes include HLA-B27, HLA-B13, HLA-B17, and HLA-DR7.[13]
A multicenter meta-analysis confirmed that deletion of 2 late cornified envelope (LCE) genes, LCE3C and LCE3B, is a common genetic factor for susceptibility to psoriasis in different populations.[14]
Obesity is another factor associated with psoriasis. Whether it is related to weight alone, genetic predisposition to obesity, or a combination of the 2 is not certain. Onset or worsening of psoriasis with weight gain and/or improvement with weight loss is observed.
Immunologic factors
Evidence suggests that psoriasis is an autoimmune disease. Studies show high levels of dermal and circulating TNF-α. Treatment with TNF-α inhibitors is often successful. Psoriatic lesions are associated with increased activity of T cells in the underlying skin.
Psoriasis is related to excess T-cell activity. Experimental models can be induced by stimulation with streptococcal superantigen, which cross-reacts with dermal collagen. This small peptide has been shown to cause increased activity among T cells in patients with psoriasis but not in control groups. Some of the newer drugs used to treat severe psoriasis directly modify the function of lymphocytes.
Also of significance is that 2.5% of those with HIV develop worsening psoriasis with decreasing CD4 counts. This is paradoxical, in that the leading hypothesis on the pathogenesis of psoriasis supports T-cell hyperactivity and treatments geared to reduce T-cell counts help reduce psoriasis severity. This finding is possibly explained by a decrease in CD4 T cells, which leads to overactivity of CD8 T cells, which drives the worsening psoriasis. The HIV genome may drive keratinocyte proliferation directly.
HIV associated with opportunistic infections may see increased frequency of superantigen exposure leading to similar cascades as above mentioned.
Guttate psoriasis often appears following certain immunologically active events, such as streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.
According to the National Institutes of Health (NIH), approximately 2.2% of the United States population has psoriasis. Internationally, the incidence of psoriasis varies dramatically. A study of 26,000 South American Indians did not reveal a single case of psoriasis, whereas in the Faeroe Islands, an incidence of 2.8% was observed. Overall, approximately 2-3% of people are affected by psoriasis worldwide. Psoriasis can begin at any age, yet there is a bimodal peak between age 20-30 years and 50-60 years. Approximately 10-15% of new cases begin in children younger than 10 years. The median age at onset is 28 years.
Psoriasis appears to be slightly more prevalent among women than among men; however, men are thought to be more likely to experience the ocular disease. Psoriasis is slightly more common in women than in men.
The incidence of psoriasis is dependent on the climate and genetic heritage of the population. It is less common in the tropics and in dark-skinned persons. Psoriasis prevalence in African Americans is 1.3% compared with 2.5% in whites.[15]
Psoriasis, even severe psoriasis, may occur in the pediatric age group, with a prevalence of 0.5-2% of children. Both biologic and immunomodulating therapies may be used safely and effectively.[16]
Although psoriasis is usually benign, it is a lifelong illness with remissions and exacerbations and is sometimes refractory to treatment. It progresses to arthritis in about 10% of cases. About 17-55% of patients experience remissions of varying lengths.
Mild psoriasis does not appear to increase risk of death.[17] However, men with severe psoriasis died 3.5 years earlier compared with men without the disease. Women with severe psoriasis died 4.4 years earlier compared with women without the disease.[17]
Psoriasis is associated with smoking, alcohol, metabolic syndrome, lymphoma, depression, suicide, potentially harmful drug and light therapies, and possibly melanoma and nonmelanoma skin cancers.
In a population-based cross-sectional study of 9035 psoriasis patients and 90,350 matched controls without psoriasis, those with more extensive psoriatic skin disease were at greater risk for major medical comorbidities, including heart and blood vessel disease, chronic lung disease, diabetes, kidney disease, joint problems, and other health conditions.[18, 19] Overall, the risk for any other type of serious illness was 11% higher for people with mild psoriasis, 15% higher for patients with moderate psoriasis, and 35% higher for those with severe psoriasis.[18, 19]
Heart disease
A systematic review of 90 studies confirmed that patients with psoriasis had a higher risk of ischemic heart disease, stroke, and peripheral arterial disease but also a greater prevalence of risk factors for cardiovascular disease, compared with controls. The authors concluded that large prospective studies with long-term followup are required to determine whether psoriasis is an independent risk factor for vascular disease or is merely associated with known risk factors.[20] Another study identified psoriasis as an independent risk factor for cardiovascular disease in women, especially if they had psoriatic arthritis and suffered from psoriasis for a longer time period (>9 y).[21]
Hypertension
In a population-based cross-sectional study of 1322 hypertensive patients with psoriasis and 11,977 controls without psoriasis, Takeshita et al found that patients with psoriasis were more likely to suffer from uncontrolled hypertension than those without psoriasis.[22, 23] Patients with moderate-to-severe psoriasis affecting more than 3% of their body surface area were at the greatest risk.
The dose-response relation between uncontrolled hypertension and psoriasis severity remained significant after adjustment for age, sex, body mass index, smoking status, alcohol use, comorbid conditions, and current use of antihypertensive medications and nonsteroidal anti-inflammatory drugs, with odds ratios of 1.20 (95% confidence interval [CI], 0.99-1.45) for moderate psoriasis and 1.48 (95% CI, 1.08-2.04) for severe psoriasis.[23]
Kidney disease
Severe psoriasis was associated with a greatly increased risk of chronic kidney disease (CKD) in a recent study of more than 800,000 patients, including 142,883 with psoriasis, 7354 with severe psoriasis, and 689,702 without psoriasis. After adjustment for age, sex, cardiovascular disease, diabetes mellitus, hyperlipidemia, hypertension, use of nonsteroidal anti-inflammatory drugs, and body mass index, the adjusted hazard ratio for CKD among patients with severe psoriasis was 1.93.[24, 25]
In a nested analysis of 8731 psoriasis patients and 87,310 controls, the odds ratio of CKD after adjustment for age, sex, cardiovascular disease, diabetes, hypertension, hyperlipidemia, body mass index, use of nonsteroidal anti-inflammatory drugs, and duration of observation was 1.36 in patients with moderate psoriasis and 1.58 in those with severe psoriasis. The relative risk for CKD was highest in younger patients.[24, 25]
Quality of life
Psoriasis can significantly influence a person’s quality of life. The physical and mental disability experienced with this disease can be comparable or in excess of that found in patients with other chronic illnesses such as cancer, arthritis, hypertension, heart disease, diabetes, and depression. A study by Kurd et al further supports the notion that psoriasis impacts quality of life and potentially long-term survival.[26] There should be a higher clinical suspicion for depression in the patient with psoriasis.
While the clinical presentation of psoriasis, and whatever improvements are made during therapy, is usually measured using the PASI (Psoriasis Area and Severity Index) score, measurement of the effect on the quality of life of the psoriasis patient may be better assessed by the DLQI (Dermatology Life Quality Index) or the CDLQI (Children’s Dermatology Life Quality Index). Measurements using these tools generally show improved quality of life with more aggressive treatment such as systemic agents.[27, 28]
Studies show that psoriasis of the palms and soles tend to have greater impact on the patient’s quality of life compared to those with more extensive psoriatic involvement not involving the palms and soles.[29, 30]
Dry eye and its manifestations may be present. Avoiding drying conditions and using lubricants can be effective. Patient recognition of these symptoms is vital for effective early treatment of this disease. Most cases of psoriasis can be controlled at a tolerable level with the regular application of care measures.
For patient education resources, see the Psoriasis Center, as well as Psoriasis, What Is Psoriasis?, Types of Psoriasis, Nail Psoriasis, and Understanding Psoriasis Medications.
Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma
Family history of similar skin condition
Pain (especially in erythrodermic psoriasis and in some cases of traumatized plaques or in the joints affected by psoriatic arthritis)
Pruritus (especially in eruptive, guttate psoriasis)
Afebrile (except in pustular or erythrodermic psoriasis in which the patient may have high fever)
Dystrophic nails
Long-term rash with recent presentation of joint pain
Joint pain without any visible skin findings
The skin almost always is affected before the eyes. Ocular findings occur in approximately 10% of patients. The most common ocular symptoms are redness and tearing due to conjunctivitis or blepharitis.
The nonocular symptoms are related to rash and psoriatic arthritis. The rash can be uncomfortable or even painful. Psoriatic arthritis can cause stiffness, pain, throbbing, swelling, or tenderness of the joints. The distal joints, such as the fingers, toes, wrists, knees, and ankles, are most often affected.
Findings on physical examination depend on the type of psoriasis present.
The most common skin manifestations are scaling, salmon-colored/erythematous macules, papules, and plaques. Typically, the macules are seen first, and these progress to maculopapules and ultimately well-demarcated, noncoherent, silvery plaques overlying a glossy homogeneous erythema. The area of skin involvement varies with the form of psoriasis.
Chronic stationary psoriasis (psoriasis vulgaris) is the most common type of psoriasis. This involves the scalp, extensor surfaces, genitals, umbilicus, and lumbosacral and retroauricular regions.
Plaque psoriasis is characterized by raised, inflamed lesions covered with a silvery white scale. The scale may be scraped away to reveal inflamed skin beneath. This is most common on the extensor surfaces of the knees, elbows, scalp, and trunk.
Guttate psoriasis presents as small salmon-pink papules, 1-10 mm in diameter, predominately on the trunk; the lesions may be scaly (see the image below). It frequently appears suddenly, 2-3 weeks after an upper respiratory infection (URI) with group A beta-hemolytic streptococci.
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Guttate psoriasis erupted in this patient after topical steroid therapy was withdrawn during a pregnancy. Contributed by Randy Park, MD.
Inverse psoriasis occurs on the flexural surfaces, armpit, groin, under the breast, and in the skin folds. It is characterized by smooth, inflamed lesions without scaling due to the moist nature of the area where this type of psoriasis is located.
Pustular psoriasis presents as sterile pustules appearing on the palms and soles or diffusely over the body. Pustular psoriasis may cycle through erythema, pustules, then scaling. The diffuse variant is termed von Zumbusch variant, which is accompanied by fever and intense ill feeling in addition to the widespread pustules. Acrodermatitis continua of Hallopeau is considered a form of pustular psoriasis that affects the hands and feet. It may prove resistant to topical and other therapies.
Erythrodermic psoriasis presents as generalized erythema, pain, itching, and fine scaling; various pustular forms also exist. It typically encompasses nearly the entire body surface area. It may be accompanied by fever, chills, hypothermia, and dehydration secondary to the large body surface area involvement. Patients with severe pustular or erythrodermic psoriasis may require hospital admission for metabolic and pain management. Older patients with erythrodermic psoriasis may experience cardiac instability and hypotension due to massive vascular shunting in the skin.
Scalp psoriasis affects approximately 50% of patients. It presents as erythematous raised plaques with silvery white scales on the scalp.
Nail psoriasis may cause pits on the nails, which often become thickened and yellowish; this is considered the most common nail finding. Oil spots, caused by exocytosis of leukocytes beneath the nail plate, are considered the most specific nail finding in psoriasis. Nails may separate from the nail bed, known as onycholysis, due to the parakeratosis of the distal nail bed. Psoriatic nails may be indistinguishable from fungal nails and, at the same time, may be more prone to developing onychomycosis because of the nail separation and subungual debris.
A retrospective study from 2014 reports that nail involvement in psoriasis is a significant predictor of the patient also having psoriatic arthritis.[31] The study looked at retrospective data from three German cross-sectional independent national studies on patients with psoriasis and psoriatic arthritis. Data on the patient’s history of psoriasis and psoriatic arthritis, clinical findings, nail involvement, and patient- and practitioner-reported outcomes were collected from standardized questionnaires. In the results, the regression model of 4146 patients indicated one of the strongest predictors of concomitant psoriatic arthritis was nail involvement.
Psoriatic arthritis affects approximately 10-30% of those with skin symptoms. The arthritis is usually in the hands and feet and, occasionally, the large joints. It produces stiffness, pain, and progressive joint damage.
Oral psoriasis may present with whitish lesions on the oral mucosa, which may appear to change in severity daily. It may also present as severe cheilosis with extension onto the surrounding skin, crossing the vermillion border. Geographic tongue is considered by many to be an oral form of psoriasis.
Eruptive psoriasis involves the upper trunk and upper extremities. Most often, it is seen in younger patients.
In addition to skin manifestations, psoriasis may also affect the lid, conjunctiva, or cornea and give rise to ocular manifestations, including ectropion and trichiasis, conjunctivitis and conjunctival hyperemia, and corneal dryness with punctate keratitis and corneal melt.[1]
Blepharitis is the most common ocular finding in psoriasis. Erythema, edema, and psoriatic plaques may develop, and they can result in madarosis, cicatricial ectropion, trichiasis, and even loss of the lid tissue.
A chronic nonspecific conjunctivitis is fairly common. It usually occurs in association with eyelid margin involvement. Psoriatic plaques can extend from the lid onto the conjunctiva. Chronic conjunctivitis can lead to symblepharon, keratoconjunctivitis sicca, and trichiasis. Nodular episcleritis and limbal lesions resembling phlyctenules also can be seen.
Corneal disease is relatively rare. Most often, it is secondary to lid or conjunctival complications, such as dryness, trichiasis, or exposure. The most common finding is punctate keratitis. Filaments, epithelial thickening, recurrent erosions, vascularization, ulceration, and scarring can occur. The vascularization tends to be superficial, peripheral, and interpalpebral or inferior. Rarely, peripheral infiltration and melting can occur in the absence of trichiasis and exposure.[32]
In one case, recurrent nasolacrimal duct occlusion was observed, presumably caused by washing of the scales into the lacrimal sac.
Usually, anterior uveitis can be seen in association with psoriatic arthritis. Acute psoriatic uveitis tends to be bilateral, prolonged, and more severe than nonpsoriatic cases.[33, 34]
Complications of psoriasis may include the following:
Secondary infections
Possible increased risk of lymphoma
Possible increased risk of cardiovascular and ischemic heart disease
Psoriatic arthritis
Mitral valve prolapse
Possibly inflammatory bowel disease[35]
Even after plaques have cleared, there may be a longstanding or permanent dyschromia. Arthritis, if not controlled, may be mutilating and crippling. Arthritic changes cannot be reversed; therefore, initiation of treatment is imperative to slow, or even halt, progression of disease. It is suggested that psoriatic patients have a higher incidence of cancer, especially lymphoma, but how much of this increased risk can be ascribed to the psoriasis and how much to the medications used for psoriasis is less certain. Psoriatic patients have a higher incidence of depression and anxiety, and, while these conditions usually improve with successful treatment, it is not guaranteed. Many other potential complications are directly related to the treatment, such as a higher incidence of skin cancer in patients treated with phototherapy and a higher incidence of infections, mild and serious, in patients on immune-suppressing medications.
Meta-analyses of cohort and case control studies of predominantly white participants reported in 2018 have shown a statistically significant association between psoriasis and inflammatory bowel disease (Crohn disease and ulcerative colitis).[36] However, a 2011 study of an Asian population showed a negative association between psoriasis and Crohn disease.[37]
The diagnosis of psoriasis is clinical. The differentiation of psoriatic arthritis from rheumatoid arthritis and gout can be facilitated by the absence of the typical laboratory findings of those conditions. Overlap with other arthritic syndromes is possible, however.
Although most cases of psoriasis are diagnosed clinically, some, particularly the pustular forms, can be difficult to recognize. In these cases, dermatologic biopsy can be used to make diagnosis. Biopsy of the skin lesion may reveal basal cell hyperplasia, proliferation of subepidermal vasculature, absence of normal cell maturation, and keratinization. A large number of activated T cells are present in the epidermis. Biopsy of acral skin may be less useful as chronic eczematous dermatitis may be psoriasiform and psoriasis of the palms and soles may show spongiosis more often associated with eczema.
Radiographs of affected joints can be helpful in differentiating types of arthritis. Joint x-rays can facilitate the diagnosis of psoriatic arthritis. Bone scans can identify joint involvement early.
Conjunctival impression cytology has demonstrated an increased incidence of squamous metaplasia, neutrophil clumping, and snakelike chromatin.
When the scales are removed, small droplets of blood appear within a few seconds from exposed vessels in the dermal papillae; this is known as the Auspitz sign.
Management of psoriasis may involve topical and systemic medication, phototherapy, stress reduction, climatotherapy, and various adjuncts such as sunshine, moisturizers, salicylic acid, and other keratolytics such as urea.
Expert dermatologists from across the globe released a consensus report on treatment optimization and transitioning for moderate-to-severe plaque psoriasis. Recommendations of the 2013 consensus report include the following:
Methotrexate may be used for as long as it remains effective and well-tolerated.
Cyclosporine is generally used intermittently for inducing a clinical response with one or several courses over a 3–6 month period.
Transition from conventional systemic therapy to a biological agent may be done directly or with an overlap if transitioning is needed because of lack of efficacy, or with a treatment-free interval if transitioning is needed for safety reasons.
Combination therapy may be helpful.
Continuous therapy for patients receiving biologicals is recommended.
Switching biologicals because of lack of efficacy should be performed without a washout period while switching biologicals for safety reasons may require a treatment-free interval.
The American Academy of Dermatology (AAD) is developing a series of recommendations under the umbrella title, Guidelines of Care for the Management of Psoriasis and Psoriatic Arthritis. The most recent addition was Section 6 (published online in November 2010; in print 2011.) All 6 sections are available online at the AAD website.[6, 39, 40, 41, 42] Section 6 of the AAD guideline recommends that psoriasis treatment be personalized for each patient’s clinical situation and discusses examples of this approach to treatment.[42]
A summary of biologic therapy guidelines from the British Association of Dermatologists can be found in Guideline Summary.
Patients with guttate, erythrodermic, or generalized pustular psoriasis may present to the emergency department. In each of these cases, restoration of the barrier function of the skin is of prime concern. This can be performed with cleaning and bandaging.
Plaque and scalp lesions are frequently encountered in patients seeking care for other problems, and initial treatment of the lesions should be offered.
The simplest treatment of psoriasis is daily sun exposure, sea bathing, topical moisturizers, and relaxation. Moisturizers, such as petrolatum jelly, are helpful. Daily application of moisturizing cream to the affected area is inexpensive and successful adjunct to psoriasis treatment. Application immediately after a bath or shower helps to minimize itching and tenderness. Section 3 (2009) of the AAD guideline discusses topical agents and recommends their use adjunctively but not as monotherapy if the disease is extensive or recalcitrant.[40]
Nonprescription tar preparations are available and have therapeutic success, especially when used in conjunction with topical corticosteroids; the newer foams are less messy preparations than some of the older ones. Anthralin, tazarotene, salicylic acid, phenolic compounds, and calcipotriene (a vitamin D analog) also may be effective especially when used in combination with topical corticosteroids. Systemic corticosteroids are generally ineffective, and they can significantly exacerbate the disease upon withdrawal.
Combination therapy with a vitamin D analog (calcipotriol and calcipotriene) or a retinoid such as tazarotene and a topical corticosteroid is more effective than therapy with either agent alone.[43] Oatmeal baths may be helpful for itching.
Solar or therapeutic ultraviolet (UV) radiation may be helpful. Various UV light treatments are used—now most commonly, UVB, although psoralen + UVB (PUVA) is still used. Among phototherapy options, Section 5 (2010) of the AAD guideline gives the highest recommendation to oral PUVA or a combination of PUVA and topical agents.[41]
Psoralen is a photosensitizer that is ingested prior to light exposure. PUVA treatment results in conjunctival hyperemia and dry eye, particularly if sun protection is not used. With proper eye protection, there does not appear to be a risk of cataract. Psoralens for either topical (bath) or systemic use may occasionally be difficult to obtain because of intermittent availability issues.
According to the AAD guidelines, PUVA can result in long remissions, but long-term use of PUVA in Caucasians may increase the risk of squamous cell carcinoma (SCC) and possibly malignant melanoma.[39, 41] A prospective study of 1380 patients found a strong correlation between number of PUVA treatments and risk of developing one or more SCC. According to the study, exposure to more than 350 PUVA treatments greatly increases the risk of SCC.[44]
In a retrospective study of 48 patients (mean age, 51 yr; 33 women, 15 men), psoralen-UVA (PUVA) therapy was found to be an appropriate treatment alternative for palmoplantar psoriasis, according to Carrascosa et al. It provided similar response rates to systemic treatment and often with increased tolerance and safety. PUVA was found to be effective in 63% of cases of palmoplantar psoriasis. Systemic therapy, however, was required in 47.9% of patients, with acitretin being the drug most often used. Adverse events occurred in 25% of patients, with the most common one being mild erythema (18%).[45]
Narrowband UVB therapy has always been accepted as a good treatment modality of psoriasis,[46] and the AAD guidelines recommend it over broad-band (UVB), although both are less effective than PUVA.[39, 41] As with PUVA, the guidelines also recommend treatment with combinations of UVB and topical or systemic agents.[41] However, a study by Keaney and Kirsner gives objective reasoning for the benefit of narrowband UV therapy by showing decreases in T cells, dendritic cells, and interleukins within responsive psoriatic plaques compared with plaques that did not respond to therapy.[10] UVB also has the advantage of not leaving the patient with a prolonged period of photosensitivity as PUVA does.
Guttate psoriasis may prove especially responsive to phototherapy. Therapies such as UVB and PUVA have low efficacy for the treatment of nail psoriasis because of the blockage of the UV radiation by the intervening nail plate, so that systemic therapy or intralesional steroids may be best for these.[47] In 2017, the US Food and Drug Administration (FDA) approved the addition of moderate-to-severe fingernail psoriasis data to the adalimumab prescribing information, based on results from a phase 3, multicenter, randomized, double-blind, parallel-arm, placebo-controlled clinical trial.[48]
Patients with psoriasis should avoid injury to skin, including sunburn and other physical trauma, as these areas may develop psoriasis. The appearance of psoriatic lesions in previously uninvolved areas after irritation or trauma is known as the Köbner phenomenon. Patients with psoriasis should also, when feasible, avoid drugs known to worsen the problem (eg, chloroquine, beta-blockers, aspirin or other NSAIDs). They should also avoid alcohol to excess. An association has been made between nonalcoholic fatty liver disease and moderate-to-severe psoriasis. What is related to treatment and what is related to psoriasis itself is still being studied.[49]
In severe cases, systemic medications such as retinoids (acitretin), methotrexate, cyclosporine, 6-thioguanine, azathioprine, a biologic, or hydroxyurea may be necessary for adequate control. Retinoids have been reported to cause dry eye, blepharitis, corneal opacities, cataracts, and decreased night vision. All of these may be associated with gastrointestinal intolerance, hepatic damage (acitretin, 6-thioguanine, azathioprine, methotrexate), marrow suppression (6-thioguanine, methotrexate, azathioprine, hydroxyurea) or renal damage (cyclosporine).
The use of biologic agents (proteins with pharmacologic activity) is discussed in Section 1 (2008) and reviewed, with updated safety information, in Section 6 of the AAD guidelines. The AAD recommends a set of baseline laboratory studies before starting treatment with a biologic agent to ensure any underlying conditions or risk factors are understood.[39, 42] Some patients with chronic hepatitis C may be safely treated with biologic agents,[50] while active hepatitis B is still considered a contraindication.
The use of these systemic medications, with appropriate safety considerations, is supported by Section 4 (2009) of the AAD guidelines.[6] Increased risk of infection applies to all systemic immune-suppressing medications, especially when used in combinations. Many of the therapies for psoriasis manipulate the function of the immune system and expose the patient to risk of severe infections while blunting the body’s response. In these patients, findings suggestive of minor infections must be taken seriously, and the risk versus the benefit of continuing the drug in the face of the infection must be weighed.
In addition, systemic retinoids and hydroxyurea may interfere with proper wound healing and elective procedures, including dental surgery, which are best performed before the start of the medications. Acitretin appears more effective than isotretinoin in psoriasis and does not require enrollment in the IPledge program. On the other hand, there is a 3-year pregnancy prohibition after its use, and many will not use this medication in any patient capable of ever becoming pregnant. Combination therapies, such as a biologic plus another immunosuppressive medication, have been used with good effect but data detailing the safest way to do this are scant. All of the systemic medications except acitretin may increase the risk of infection.
Abruptly stopping steroid therapy in psoriasis or adding known irritant drugs can result in the sudden worsening of psoriasis or appearance of a new form. Commonly, this new form is guttate psoriasis, which is much more severe and cosmetically problematic than the preexisting plaque type. It may also present with a more threatening pustular or erythrodermic psoriatic flare.
Because of concerns that immune-suppressing medications may blunt the body response to malignancies, most consider active or untreated cancer a contraindication to starting such medications.
Keratoconjunctivitis sicca can be treated with ocular lubricants and punctal occlusion. Trichiasis and cicatricial ectropion usually require surgical treatment. Conjunctival, corneal, and anterior chamber inflammation can be treated with topical corticosteroids. Nonsteroidal anti-inflammatory agents or oral corticosteroids are occasionally necessary. Whether systemic immunosuppression is effective for ocular disease is not clear. Corneal melting, inflammation, and vascularization can be difficult to treat. A bandage contact lens may retard the melting. Topical corticosteroids can control the infiltration and delay the vascularization. In some cases, progression can occur in spite of these treatments and can lead to the need for lamellar or penetrating keratoplasty.
Psoriasis is a chronic problem, and consultation for follow-up with a dermatologist or a rheumatologist is appropriate. Close follow-up is necessary to design an optimal treatment plan in accordance with the severity of disease.
Severity of psoriasis can be classified as follows:
Mild - Less than 2% of the body is affected
Moderate - From 3-10% of the body is affected
Severe - More than 10% of the body is affected
Of note, the palm of the patient’s hand is equal to 1% body surface area.
Determining the severity of psoriasis requires combining objective measures, such as body surface area involvement; disease location; symptoms; and presence of psoriatic arthritis with subjective measures such as the physical, financial, and emotional impact of the disease.
Patients with infectious diseases and psoriasis may be using drugs that modify immunologic response and render them immunocompromised. Investigation into the type of therapy is important and, if such an agent is identified, referral and close follow-up is needed.
Many suggest that because of the comorbidities of heart disease and cardiovascular disease that if adult patients have not been recently evaluated and screened for these, they should either be tested or referred back to their primary care provider to consider what is appropriate for any particular patient.
Patients with psoriasis, especially widespread and severe, have a higher incidence of depression, which may require medical intervention. If this cannot be managed by their primary care provider, referral to a mental health specialist might be appropriate.
Autoimmune diseases are generally associated with increased rates of lymphoma and myelodysplastic disease. Whether this is related to the disease itself or to its treatment is not yet determined. Patients who have laboratory abnormalities or physical findings of hematologic disease or malignancy should be evaluated by a hematologist and/or oncologist as appropriate.[51]
No specific surgical treatments are available for psoriasis, other than procedures relating to ophthalmic complications as described in other sections. The development of psoriasis at surgical sites (and after sunburn) is a recognized phenomenon.
See above Treatment of Skin Lesions for a discussion on different treatment options. All newer medications, especially the biologic therapies, are extremely expensive, with cash prices ranging from $30,000 per year to over $80,000 per year. Other medications, topical and systemic, that have been available for decades have been subjected to regular price increases, which, while keeping them less expensive than a newer biologic agent, has still resulted in them being very expensive. This usually includes generic medications, when generics are available.
Industry communications reveal that the list cost of a new medication has little to do with the cost of research and manufacturing expenses, but more to do with target income goals and considerations of what the market will bear. For this reason, most insurance plans do not do blanket approval of any and all FDA-approved medications and will often require a staged approval process, where a patient will have to have been unresponsive or have had significant adverse effects to less expensive medications before more expensive treatments are considered. This is even more problematic when there are attempts to do off-label psoriasis treatment using medications indicated for other inflammatory and arthritic conditions. Such use, even if supported by the scientific literature, is often be branded "experimental", and insurance coverage may be difficult or impossible to obtain.
Difficulty in reliably obtaining, storing, and using some of these newer medications may explain why the biologics seem to be less efficacious in patients with lower socioeconomic status.[52]
Ample literature suggests that weight loss can help psoriasis, but other attempts to show improvement with more specific diets, such as a gluten-free diet, are less conclusive. Studies of very-low-calorie diets and the “Mediterranean Diet" have both shown improvement in anecdotal reports and small studies.[53, 54] Nutritional supplements have shown limited benefit, with the exception of fish oil.[55] Vitamin D itself has also been reported to be of benefit in small studies.[56] Much more work needs to be done before enthusiastic support of any particular supplement or dietary plan may be offered.
Any restrictions on activity would relate to concomitant arthritis and how well it is being controlled. Natural sunlight can help psoriasis and may explain why it is relatively rare on the face. It has been suggested that a more active lifestyle can help psoriasis, but whether this is an independent factor or more related to better weight control is less certain.
No specific strategies prevent psoriasis, although healthy lifestyles that avoid obesity and reduced alcohol use can make control easier and increase the chances of at least temporary remission. Whenever possible, patients who are currently being treated for psoriasis or have a history of psoriasis should avoid over-the-counter and prescription medications known to exacerbate it. This includes the use of over-the-counter NSAIDs such as ibuprofen and naproxen.
Other than age-appropriate screening for cardiovascular disease, long-term monitoring is generally treatment specific (eg, skin cancer in phototherapy patients, liver disease in methotrexate patients, tuberculosis exposure in patients on biologic medications).
Guidelines on screening for comorbidities in pediatric patients with psoriasis have been issued by the Pediatric Dermatology Research Alliance and National Psoriasis Foundation.[57] Features include the following:
Overweight or obesity - Start at age 2 years; use body mass index criteria
Type 2 diabetes -Starting at age 10 years or puberty onset in overweight patients with two risk factors, screen every 3 years; screen obese patients every 3 years regardless of risk factors; use fasting serum glucose value for screening
Dyslipidemia - Start at age 9-11 years and then again at age 17-21 years; use universal lipid screening; fasting lipid panel recommended
Hypertension - Starting at age 3 years, screen yearly using age, sex, and height reference charts
Nonalcoholic fatty liver disease (NAFLD) - Starting at age 9-11 years, use alanine aminotransferase in overweight or obese children with risk factors (eg, insulin resistance, prediabetes or diabetes, central adiposity, dyslipidemia, sleep apnea, family history of NAFLD/nonalcoholic steatohepatitis (NASH); consider screening at a younger age if patients have greater risk factors (eg, severe obesity, family history of NAFLD/NASH, hypopituitarism); with normal screening results, repeat alanine aminotransferase screening every 2-3 years based on risk factors (or sooner if they increase in number or severity)
Polycystic ovary syndrome - Consider screening in patients with symptoms (eg, oligomenorrhea, hirsutism)
Gastrointestinal disease - Considering evaluating patients with decreased growth rate, unexplained weight loss, or symptoms of inflammatory bowel disease
Arthritis - Screen periodically with review of systems and physical examination
Uveitis - Only warranted in psoriatic arthritis.
Mood disorders and substance abuse - Regardless of age, annually for depression and anxiety; at age 11 years, annually for substance abuse
Quality of life - Consider using formal instrument (eg, Children's Dermatology Life Quality Index)
Guidelines on psoriasis biologic therapy from the British Association of Dermatologists[58]
Offer biologic therapy to people with psoriasis who require systemic therapy if methotrexate and cyclosporine have failed; if these agents are not tolerated or are contraindicated; and if the psoriasis has a large impact on physical, psychological, or social functioning (eg, Dermatology Life Quality Index [DLQI] or Children's DLQI score >10 or clinically relevant depressive or anxiety symptoms) and one or more of the following disease severity criteria apply:
Psoriasis is extensive (defined as body surface area [BSA] >10% or PASI ≥10)
Psoriasis is severe at localized sites and associated with significant functional impairment and/or high levels of distress (eg, nail disease or involvement of high-impact and difficult-to-treat sites such as the face, scalp, palms, soles, flexures, and genitals)
Consider biologic therapy earlier in the treatment plan (eg, if methotrexate has failed, is not tolerated, or is contraindicated) in people with psoriasis who fulfill the disease severity criteria and who also have active psoriatic arthritis or who have psoriasis that is persistent (ie, that relapses rapidly, defined as >50% baseline disease severity within 3 mo of completion of any treatment) while not on a therapy that cannot be continued in the long term (eg, narrow-band UVB).
Assess whether the minimal response criteria have been met, which are defined by the following:
Fifty percent or greater reduction in baseline disease severity (eg, PASI 50 response, or percentage BSA where PASI is not applicable) and
Clinically relevant improvement in physical, psychological, or social functioning (eg, ≥4-point improvement in DLQI or resolution of low mood)
Specific agents should be used as follows:
Ustekinumab: Offer ustekinumab as a first-line biologic agent to adults with psoriasis who fulfil the criteria for biologic therapy.
Adalimumab: Offer adalimumab as a first-line biologic agent to adults with psoriasis, particularly when psoriatic arthropathy is a consideration.
Secukinumab: Consider secukinumab as a first-line biologic agent in adults with psoriasis, with or without psoriatic arthritis.
Infliximab: Reserve infliximab for use in people with very severe disease or people in whom other available biologic agents have failed or cannot be used.
Others: Offer adalimumab (age ≥4 y), etanercept (≥6 y), or ustekinumab (≥12 y) to children and young people who fulfill the criteria for biologic therapy.
Advise women of childbearing potential who are starting biologic therapy for psoriasis to use effective contraception and discuss conception plans with the consultant supervising their care. There are no known interactions between biologic therapies and contraceptive methods.
Advise mothers who have received biologic therapy for psoriasis beyond 16 weeks' gestation that their infants should not receive any live vaccinations until they have reached age 6 months (eg, rotavirus and BCG). Do not give live vaccines to people on biologic therapy or to infants (up to age 6 mo) whose mothers have received biologic therapy beyond 16 weeks' gestation. Stop biologic therapy for at least 6 months before giving live vaccines and for 12 months in the case of the shingles (herpes zoster) vaccine. In general, biologic therapy can be started 4 weeks after administration of a live vaccine. Whenever possible, complete all required vaccinations prior to the initiation of biologic therapy, and review vaccination requirements during therapy with reference to the Green Book and the clinical risk category of “immunosuppression.”
Do not use TNF antagonists in people with demyelinating diseases, and review alternative interventions in people who have an affected first-degree relative with demyelinating disease. Stop treatment and seek specialist advice if neurologic symptoms suggestive of demyelinating disease develop during TNF antagonist therapy. Symptoms include loss or reduction of vision in one eye with painful eye movements; double vision; ascending sensory disturbance and/or weakness; problems with balance, unsteadiness, or clumsiness; and altered sensation traveling down the back and sometimes into the limbs when bending the neck forward.
Avoid TNF antagonist therapy in people with severe cardiac failure. Stop TNF antagonist therapy in the event of new or worsening preexisting heart failure and seek specialist advice.
Exercise caution and consult a gastroenterology specialist before using secukinumab or ixekizumab in people with inflammatory bowel disease.
Guidelines on the management and treatment of psoriasis with biologics by the American Academy of Dermatology and the National Psoriasis Foundation[59]
TNF-alpha Inhibitors
Etanercept recommendations are as follows:
Monotherapy treatment option for adults with moderate-to-severe plaque psoriasis
Recommended starting dose of 50 mg; self-administered SC injection twice weekly for 12 consecutive weeks
Recommended maintenance dose of 50 mg once weekly; 50 mg twice weekly is more efficacious than once weekly and may be required for better disease control in some patients
Recommended as monotherapy option in adults with moderate-to-severe plaque psoriasis affecting the scalp or nails
Can be recommended as monotherapy option for adults with other subtypes (ie, pustular, erythrodermic) of moderate-to-severe plaque psoriasis
Recommended monotherapy option in adults with plaque psoriasis of any severity when associated with significant psoriatic arthritis
Recommended combination treatment option with topicals (eg, high-potency corticosteroids with or without a vitamin D analogue) to augment treatment of moderate-to-severe plaque psoriasis
Recommended combination treatment option with methotrexate for moderate-to-severe plaque psoriasis in adults
May be combined with acitretin, apremilast, cyclosporine, or narrowband ultraviolet phototherapy for moderate-to-severe plaque psoriasis in adults
Infliximab recommendations are as follows:
Monotherapy treatment option for adults with moderate-to-severe plaque psoriasis
Recommended starting dose is an infusion of 5 mg/kg administered at week 0, week 2, and week 6; thereafter, administered every 8 weeks
Recommended to be administered at more frequent intervals (less than q8wk and as frequently as q4wk during maintenance phase) and/or at a higher dose (up to 10 mg/kg) for better disease control in some adults
Recommended as monotherapy option for moderate-to-severe plaque psoriasis affecting the palms and soles (plaque-type palmoplantar psoriasis), nails, or scalp in adults
Can be recommended as monotherapy option in adults with other subtypes (ie, pustular, erythrodermic) of moderate-to-severe plaque psoriasis
Recommended as monotherapy option in adults with plaque psoriasis of any severity when associated with significant psoriatic arthritis; it also inhibits radiographically detected joint damage in psoriatic arthritis
Recommended combination treatment option with topicals (eg, high-potency corticosteroids with or without a vitamin D analogue) to augment treatment of moderate-to-severe plaque psoriasis
May be combined with acitretin, methotrexate, or apremilast for moderate-to-severe plaque psoriasis in adults
Adalimumab recommendations are as follows:
Monotherapy treatment option for adults with moderate-to-severe plaque psoriasis
Recommended starting dose of 80 mg taken as two self-administered SC 40-mg injections, followed by a 40-mg self-administered SC injection 1 week later, followed by 40-mg self-administered SC injections every 2 weeks thereafter
Maintenance dose of 40 mg/wk recommended for better disease control in some patients
Recommended as monotherapy option for adults with moderate-to-severe plaque psoriasis affecting the palms and soles (palmoplantar psoriasis), nails, or scalp
Can be recommended as monotherapy option for adults patients with other subtypes (ie, pustular, erythrodermic) of moderate-to-severe psoriasis
Recommended as monotherapy option in adults with plaque psoriasis of any severity when associated with psoriatic arthritis
Can be recommended combination treatment option with topicals (eg, high-potency corticosteroids with or without a vitamin D analogue) to augment treatment of moderate-to-severe plaque psoriasis
May be combined with acitretin, methotrexate, apremilast, cyclosporine, or narrowband ultraviolet phototherapy for moderate-to-severe plaque psoriasis in adults
Certolizumab has been approved by the FDA for the treatment of plaque psoriasis, psoriatic arthritis, Crohn disease, ankylosing spondylitis, and rheumatoid arthritis. Approved dosing for moderate-to-severe psoriasis is 400 mg (two 200-mg SC injections) every other week. It is likely to possess class characteristics similar to those of other TNF-alpha inhibitors.
Interleukin-12/23 Inhibitors
Ustekinumab recommendations are as follows:
Monotherapy treatment option for adults with moderate-to-severe plaque psoriasis
Recommended starting doses: (1) patients weighing 100 kg or less, 45 mg SC initially and 4 weeks later, followed by 45 mg administered SC every 12 weeks; (2) patients weighing more than 100 kg, 90 mg administered SC initially and 4 weeks later, followed by 90 mg administered SC every 12weeks
Recommended alternate dosages are higher doses (90 mg instead of 45 mg in patients weighing ≥100 kg) or with greater frequency (eg, every 8 wk in maintenance phase) if response to standard dosing is inadequate
Can be used as monotherapy option for adults with moderate-to-severe plaque psoriasis affecting the palms and soles (plaque-type palmoplantar psoriasis), nails, or scalp
Can be used as monotherapy option for adults with other subtypes (ie, pustular, erythrodermic) of moderate-to-severe psoriasis; evidence is limited for use in inverse and guttate psoriasis
Recommended as monotherapy option in adults with plaque psoriasis of any severity when associated with psoriatic arthritis
Can be recommended combination treatment option with topicals (eg, high-potency corticosteroids with or without a vitamin D analogue) to augment treatment of moderate-to-severe plaque psoriasis
May be combined with acitretin, methotrexate, apremilast, cyclosporine, or narrowband ultraviolet phototherapy for moderate-to-severe plaque psoriasis in adults
Interleukin-17 Inhibitors
Secukinumab recommendations are as follows:
Monotherapy treatment option in adults with moderate-to-severe plaque psoriasis
Recommended starting dose of 300 mg by self-administered SC injection at week 0, week 1, week 2, week 3, and week 4, followed by 300 mg every 4 weeks
Recommended maintenance dose of 300 mg every 4 weeks
Recommended dose of 300 mg is more effective than 150 mg
Can be recommended as monotherapy in adults with moderate-to-severe plaque psoriasis affecting the head and neck (including the scalp) or nails
Recommended as monotherapy option in adults with moderate-to-severe palmoplantar plaque psoriasis
Can be recommended as monotherapy option in adults with moderate-to-severe palmoplantar pustulosis
Can be used as monotherapy in adults with erythrodermic psoriasis
May be used as monotherapy in adults with plaque psoriasis when associated with psoriatic arthritis
Ixekizumab recommendations are as follows:
Monotherapy treatment option for adults with moderate-to-severe plaque psoriasis
Recommended starting dose of 160 mg by self-administered SC injection, followed by 80 mg at week 2, week 4, week 6, week 8, week 10, and week 12
Recommended maintenance dose of 80 mg every 4 weeks
Can be recommended as monotherapy option in adults with moderate-to-severe plaque psoriasis affecting the scalp or nails
Can be recommended as monotherapy option in adults with erythrodermic psoriasis or generalized pustular psoriasis
Recommended as monotherapy option in adults with plaque psoriasis when associated with psoriatic arthritis
Brodalumab recommendations are as follows:
Recommended as monotherapy treatment option in adults with moderate-to-severe plaque psoriasis
Can be used as monotherapy option in adults with generalized pustular psoriasis
Recommended dose of 210 mg by self-administered SC injection at week 0, week 1, and week 2, followed by 210 mg every 2 weeks
Interleukin-23 Inhibitors
Guselkumab recommendations are as follows:
Recommended as monotherapy treatment option for adults with moderate-to-severe plaque psoriasis
Recommended dose of 100 mg by self-administered SC injection at week 0 and week 4, followed by every 8 weeks thereafter
Recommended as monotherapy option in adults with scalp, nail, or plaque-type palmoplantar psoriasis
Tildrakizumab recommendations are as follows:
Recommended as monotherapy treatment option in adults with moderate-to-severe plaque psoriasis
Recommended dose of 100 mg given in office by physician-administered SC injection at week 0 and week 4, followed by every 12 weeks thereafter
Risankizumab is not approved by the FDA, but it can be used as monotherapy in adults with moderate-to-severe plaque psoriasis. When approved, the dose will likely be 150 mg given by self-administered subcutaneous injections at week 0 and week 4, followed by every 12 weeks.
Guidelines on the safe and effective prescribing of oral cyclosporine in dermatology by the British Association of Dermatologists[60]
Cyclosporine is licensed for use in the following indications:
Atopic dermatitis (in persons aged 16 years or older)
Psoriasis (in persons aged 16 years or older)
Good evidence supports the use of cyclosporine outside its product license for the following indications:
Atopic dermatitis (in persons younger than 16 years)
Behçet disease
Chronic spontaneous (idiopathic) urticaria
Graft versus host disease
Palmoplantar pustulosis
Pyoderma gangrenosum
Cyclosporine should be used only as a last resort in the following indications, and current evidence shows it is unlikely to be beneficial:
Alopecia areata
Discoid lupus erythematosus
Pemphigus foliaceous
Pemphigus vulgaris
Continuous treatment may be considered for select patients with chronic skin disease in the appropriate situation; however, in an effort to reduce nephrotoxicity, use single or intermittent short courses of up to 16 weeks if possible. Cyclosporine dose titration during therapy also should be used to reduce nephrotoxicity.
If hypertension occurs, the cyclosporine dose should be reduced and/or the hypertension should be treated. If appropriate blood pressure cannot be maintained, discontinue cyclosporine.
If infection is suspected, consider obtaining consult on the safety of inducing immunosuppression; ensure all necessary treatment is being administered before beginning cyclosporine.
Patients should be advised to seek advice early if febrile illness occurs or their skin condition rapidly worsens.
Owing to a long‐term risk of developing nonmelanoma skin cancer, cyclosporine should not be administered concurrently with phototherapy.
Serum lipid levels should be measured for a baseline and should be monitored throughout treatment; this is especially important in patients considered high risk (eg, diabetics, those with preexisting hyperlipidemia).
Guidelines on the management and treatment of psoriasis with phototherapy from the American Academy of Dermatology and the National Psoriasis Foundation[61]
Narrowband ultraviolet B phototherapy
Phototherapy using narrowband ultraviolet B (NB-UVB) is recommended as monotherapy for adults with plaque psoriasis.
For adults with generalized plaque psoriasis, the recommended NB-UVB phototherapy starting dose should be based on the minimal erythema dose or it should be determined based on a fixed-dose or skin-phototype protocol.
For adults with generalized plaque psoriasis, a treatment phase of thrice-weekly dosing of NB-UVB phototherapy is recommended.
For adults with psoriasis, treatment with short-term psoralen plus ultraviolet A (PUVA) monotherapy is more effective than NB-UVB.
Owing to its increased safety, higher convenience, and lower cost, NB-UVB is preferred over PUVA monotherapy for psoriasis in adults, even though it is less effective.
In adults with generalized plaque psoriasis, NB-UVB is recommended over broadband ultraviolet B (BB-UVB) monotherapy.
Treatment with NB-UVB monotherapy is recommended for guttate psoriasis patients, regardless of their age.
For appropriate patients with generalized plaque psoriasis, home-based NB-UVB phototherapy is recommended as an alternative to in-office NB-UVB phototherapy.
Treatment with NB-UVB phototherapy is recommended for pregnant patients who have guttate psoriasis or generalized plaque psoriasis.
As a measure to possibly improve efficacy, NB-UVB phototherapy can be safely augmented with concomitant topical therapy using retinoids, vitamin D analogues, and corticosteroids.
Oral retinoids can be combined with NB-UVB phototherapy in appropriate patients with generalized plaque psoriasis if they have not responded adequately to monotherapy.
Owing to an increased risk of developing skin cancer, long-term combination therapy with NB-UVB and cyclosporine is not recommended for adults with generalized plaque psoriasis.
Apremilast combined with NB-UVB phototherapy can be considered for adult patients with generalized plaque psoriasis if they have not responded adequately to monotherapy.
To reduce the risk of genital skin cancer, all patients receiving NB-UVB phototherapy should be provided genital shielding.
To reduce the risk of ocular toxicity, all patients receiving NB-UVB phototherapy should be provided eye protection with goggles.
Owing to the risk of photocarcinogenesis, use caution when administering NB-UVB phototherapy to patients with a history of melanoma or multiple nonmelanoma skin cancers, arsenic intake, or prior exposure to ionizing radiation.
Folate supplementation is recommended for females of childbearing age who are receiving NB-UVB phototherapy.
To maintain the clinical response from NB-UVB phototherapy, maintenance therapy can be considered.
BB-UVB phototherapy
In adults with generalized plaque psoriasis, BB-UVB phototherapy is recommended as monotherapy if NB-UVB is not available.
In adults with generalized plaque psoriasis, BB-UVB monotherapy is considered less efficacious than NB-UVB or oral PUVA monotherapy.
Monotherapy with BB-UVB may be considered for adults with guttate psoriasis.
To reduce the risk of genital skin cancer, all patients being offered BB-UVB phototherapy should be provided with genital shielding.
To reduce the risk of ocular toxicity, all patients receiving BB-UVB phototherapy should be provided eye protection with goggles.
Owing to the risk of photocarcinogenesis, use caution when administering BB-UVB phototherapy to patients with a history of melanoma or multiple nonmelanoma skin cancers, arsenic intake, or prior exposure to ionizing radiation.
Combination therapy with acitretin and BB-UVB can be considered in adults with generalized plaque psoriasis.
Targeted UVB phototherapy
The recommended targeted UVB phototherapy for adults with localized plaque psoriasis (< 10% body surface area), for individual plaque psoriasis lesions, or for patients with more extensive disease includes excimer 308-nm laser, excimer 308-nm light, and targeted NB-UVB 311- to 313-nm light.
For maximal efficacy, the recommended treatment frequency for targeted UVB phototherapy in adults with localized plaque psoriasis is 2-3 times per week, rather than once every 1-2 weeks.
In adults with localized plaque psoriasis, the initial dose of targeted UVB phototherapy is based on the minimal erythema dose or by a fixed-dose or skin-phototype protocol.
For treating localized plaque psoriasis in adults, the most effective targeted UVB phototherapy is excimer 308-nm laser, followed by excimer 308-nm light, followed by localized NB-UVB 311- to 312-nm light.
For adults with plaque psoriasis (including palmoplantar psoriasis), a recommended targeted UVB phototherapy includes excimer 308-nm laser and excimer 308-nm light.
Treatment of plaque psoriasis in adults with excimer 308-nm laser may be combined with topical steroid therapy.
A recommended targeted UVB phototherapy treatment for adults with scalp psoriasis is excimer 308-nm laser.
PUVA therapy
In the treatment of localized plaque psoriasis in adults, particularly those with palmoplantar psoriasis or palmoplantar pustular psoriasis, topical phototherapy with PUVA is deemed superior to NB-UVB 311- to 313-nm light.
A recommended treatment for psoriasis in adults is oral PUVA.
A recommended treatment for moderate-to-severe psoriasis in adults is bath PUVA.
Photodynamic therapy
Photodynamic therapy with either aminolevulinic acid or methyl aminolevulinate is not recommended for adults with localized psoriasis, including the palmoplantar variety or nail psoriasis.
Grenz ray, climatotherapy, visible light, Goeckerman, and pulsed-dye laser therapies
Evidence is insufficient to recommend grenz ray therapy (long-wavelength ionizing radiation) for the treatment of psoriasis.
Sufficient evidence exists to recommend climatotherapy (temporary or permanent relocation geographically) for the treatment of psoriasis.
Evidence is insufficient to recommend the use of visible light (blue or red) as a more effective treatment for psoriasis, except in nail psoriasis.
Sufficient evidence exists to recommend Goeckerman therapy (coal tar in combination with UVB phototherapy) for the treatment of psoriasis.
Pulsed-dye laser can be considered for nail psoriasis.
Many drugs that affect the rate of skin cell production are used in psoriasis therapy alone or in combination with light therapy, stress reduction, and climatotherapy. Adjuncts to treatment include sunshine, moisturizers, and salicylic acid as a scale-removing agent. Generally, these therapies are used for patients with less than 20% of body surface area involved, unless the lesions are physically, socially, or economically disabling.
Treatments for more advanced psoriasis include narrowband ultraviolet B (UVB) light, psoralen with ultraviolet A (UVA) light retinoids (eg, isotretinoin [Accutane, Claravis], acitretin [Soriatane]), methotrexate (particularly for arthritis), cyclosporine (Neoral, Sandimmune), infliximab (Remicade), etanercept (Enbrel), adalimumab (Humira), apremilast (Otezla), and secukinumab (Cosentyx). Decreased effectiveness of infliximab or adalimumab in a patient previously well controlled on the medication may mean that antibodies to the medication are being produced.[62]
In a study of ustekinumab in patients with moderate-to-severe psoriasis, investigators did not observe an increased trend in dose-related or cumulative toxicity with the duration of ustekinumab treatment. The investigators also reported rates of adverse events generally comparable to those of other biologics approved for managing moderate-to-severe psoriasis.[2] It is approved in two dosages, administered subcutaneously, with the higher dose given to those weighing 100 kg (220 pounds) or more. It has been suggested that 91 kg (200 pounds) might be a better cutoff for the higher dose for optimal control.[3]
Recommendations from a 2013 international consensus report on treatment optimization and transitioning for moderate-to-severe plaque psoriasis include methotrexate and cyclosporine, biologic agents, and combination therapy.[7]
The AAD guidelines recommend treatment with methotrexate, cyclosporine, and acitretin, with consideration of the contraindications and drug interactions noted in the discussion of each medication below.[6]
Many other medications are used off label for psoriasis. Many of these are drugs approved initially for rheumatoid arthritis or inflammatory bowel disease but are found to also have benefits in skin psoriasis. Tofacitinib citrate, a Janus kinase inhibitor, is such a medication that has shown promise in the treatment of psoriasis.[63] Caution must be taken any time a medication is used off label because the true risks and benefits may not yet have been defined for a different patient population than that originally studied.
Clinical Context:
Triamcinolone treats inflammatory dermatosis responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It has mild potency and is the first drug of choice for most patients.
Clinical Context:
Betamethasone treats inflammatory dermatosis responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It is a potent topical steroid and is the drug of choice if psoriasis is resistant to milder forms.
Topical corticosteroids are the mainstay of treatment for mild and limited psoriasis. They can reduce plaque formation. These agents have anti-inflammatory effects and may cause profound and varied metabolic activities.
The strength of topical steroid and vehicle are chosen according to the thickness of plaques and body location. No topical corticosteroids are conclusively superior in efficacy or adverse effects than others in the same class. Some formulations such as foams and solutions are easier to use in the scalp than either creams or ointments. A patient who has been doing well on a topical steroid who begins to have worsening, especially with itching, should be evaluated for either a concomitant fungal infection or the development of allergic contact dermatitis to a steroid or vehicle component. Potent and superpotent corticosteroids generally only need be applied once daily unless the scale on a plaque is particularly thick. Extended use of very potent steroids should be avoided when possible in the treatment of genital and inverse psoriasis.
Clinical Context:
Prednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.
Clinical Context:
Dexamethasone is used for various allergic and inflammatory diseases. It decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Ophthalmic corticosteroids treat conjunctival, corneal, and anterior chamber inflammation. These agents help control infiltration and delay vascularization. Care must be taken with long-term use because of concerns about infection with viruses such as herpes simplex or fungal infections.
Clinical Context:
Coal tar is antipruritic and antibacterial and inhibits deregulated epidermal proliferation and dermal infiltration. It does not injure the normal skin when applied widely, and it enhances the usefulness of phototherapy. It generally is used as a second-line drug therapy due to messy application, except for shampoos, which may be used and rinsed at once.
Coal tar is an inexpensive treatment that is available over the counter in shampoos, lotions, creams, or foam for use in widespread areas of involvement. It is particularly useful in hair-bearing areas. Some recent research has shown the 1% concentration may be superior in control of lesions to more concentrated preparations. Tar preparations may be especially useful when combined with topical corticosteroids. This may be accomplished by applying the products sequentially or, when available, obtaining them from a compounding pharmacy. Treatment with tar preparations may be especially useful when combined with topical corticosteroids.
Clinical Context:
Anthralin reduces the rate of cell proliferation. Its chemically reducing properties may also upset the oxidative metabolic processes, further reducing epidermal mitosis. It is not the first or second drug of choice due to irritation problems of normal skin surrounding lesions and staining of the skin.
Keratolytic agents are used to remove scale, to smooth the skin, and to treat hyperkeratosis.
Removing the thick scale allows topical corticosteroids and other topical medications to better reach the target tissues and achieve better results. This is especially important on the scalp. Many over-the-counter preparations can be used for this, most of which contain salicylic acid. Lactic acid, ammonium lactate, and urea are other ingredients that may be applied before or at the same time as other topical medications. Urea preparations stronger than 30% require a prescription, a variety of creams, lotions, and foams are available for this. Many “foot creams” contain combinations of keratolytics and may be applied to any area of the body needing scale removal.
Anthralin is also considered to be in the antipsoriatic therapeutic class.
Clinical Context:
Calcipotriene is a synthetic vitamin D-3 analog that regulates skin cell production and development. It is used in the treatment of moderate plaque psoriasis. This treatment does not cause long-term skin thinning or systemic effects. Sorilux is a newer foam version of this medication.
Clinical Context:
Calcipotriene is a synthetic vitamin D-3 analog that regulates skin cell production and development. It inhibits epidermal proliferation, promotes keratinocyte differentiation, and has immunosuppressive effects on lymphoid cells. Betamethasone is a corticosteroid that decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. The combination is available as a topical ointment, foam, or as a solution that can be applied to the body or scalp. The products contain calcipotriene 0.005% and betamethasone dipropionate 0.064%.
The combination product is quite expensive and the same results may be obtained by using a generic corticosteroid sequentially in combination with one of the other vitamin D analog products.
Vitamin D analogs are used in patients with lesions resistant to topical therapy or with lesions on the face or exposed areas where thinning of the skin would pose cosmetic problems. These come as ointments, solutions, and foams. The latter two are especially useful for scalp treatments.
Clinical Context:
Tazarotene is a retinoid prodrug that is converted to its active form in the body and modulates differentiation and proliferation of epithelial tissue and perhaps has anti-inflammatory and immunomodulatory activities. It may be the drug of choice for those with facial lesions who are not at risk of pregnancy.
Tazarotene, although topical, is a category X medication. Topical tretinoin is of less use in psoriatic patients. A strategy that may be tried in patients who experience unacceptable irritation is to use short contact times. There are several protocols, but the least irritating is to apply the medication for 15-20 min and then wash off. The total time on may be increased by 15-20 minutes every few weeks until clinical efficacy or adverse cutaneous effects are seen. This short-contact method may be especially useful when one is using it in skin folds but is less effective for the plaque with very thick scale.
Aqueous gel formulations are odorless and colorless, and no long-term skin damage has been noted with topical retinoids. There is also no threat of worsening if the therapy is withdrawn, as with steroids. These drugs should not be used in women if pregnancy is a possibility.
Clinical Context:
Methotrexate inhibits dihydrofolic acid reductase. Dihydrofolates must be reduced to tetrahydrofolates by this enzyme before they can be utilized as carriers of one-carbon groups in the synthesis of nucleotides and thymidylate. Subsequently, methotrexate interferes with DNA synthesis, repair, and cellular replication. Actively proliferating tissues are in general more sensitive to this effect of methotrexate.
Clinical Context:
Topical tacrolimus has been used in the past for management of refractory atopic dermatitis. However, multiple studies have shown effectiveness with psoriasis affecting intertriginous regions as well as the face. Generally, it seems to be effective in thin-skinned areas. However, it has become somewhat of a second-line agent given other studies showing topical steroids may be more effective and potential serious disease association.
Clinical Context:
Cyclosporine is an 11-amino acid cyclic peptide and natural product of fungi. It acts on T-cell replication and activity.
Cyclosporine is a specific modulator of T-cell function and an agent that depresses cell-mediated immune responses by inhibiting helper T-cell function. Preferential and reversible inhibition of T lymphocytes in the G0 or G1 phase of cell cycle is suggested. The drug binds to cyclophilin, an intracellular protein, which, in turn, prevents formation of interleukin (IL)-2 and the subsequent recruitment of activated T cells.
Cyclosporine has about 30% bioavailability, but there is marked interindividual variability. It specifically inhibits T-lymphocyte function with minimal activity against B cells. Maximum suppression of T-lymphocyte proliferation requires that the drug be present during first 24 h of antigenic exposure.
Cyclosporine suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions (eg, delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease) for a variety of organs.
Cyclosporine is used in extensive disease refractory to other treatments, especially when used at 5 mg/kg/d. Remission is usually rapid with this therapy; however, skin lesions tend to recur within days to weeks after treatment is stopped (although patients do not usually have the severe rebound that patients withdrawing from therapy may have). Maintenance therapy (3 mg/kg/d) usually is required with lower doses of this drug.
Clinical Context:
Infliximab is a chimeric antibody that binds both the soluble and transmembrane TNF-α molecules, thereby neutralizing the effects of TNF-α. It is indicated for chronic severe (ie, extensive and/or disabling) plaque psoriasis in adults who are candidates for systemic therapy and when other systemic therapies are medically less appropriate. It is also indicated to reduce signs and symptoms, and to improve physical function of patients with psoriatic arthritis. Screen patients for tuberculosis (TB) and hepatitis B, as reactivation of both illnesses is associated with TNF-α inhibitors.
Clinical Context:
Etanercept is a recombinant human TNF-α receptor protein fused with the Fc portion of IgG1 that binds to soluble and membrane-bound TNF-α, thereby neutralizing the effects of TNF-α. It is indicated for adults and children aged 4 years and older with moderate-to-severe psoriasis. It is also indicated for adults with moderate-to-severe psoriatic arthritis. Screen patients for TB and hepatitis B, as reactivation of both illnesses is associated with TNF-α inhibitors.
Clinical Context:
Adalimumab is a fully human anti–TNF-α monoclonal antibody. It binds specifically to soluble and membrane-bound TNF-α, thereby neutralizing the effects of TNF-α. It is used to treat moderate-to-severe psoriasis and moderate-to-severe psoriatic arthritis. Screen patients for TB and hepatitis B, as reactivation of both illnesses is associated with TNF-α inhibitors.
These agents neutralize the effects of tumor necrosis factor-α (TNF-α). For adalimumab, weight-based dosing regimens exist for pediatric-aged patients. For etanercept, some patients will require twice-weekly dosing of the induction period indefinitely in order to maintain satisfactory control. Decreased effectiveness of infliximab or adalimumab in a patient previously well controlled on the medication may mean that antibodies to the medication are being produced.
Clinical Context:
Apremilast is a phosphodiesterase-4 inhibitor specific for cAMP, resulting in increased intracellular cAMP levels. It may affect cytokines and chemokine synthesis, leading to anti-inflammatory effects. It is indicated for moderate-to-severe plaque psoriasis in adults who are candidates for phototherapy or systemic therapy.
The mechanisms by which phosphodiesterase-4 (PED4) inhibitors elicit anti-inflammatory effects are not completely understood. Unlike biologics that neutralize inflammatory mediators at the protein level, apremilast modulates mediator production at the level of mRNA expression.
Clinical Context:
Secukinumab is a human IgG1 monoclonal antibody that selectively binds to and neutralizes the proinflammatory cytokine IL-17A. IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses and plays a key role in the pathogenesis of plaque psoriasis. Following the initial once-weekly SC dosage regimen, the drug is given as a maintenance dose once monthly. It is indicated for moderate-to-severe plaque psoriasis in patients who are candidates for systemic therapy or phototherapy.
Clinical Context:
Ixekizumab is a humanized monoclonal IgG4 antibody that targets IL-17A and neutralizes the proinflammatory effects of IL-17A. It is administered as a SC injection. It is indicated for adults with moderate-to-severe plaque psoriasis.
Clinical Context:
Brodalumab is a human monoclonal IgG2 antibody that selectively binds to the human IL-17A receptor and inhibits its interactions with cytokines IL-17A, IL-17F, IL-17C, IL-17A/F heterodimer, and IL-25. It is indicated for moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy and have failed to respond or have lost response to other systemic therapies.
Clinical Context:
Ustekinumab is a human monoclonal antibody directed against IL-12 and IL-23, thereby interfering with T-cell differentiation and activation and subsequent cytokine cascades. It is indicated for moderate-to-severe plaque psoriasis.
Clinical Context:
Risankizumab is a humanized immunoglobulin G1 (IgG1) monoclonal antibody that selectively binds to the p19 subunit of human interleukin 23 (IL-23) cytokine and inhibits its interaction with the IL-23 receptor. IL-23 is a naturally occurring cytokine that is involved in inflammatory and immune responses. It is indicated for treatment of moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy.
Clinical Context:
Guselkumab is a human monoclonal IgG1-lambda antibody that selectively binds to the p19 subunit of IL-23. IL-23 is a natural cytokine associated with inflammatory and immune responses. Guselkumab inhibits the proinflammatory actions of IL-23, thereby decreasing cytokine and chemokine release. It is indicated for adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy.
Clinical Context:
This humanized IgG1/k monoclonal antibody selectively binds to the p19 subunit of IL-23 and inhibits its interaction with the IL-23 receptor. IL-23 is a natural cytokine associated with inflammatory and immune responses. Tildrakizumab inhibits the release of proinflammatory cytokines and chemokines. It is indicated for adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy.
Clinical Context:
This combination is indicated for the treatment of plaque psoriasis in adults. It is a combination lotion containing a topical corticosteroid and a retinoid.
Clinical Context:
For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Many other topical steroids also are available.
Up to 0.4 mL may be injected, after ring block, into the nail bed and matrix to improve psoriatic dystrophy. Results may be long lasting but more than one treatment may be required.
Intramuscular corticosteroids are not recommended for the management of psoriasis because of the risk of flare upon withdrawal. On the other hand, isolated plaques may be injected intralesionally, as may the nail matrix in cases of severe psoriatic nails.
Clinical Context:
Artificial tears contain the equivalent of 0.9% NaCl and are used to maintain ocular tonicity. They act to stabilize and thicken precorneal tear film and prolong tear film breakup time, which occurs with dry eye states.
Artificial tears are used to treat dry eye irritation. Many types of artificial tears are available over the counter. In mild cases, preserved tears can be used. In severe cases, only nonpreserved tears should be used. Preserved tears include GenTeal, Refresh Tears, and Tears Naturale II. Nonpreserved tears include Refresh, Refresh Plus, OcuCoat, Bion, and Hypo Tears PF.
What are the signs and symptoms of psoriasis?What is psoriasis?What are the types of psoriasis?What should be included in the physical exam of psoriasis?What is the role of lab studies in the workup of psoriasis?Which lab studies should be performed prior to initiating systemic therapy for psoriasis?Which imaging studies and procedures are indicated in the workup of psoriasis?Which medications are used in the treatment of psoriasis?What are the treatment guidelines for moderate-to-severe plaque psoriasis?What are the nonpharmacologic treatment options for psoriasis?When is surgery indicated in the treatment of psoriasis?What is psoriasis?What is the most common type of psoriasis?How prevalent are ocular symptoms in psoriasis?What are the treatment options for psoriasis?What causes psoriasis?What is the pathogenesis of psoriasis?What is the pathophysiology of psoriasis?What is the role of keratinocytes in the etiology of psoriasis?Which environmental factors exacerbate psoriasis?What is the role of genetics in psoriasis?Which immunologic factors are associated with psoriasis?What is the prevalence of psoriasis?Is psoriasis more common in males or females?How does the prevalence of psoriasis vary among races?What is the prevalence of psoriasis in children?What is the disease course of psoriasis?What is the mortality risk of psoriasis?What are the risk factors and comorbidities of psoriasis?How much does psoriasis increase risk for major medical comorbidities?What is the relationship between psoriasis and heart disease?What is the relationship between psoriasis and hypertension?How does psoriasis affect the risk for chronic kidney disease (CKD)?How does psoriasis affect quality of life?What education about psoriasis should be given to patients?What are the symptoms of psoriasis?Which physical findings suggest psoriasis?What areas of the body are affected in chronic stationary psoriasis (psoriasis vulgaris)?Which physical findings are characteristic of plaque psoriasis?Which physical findings are characteristic of guttate psoriasis?Which physical findings are characteristic of inverse psoriasis?Which physical findings are characteristic of pustular psoriasis?Which physical findings are characteristic of erythrodermic psoriasis?Which physical findings are characteristic of scalp psoriasis?Which physical findings are characteristic of nail psoriasis?Which physical findings suggest psoriatic arthritis?Which physical findings are characteristic of oral psoriasis?What areas of the body are affected in eruptive psoriasis?Which ocular findings suggest psoriasis?What are the possible complications of psoriasis?What are the differential diagnoses for Psoriasis?How is psoriatic arthritis differentiated from rheumatoid arthritis and gout?What is the role of lab studies in the diagnosis of psoriasis?Which lab studies are indicated prior to systemic therapy for psoriasis?What is the role of imaging studies and procedures in the diagnosis of psoriasis?What is the role of punch biopsy in the diagnosis of psoriasis?Which histologic findings are characteristic of psoriasis?What are the treatment options for psoriasis?What are the treatment guidelines for psoriasis?What is the role of the emergency department (ED) in the treatment of psoriasis?What types of psoriatic lesions may be identified during treatment for other conditions?What are the conservative treatment options for psoriasis?How effective are nonprescription tar preparations for the treatment of psoriasis?How effective is combination drug treatment for psoriasis?How effective is ultraviolet (UV) radiation in the treatment of psoriasis?What should patients with psoriasis avoid?What is the role of systemic medications in the treatment of psoriasis?What are the possible complications of abrupt discontinuation of steroid therapy for psoriasis?When are immune-suppressing medications contraindicated in the treatment of psoriasis?What are the treatment options for ocular complications of psoriasis?How is the severity of psoriasis determined, and which specialist consultations may be indicated in the treatment of psoriasis?When is surgery indicated for treatment of psoriasis?How does the cost of medication affect treatment selection for psoriasis?What is the role of dietary modifications in the treatment of psoriasis?What is the role of activity modification in the treatment of psoriasis?Can psoriasis be prevented?What long-term monitoring is indicated in the treatment of psoriasis?What are the PeDRA/NPF guidelines for screening studies in pediatric patients with psoriasis?What are the guidelines on psoriasis biologic therapy?Which medications are used to treat psoriasis?Which medications in the drug class Injectable Corticosteroids are used in the treatment of Psoriasis?Which medications in the drug class Topical Combinations are used in the treatment of Psoriasis?Which medications in the drug class Interleukin Inhibitors are used in the treatment of Psoriasis?Which medications in the drug class Phosphodiesterase-4 Enzyme Inhibitors are used in the treatment of Psoriasis?Which medications in the drug class Tumor Necrosis Factor Inhibitors are used in the treatment of Psoriasis?Which medications in the drug class Immunomodulators are used in the treatment of Psoriasis?Which medications in the drug class Antimetabolites are used in the treatment of Psoriasis?Which medications in the drug class Topical Retinoids are used in the treatment of Psoriasis?Which medications in the drug class Vitamin D Analogs are used in the treatment of Psoriasis?Which medications in the drug class Keratolytic Agents are used in the treatment of Psoriasis?Which medications in the drug class Coal Tar are used in the treatment of Psoriasis?Which medications in the drug class Ophthalmic Corticosteroids are used in the treatment of Psoriasis?Which medications in the drug class Topical Corticosteroids are used in the treatment of Psoriasis?Which medications in the drug class Ophthalmic agents, Miscellaneous are used in the treatment of Psoriasis?
Jacquiline Habashy, DO, MSc, Resident Physician, Department of Dermatology, Western University of Health Sciences College of Osteopathic Medicine of the Pacific
Disclosure: Nothing to disclose.
Coauthor(s)
David T Robles, MD, PhD, FAAD, Director, Dermatology Division, Chaparral Medical Group
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Jeffrey Meffert, MD, † Former Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio
Disclosure: Nothing to disclose.
Acknowledgements
Robert Arffa, MD Clinical Assistant Professor, University of Pittsburgh School of Medicine
Robert Arffa, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.
Richard Gordon Jr, MD Staff Physician, Department of Emergency Medicine, Detroit Receiving Hospital University Health Center
Richard Gordon Jr, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, American Medical Student Association/Foundation, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Ryan I Huffman, MD Resident Physician, Department of Ophthalmology, Yale-New Haven Hospital
Disclosure: Nothing to disclose.
Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.
Randy Park, MD Chair, Associate Professor, Department of Emergency Medicine, Denton Regional Medical Center
Disclosure: Nothing to disclose.
Brian A Phillpotts, MD Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine
Brian A Phillpotts, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, and National Medical Association
Disclosure: Nothing to disclose.
Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Institute
Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, and International Society of Refractive Surgery
Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; RPS Ownership interest Other; Bausch & Lomb Honoraria Speaking and teaching; Merck Consulting fee Consulting; Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching
Adam J Rosh, MD Assistant Professor, Program Director, Emergency Medicine Residency, Department of Emergency Medicine, Detroit Receiving Hospital, Wayne State University School of Medicine
Adam J Rosh, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.
Dana A Stearns, MD Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery, Harvard Medical School
Dana A Stearns, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Laidman J. Moderate and Severe Psoriasis Linked to Higher Kidney Risks. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/812730. Accessed: October 21, 2013.
Lipper GM. Psoriasis and IBD: Is This Comorbidity for Real?. Medscape Dermatology. Available at https://www.medscape.com/viewarticle/907240. January 11, 2019; Accessed: January 15, 2019.
Brown T. Fingernail Psoriasis Data Added to Humira Prescribing Info. Medscape News & Perspective. Available at http://www.medscape.com/viewarticle/877985?src=soc_fb_170405_mscpedt_news_pharm_humira. March 30, 2017; Accessed: April 6, 2017.
Hackethal V. Guidelines on Psoriasis Comorbidity Screening in Kids Issued. Medscape News & Perspective. Available at http://www.medscape.com/viewarticle/880462?nlid=115307_1584&src=WNL_mdplsfeat_170530_mscpedit_derm&uac=106950CX&spon=33&impID=1357759&faf=1#vp_1. May 23, 2017; Accessed: May 31, 2017.
Plaque psoriasis is raised, roughened, and covered with white or silver scale with underlying erythema. Contributed by Randy Park, MD.
Plaque psoriasis is most common on the extensor surfaces of the knees and elbows. Contributed by Randy Park, MD.
Guttate psoriasis erupted in this patient after topical steroid therapy was withdrawn during a pregnancy. Contributed by Randy Park, MD.
Plaque psoriasis is raised, roughened, and covered with white or silver scale with underlying erythema. Contributed by Randy Park, MD.
Guttate psoriasis erupted in this patient after topical steroid therapy was withdrawn during a pregnancy. Contributed by Randy Park, MD.
Plaque psoriasis is most common on the extensor surfaces of the knees and elbows. Contributed by Randy Park, MD.
Nail psoriasis. Pits, distal onycholysis (nail separation), and brownish staining ("oil spots") are classic nail findings
Inverse psoriasis. Occurring in skin folds, this will often lack the scale seen in other locations.
Pustular psoriasis of the soles. This may be confined to the hands and feet (Acrodermatitis Continua of Hallepeau) or may be part of a generalized pustular psoriasis (Von Zumbusch disease)
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